Effect of schisandrin B on lung mRNA expression of transforming growth factor-β1 signal transduction molecule in rat lungs exposed to silica

Objective To investigate the effects of schisandrin B (Sch-B) on expression of transforming growth factor-β1 (TGF-β1) and signal transduction molecule mRNA in rat lungs exposed to SiO2,and explore the intervention mechanism of Sch-B on pulmonary fibrosis induced by SiO2. Methods Ninety six Wistar rats were randomly divided into control (normal saline) group, SiO2 group and SiO2 plus Sch-B group.The rats were exposed to SiO2 by direct tracheal instillation to establish the silicotic animal models. SiO2 group and SiO2 plus Sch-B group were treated with 1ml SiO2 (50 mg/ml) for each rat From the first day after model establishment, SiO2 plus Sch-B group were orally given Sch-B (80 mg/kg) a day, control group and silica group were orally given olive oil. On the 3rd, 7th,14th and 28th days after treatment, 8 rats in each group were sacrificed and samples were collected. The histo-pathological examination of lung was performed by HE staining. The expression levels of TGF-β1 、TGFβR Ⅱ and Smad4 mRNA in the lung tissues were detected by RT-PCR. Results The results of histo-pathological examination showed that in SiO2 group, lung tissues were injured obviously; the alveolar inflammation with alveolus interval edema and inflammation cell infiltration appeared on the 3rd and 7th days; the alveolus interval became thicker, became thicker, fibroblast and collagen matiix increased markedly on 14th day; the alveolar structure was damaged, alveolar wall thickened obviously,collagen aggradation and pulmonary fibrosis displayed on 28th day. The alveolar inflammation and pulmonary fibrosis in SiO2 plus Sch-B group were significantly less than those in SiO2 group. The expressions levels of TGF-β1、TGFβR Ⅱ and Smad4 mRNA (TGF-β1: 1.03±0.31 、1.33±0.39、1.08±0.26、0.82±0.16,TGF-βR Ⅱ:0.65 ±0.11、0.80 ±0.16、0.83 ±0.24、0.62 ±0.15, Smad4: 0.87 ±0. 15、0.68 ±0.11、0.78 ±0.19、0.30 ±0.08) in SiO2group were significantly higher than those in the control group (TGF-β1:0.59±0.22、0.55 ±0.25、0.56±0.20、0.55 ±0.12,TGR-βR Ⅱ:0.28 ±0.13、0.31 ±0. 15、0.34 ±0.15、0.27 ±0.09,Smad4:0.23 ±0.11、0.40 ±0. 12、0.39 ±0.12、0.18±0.06)(P＜0.01 or P＜0.05), but the expression level of TGF-β1 mRNA was the highest on the 7th day. The expression levels of TGF-β1 and Smad4 mRNA (TGF-β1: 0.68 ±0.28、0.88 ±0.25、0.75 ±0.11、0.61 ±0. 14,Smad4:0.25 ±0.12、0.45 ±0.09、0.44 ±0.07、0.21 ±0.04) in SiO2 plus Sch-B group were significantly lower than those in SiO2 group (P＜0.01 or P＜0.05),but there were no significant differences of the TGFβR Ⅱ mRNA expression levels between SiO2 group and SiO2 plus Sch-B group. Conclusion Sch-B can reduce the pulmonary fibrosis induced by SiO2 through inhibition of the mRNA express of TGF-β1 and Smad4 in the lung tissue, modulating the TGF-β1/Smad4 signal transduction pathway and inhibiting the target gene activation.     

地塞米松预处理对大鼠光气吸入性肺损伤基质金属蛋白酶-9表达的影响

Objective To investigate the effects of dexamethasone on expression of matrix metalloproteinase-9 (MMP-9) in rats with acute lung injury induced by phosgene. Methods The rats were randomly divided into 3 groups: normal control group that consists of the rats with air exposure, phosgene group that consists of the rats with phosgene exposure and dexamethasone group that consists of the rats with phosgene exposure after 2.5 mg/kg dexamethasone being injected. Wet and dry ratio of the lung (W/D) was calculated, and leukocyte count and total protein content of bronchoalveolar lavage fluid (BALF) were recorded at 2 h after exposure. The concentrations of MMP-9 in the serum and BALF were measured by enzyme-linked immunosorbent assay. The pathologic changes of lung tissues were observed under light microscopy. The immunohistochemistry and the RT-PCR were used to detect the contents of MMP-9 in the lung tissue. Results Compared with phosgene group, the lung W/D, protein content and WBC count in of BALF dexamethasone group was significantly decreased (P＜0.01). MMP-9 levels of the serum and BALF in dexamethasone group were (4.799±0.043) μg/L and (15.052±0.029) μg/L, respectively, which were significantly lower than those [(9.439±0.100) and (20.640±0.446) μg/L] in phosgene group (P＜0.01). Compared with phosgene group (2.789±0.282), the expression level(1.183±0.260) of lung M MP-9 mRNA in dexamethasone group was significantly lower than that in phosgene group (P＜0.01).Histological experimental results showed the marked hyperemia and thickening of alveolar wallsand stroma cells infiltrating and more visible alveolar structure damage of alveolar walls in phosgene group while the alveolar structure and the alveolar walls were clear and slightly thickened with inflammatory cells in dexamethasone group. Immunohistochemical results showed that MMP-9 protein expression levels of lung and brochus tissues in normal control group and dexamethasone group were weakly positive, which in phosgene group were strongly positive. Conclusion Dexamethasone has a beneficial effects on acute lung injury induced by phosgene in rats due to the inhibiting MMP-9.     

大剂量N-乙酰半胱氨酸对染尘大鼠肺组织的影响

目的 观察大剂量N-乙酰半胱氨酸(NAC)对矽肺形成过程中炎症和纤维化反应的影响.方法 将Wisar大鼠随机分为模型组、干预组、对照组,每组32只.模型组和干预组以二氧化硅结晶体诱发染尘大鼠模型,干预组以大剂量NAC进行干预.分别在染尘后的第3、7、14、28天处死8只大鼠.对大鼠肺组织进行HE染色及Masson染色,观察肺组织病理变化.用酶联免疫法(EusA)测定肺泡灌洗液中肿瘤坏死因子-α(TNF-α)和白细胞介素-8(IL-8)的含量.结果 NAC干预组病理观察显示,肺泡炎症和纤维化程度均较模型组明显减轻.与模型组(13.84±1.61、9.23±0.87、11.23±1.25、9.56±0.76)比较,第3、7、14、28天十预组肺脏系数(9.30±0.78、6.29±0.74、7.63±0.88、6.06±1.16)均明显降低.差异有统计学意义(P＜0.01.与对照组相比,各时间点模型组肺泡灌洗液中TNF-α和IL-8含量均明显升高,差异有统计学意义(P＜0.01);与模型组相比,各时间点干预组的TNF-α和IL-8含量均明显降低,差异有统计学意义(P＜0.01).结论 早期大剂量NAC干预能够明显减轻染尘大鼠的肺组织炎症,降低肺泡灌洗液中TNF-α和IL-8含量,抑制和延缓肺纤维化的发生.

Abstract：

Objective To explore the effects of high-dose N-acetylcysteine on the lung tissues of rats exposed to silica. Methods Ninety-six Wistar rats were randomly divided into model group, intervention group and control group (32 rats for each group). The rats of model group and intervention group were exposed to silica by intratracheal infusion of silica dust suspension. The rats in the intervention group were orally given high dose N-acetylcysteine. In 3,7,14,28 days after exposure, eight rats in each group were sacrificed, respectively and the lung samples were collected. The pathological changes of lung were evaluated by HE and Masson staining methods. The levels of TNF-α and IL-8 in the BALF were detected by ELISA. Results Compared with the control group, the alveolitis and pulmonary fibrosis in the intervention group were significantly reduced. In 3,7,14,28 days after exposure, the lung/body coefficients in the intervention group were 9.30±0.78, 6.29±0.74,7.63±0.88,6.06+1.16 respectively, which were significantly lower than those (13.84±1.61,9.23±0.87, 11.23±1.25,9.56±0.76, P＜0.01 )in the model group (P＜0.01). At the different time points, the levels of TNF-α and IL-8 in the BALF in the intervention group were significantly higher than those in the control group (P＜0.01), but were significantly lower than those in the model group (P＜0.01). Conclusion The intervention with high dose N-acetylcysteine can significantly reduce the alveolitis and the TNF-α and IL-8 levels in the BALF, therefore, inhibit and delay the development of pulmonary fibrosis of rats exposed to silicon dioxide.     

博莱霉素致大鼠肺纤维化原癌基因c-erbB2和肺表皮生长因子受体的表达

目的 探讨肺纤维化模型大鼠肺组织中原癌基因c-erbB2激活和肺表皮生长因子受体(EGFR)的表达.方法 将54只Wistar大鼠随机分成博莱霉素(BLM)组、EGFR拮抗剂Iressa组和对照组,每组18只.用BLM(5 mg/kg)气管注射制造大鼠肺纤维化模型,对照组气管注入生理盐水O.2～0.3ml;Iressa组造模前1 h灌胃给予Iressa(200 mg/kg),BLM组和对照组用生理盐水10 ml/kg灌胃,每组均灌胃5次/周,分别于第1、14、28天处死大鼠.观察大鼠肺组织病理改变,用免疫组化法检测肺组织原癌基因c-erbB2和EGFR的表达.结果 Iressa组大鼠肺组织可见纤维化并炎性细胞浸润,与BLM 组变化规律相同,肺纤维化程度低于BLM组.第28天Iressa组肺纤维化评分(2.17±0.41)明显低于BLM组(3.50±0.84),差异有统计学意义(P＜0.01).各时间点BLM组和Iressa组c-erbB2和EGFR表达均明显高于对照组,差异有统计学意义(P＜0.01).Iressa组的c-erbB2表达与BLM组变化规律一致,均随时间的延长,c-erbB2表达逐渐下降,不同时间的c-erbB2表达比较,差异有统计学意义(P＜0.01).Iressa组的c-erbB2表达与BLM组比较,差异无统计学意义(P＞0.05).Iressa组于第14、28天时肺组织中EGFR表达水平为0.17±0.02和0.28+0.04,明显低于BLM组(0.27+0.04、0.34±0.02),差异有统计学意义(P＜0.01).Iressa组第28天EGFR表达明显高于第14天,差异有统计学意义(P＜0.01).结论 c-erbB2和EGFR在大鼠肺泡炎及肺纤维化不同阶段表达增强,c-erbB2和EGFR可能参与了肺纤维化的发生.

Abstract：

Objective To study the expression of the epidermal growth factor receptor( EGFR) and the oncogene c-erbB2 on pulmonary fibrosis induced by bleomycin( BLM) in rats. Methods Fifty-four Wistar rats were randomly divided into three groups, the pulmonary fibrosis group (BLM), Iressa group and the control group. There were 18 rats in each group. Control group were injected with saline 0.2~0.3 ml in trachea.Iressa group and BLM group were injected with BLM intratracheal. After the fibrosis models were build, Iressa group were given orally Iressa(200 mg/kg)l h before modeling in Iressa group, saline were fed 10 ml/kg in BLM group and control group. The three groups were fed 5 times per week; and were sacrificed after treatment on days 1, 14and 28 respectively. The lungs were harvested for histological studies. Results The lung tissue in Iressa group showed fibrosis and inflammatory cell infiltration, the same as shown in the BLM group. The pulmonary fibrosis score was significantly lower than the BLM group on the 28 th day (2.17±0.41 vs 3.50±0.84, P＜0.01). Compared with the control group, c-erbB2 and EGFR were hyperexpressed significantly both in BLM group and Iressa group at all time points (P＜0.01); c-erbB2 expression had no changes between the Iressa group and the BLM (P＞0.05), that were gradually decreased, and was significantly different at each time point (P＜0.01). EGFR expression was increased gradually on the 14th and 28th day (0.17±0.02 and 0.28±0.04)in Iressa group ,that was significantly lower than the BLM group (0.27±0.04 and 0.34±0.02)(P＜0.01). EGFR expression increased significantly on the 28th day than on the 14th day in the Iressa group(P＜0.01). Conclusion The expression of C-erbB2 and EGFR are enhanced in different stages of alveolitis and pulmonary fibrosis, c-erbB2 and EGFR may be participated in different stages of pulmonary fibrosis.     

五味子乙素对染矽尘大鼠肺组织转化生长因子β1信号转导通路分子mRNA表达的影响

目的 观察五味子乙素(sehisandrin B,Sch-B)对染矽尘大鼠肺组织转化生长因子β1(TGF-β1)信号通路分子mRNA表达的影响,探讨其防治矽肺纤维化的作用及机制.方法 将96只Wistar大鼠随机分为对照组、染矽尘组、Sch-B干预组,每组32只,气管暴露法一次性染尘建立大鼠矽肺模型,染矽尘组和Sch-B干预组每只大鼠气管内注入1 ml(50 mg/ml)SiO2混悬液,对照组注入1 ml灭菌生理盐水.染尘后第1天开始灌胃干预,Sch-B组给予Sch-B(80mg·kg-1/d-1),染矽尘组和对照组给予等体积的橄榄油.不同处理3、7、14和28 d后,各组处死8只大鼠,对肺组织HE染色观察病理改变;用反转录-聚合酶链式反应(RT-PCR)法测定大鼠肺组织中TGF-β1、转化生长因子βⅡ型受体(TGF-βRⅡ)和Smad4基因表达.结果 染矽尘组肺损伤明显,在3和7 d时表现为明显的肺泡炎,可见肺泡间隔水肿,大量炎性细胞浸润,在14d时,肺泡间隔明显增宽,成纤维细胞和胶原基质明显增多;在28 d时,肺泡结构破坏,肺泡壁明显增厚,肺组织以胶原沉积和肺纤维化改变为主.Sch-B组肺泡炎和肺纤维化程度均较染矽尘组明显减轻.染矽尘组3、7、14、28 d时大鼠肺内TGF-β1、TGF-βRⅡ和Smad4的mRNA表达(TGF-β1:1.03±0.31、1.33±0.39、1.08±0.26、0.82±0.16,TGF-βRⅡ:0.65±0.11、0.80±0.16、0.83±0.24、0.62±0.15,Smad4:0.87±0.15、0.68±0.11、0.78±0.19、0.30±0.08)均明显高于对照组(TGF-β1:0.59±0.22、0.55±0.25、0.56±0.20、0.55±0.12,TGR-βRⅡ:0.28±0.13、0.31 ±0.15、0.34±0.15、0.27±0.09,Smad4:0.23±0.11、0.40±0.12、0.39±0.12、0.18±0.06),差异均有统计学意义(P＜0.01或P＜0.05),其中TGF-β1在第7天时达高峰后开始下降.Sch-B干预组各时间点TGF-β1和Smad4(TGF-β1:0.68±0.28、0.88±0.25、0.75±0.11、0.61±0.14,Smad4:0.25±0.12、0.45±0.09、0.44±0.07、0.21±0.04)均低于染矽尘组,差异有统计学意义(P＜0.01或P＜0.05).与染矽尘组相比,Sch-B干预组TGF-βRⅡmRNA表达无明显改变,差异无统计学意义(P＞0.05).结论 Sch-B能减轻染矽尘大鼠肺组织的纤维化程度,其作用机制可能是通过抑制TGF-β1和Smad4的mRNA表达上调,从而干扰TGF-β1/Smad4信号通路对靶基因的激活来实现的.

Abstract：

Objective To investigate the effects of schisandrin B (Sch-B) on expression of transforming growth factor-β1 (TGF-β1) and signal transduction molecule mRNA in rat lungs exposed to SiO2,and explore the intervention mechanism of Sch-B on pulmonary fibrosis induced by SiO2. Methods Ninety six Wistar rats were randomly divided into control (normal saline) group, SiO2 group and SiO2 plus Sch-B group.The rats were exposed to SiO2 by direct tracheal instillation to establish the silicotic animal models. SiO2 group and SiO2 plus Sch-B group were treated with 1ml SiO2 (50 mg/ml) for each rat From the first day after model establishment, SiO2 plus Sch-B group were orally given Sch-B (80 mg/kg) a day, control group and silica group were orally given olive oil. On the 3rd, 7th,14th and 28th days after treatment, 8 rats in each group were sacrificed and samples were collected. The histo-pathological examination of lung was performed by HE staining. The expression levels of TGF-β1 、TGFβR Ⅱ and Smad4 mRNA in the lung tissues were detected by RT-PCR. Results The results of histo-pathological examination showed that in SiO2 group, lung tissues were injured obviously; the alveolar inflammation with alveolus interval edema and inflammation cell infiltration appeared on the 3rd and 7th days; the alveolus interval became thicker, became thicker, fibroblast and collagen matiix increased markedly on 14th day; the alveolar structure was damaged, alveolar wall thickened obviously,collagen aggradation and pulmonary fibrosis displayed on 28th day. The alveolar inflammation and pulmonary fibrosis in SiO2 plus Sch-B group were significantly less than those in SiO2 group. The expressions levels of TGF-β1、TGFβR Ⅱ and Smad4 mRNA (TGF-β1: 1.03±0.31 、1.33±0.39、1.08±0.26、0.82±0.16,TGF-βR Ⅱ:0.65 ±0.11、0.80 ±0.16、0.83 ±0.24、0.62 ±0.15, Smad4: 0.87 ±0. 15、0.68 ±0.11、0.78 ±0.19、0.30 ±0.08) in SiO2group were significantly higher than those in the control group (TGF-β1:0.59±0.22、0.55 ±0.25、0.56±0.20、0.55 ±0.12,TGR-βR Ⅱ:0.28 ±0.13、0.31 ±0. 15、0.34 ±0.15、0.27 ±0.09,Smad4:0.23 ±0.11、0.40 ±0. 12、0.39 ±0.12、0.18±0.06)(P＜0.01 or P＜0.05), but the expression level of TGF-β1 mRNA was the highest on the 7th day. The expression levels of TGF-β1 and Smad4 mRNA (TGF-β1: 0.68 ±0.28、0.88 ±0.25、0.75 ±0.11、0.61 ±0. 14,Smad4:0.25 ±0.12、0.45 ±0.09、0.44 ±0.07、0.21 ±0.04) in SiO2 plus Sch-B group were significantly lower than those in SiO2 group (P＜0.01 or P＜0.05),but there were no significant differences of the TGFβR Ⅱ mRNA expression levels between SiO2 group and SiO2 plus Sch-B group. Conclusion Sch-B can reduce the pulmonary fibrosis induced by SiO2 through inhibition of the mRNA express of TGF-β1 and Smad4 in the lung tissue, modulating the TGF-β1/Smad4 signal transduction pathway and inhibiting the target gene activation.     

石英尘和博莱霉素诱导的大鼠肺纤维化模型的比较研究

目的 比较石英尘和博莱霉素诱导的大鼠肺纤维化模型中的肺泡炎和早期纤维化改变,并对其机制进行探讨.方法 将大鼠随机分为SiO2组(14只,气管内注入40mg/ml SiO2混悬液1 ml)、BLM组(14只,气管内注入5 mg/kg BLM A5)和对照组(14只,气管内注入1 ml无菌生理盐水).在造模后7、14 d每组各处死7只动物,取肺组织病理切片行HE染色,对肺泡炎进行计分,行饱和苦味酸天狼猩红染色,采用图像分析系统测得各组胶原面积后,进行定量分析,免疫组织化学技术检测肺组织中CD68和TNF-α蛋白表达情况,采用图像分析计算累积吸光度值,进行半定量分析.结果 (1)HE染色光学显微镜下可见,BLM组7d时肺泡炎(肺泡炎评分2.814±0.832)最明显,偏振光下显示BLM组14d时肺纤维化[胶原面积(1284.57±554.72)μm2)]最严重,均明显高于对照组和同期SiO2组,差异有统计学意义(P＜0,05).(2)免疫组化结果显示,BLM组7 d时TNF-α表达最高(17.100±1.831),明显高于对照组(0.420±0.020)、SiO2组7 d(7.909±1.275)及BLM组14d(13.506±1.454),差异均有统计学意义(P＜0.05);在SiO2组14 d时TNF-α表达为22.778±2.512,明显高于BLM组(14 d)、对照组及SiO2组(7 d),差异有统计学意义(P＜0.05).14 d时,SiO2组CD68表达明显高于对照组、BLM组(14 d)及SiO2组(7d),差异有统计学意义(P＜0.05).结论 BLM诱导的大鼠肺损伤模型的早期肺泡炎重于SiO2诱导的大鼠肺损伤模型,纤维化进程早于SiO2诱导的大鼠肺损伤模型,TNF-α在两种模型的病程中均起着重要的作用,而巨噬细胞更为持续地参与了SiO2诱导的肺纤维化.

Abstract：

Objective To compare the pulmonary alveolitis and the early fibrosis of pulmonary fibrosis induced by quartz dust and bleomycin in rats, and investigate their mechanism. Methods The female rats were divided into three groups: control group exposed to normal saline by the trachea; SiO2 group exposed to SiO2 by the trachea; BLM group exposed to BLM A5 by the trachea. Each half of the animals were sacrificed on the 7th andl4th day after expoasure. The lungs of rats were collected to observe pulmonary alveolitis by HE staining and to observe fibrosis by saturated picric acid sirius red staining. The expression of tumor necrosis factor-α (TNF-α) and CD68 in pulmonary tissues were analyzed quantitatively by immunohistochmistry and image analysis system. Results (1) The alveolitis and pulmonary fibrosis of rats in both SiO2 group and BLM group were became more serious gradually over time, HE staining under light microscope showed that BLM group on the 7th day had the most obvious alveolitis (2.814±0.832), the saturated picric acid sirius red staining under polarized light showed that BLM group on the 14th day had the worst pulmonary fibrosis (1284.57±554.72), which were significantly higher than those (103.69±18.29 and 111.78±37.45) in control group and SiO2 group on the 7th day (P＜0.05). (2) The results of immunohistochmistry examination indicated that the expression (17.100±1.831) of TNF-α in the BLM group on the 7th day was significantly higher than those (0.451 ±0.441, 7.909±1.275 and 13.506±1.454) in control group, SiO2 group on 7th day and BLM group on 14th day (P＜0.05). The expression (22.778 ±2.512) of TNF-a in the SiO2 group on the 14th day was significantly higher than those in control group, SiO2 group on 7th day and BLM group on 14th day (P＜0.05).The expression (134.941 ±35.951) of CD68 in the SiO2 group on the 14th day was significantly higher than those in control group,SiO2 group on 7th day and BLM group on 14th day(P＜0.05).Conclusion The early alveolitis of BLM-induced lung injury model was more serious than that of SiO2-induced lung injury model,and the fibrosis process of BLM-induced lung injury model was earlier than that of SiO2-induced lung injury model.TNF-α plays an important role in the conrse of both models.but macrophages is involved in Si06nduced pulmonary in a more continuous way than in BLM-induced pulmonary fibrosis.     

甲醛吸入急性肺水肿大鼠心、肺、脑、肝和血清蛋白浓度及一氧化氮合酶活力变化

目的 研究甲醛吸人性急性肺水肿模型大鼠心、肺、脑、肝和血清蛋白浓度及一氧化氮合酶(NOS)活力的变化,为研究此类肺水肿提供实验依据.方法 健康成年清洁级SD大鼠18只随机分为对照组和模型组,在染毒箱内以"静态+喷雾"吸入40%甲醛2 h复制急性肺水肿模型,8 h后眼球采血并处死,按试剂盒说明书测定血清及心、肺、脑、肝组织匀浆的蛋白浓度和NOS活力,并计算心肺系数、心指数和肺指数,肺组织作常规病理检查.对照组将甲醛换为生理盐水,处理方法同模型组.结果 与生理盐水对照组比较,模型组心肺系数显著增大(P<0.05),病理切片显示模型组出现肺组织间隙增大、大量有核细胞浸润等肺水肿改变;血清、心脏、脑和肺匀浆蛋白浓度显著增加(P<0.05或P<0.01),肝蛋白浓度差异无统计学意义(P>0.05);血清、心、肺、脑、肝NOS活力无统计学意义(均P>0.05).结论 甲醛吸入性急性肺水肿大鼠血清、心脏、脑和肺蛋白含量增加.NOS活力变化不大.

Abstract：

Objective To study the changes of the protein concentration (Cpro) and nitric oxide synthase (NOS) of serum, heart, lungs, brain and liver in acute pulmonary edema rats model induced by formaldehyde inhalation, to provide data for studying in acute pulmonary edema animal model induced by formaldehyde inhalation. Methods Eighteen SD female rats were randomly divided into the control group and the model group, and the model group rats were inhaled vaporous formaldehyde in a self-made cabinet for 2 hours and were sacrificed 8 hours later. The blood sampling, lungs, heart, brain and liver were collected and lungs/ heart index, heart/body weight index and lungs/body weight index were calculated, NOS were detected with NOS kit and protein determination kit, and the pathological examination of lungs tissue was done. Rats of control group were treated as the same as model group, but formaldehyde was replaced by normal saline. Results Compared with the control, lungs/heart index increased significantly (P<0.05) in the model rats, the lungs pathological examination showed that pulmonary tissue space broadening and filled with lots of nucleated cells in the model rats. Protein concentration of serum, heart, brain and lungs increased significantly (P<0.05 or P<0.01) in model rats, but no significant change was seen in NOS of serum, brain, heart, liver and lungs (P>0.05). Conclusion In acute pulmonary edema rats induced by formaldehyde inhalation, the protein concentration of serum, heart, brain and lungs tissues increase significantly, NOS does not change obviously.     

Effects of silicotic alveolar macrophages exposed to SiO2 on the expression of type Ⅲ collagen and type Ⅲ procollagen in human lung fibroblasts

Objective To study the effects of supernatant of alveolar macrophages (AM) exposed to SiO2 on the expression of type Ⅲ collagen and type Ⅲ procollagen in human lung fibroblasts (HELF) and the intervention effects of anti-TGF-β1 antibody Methods AMs collected from a silicotic by bronchoalveolar lavage were divided into 2 parts, one part was exposed to SiO2 and other part served as control. The supernatant was obtained from AMs cultured for 18 h. HELF were divided into (1) exposure group, which was added with supernatant from AMs exposed to SiO2; (2) control group, which was added with the supernatant from AMs not exposed to SiO2; (3) blank control group, which was added with DMEM; (4) exposure group plus anti-TGF-β1antibody (10μg/ml); (5) control group plus anti-TGF-β1 antibody (10 μg/ml). (1)-(3) groups were cultured for 6, 12, 18, 24, 36, 48h, respectively. (4)-(5) groups were cultured for 18, 24, 36, respectively.Immunocytochemical test and Western blot assay were used to detect pC Ⅲ expression levels in HELF and C Ⅲ expression levels in the supernatant of HELF culture, respectively. Results The pC Ⅲ expression levels of exposure group were 0.1423 ±0.0107,0.1624±0.0011,0.1925 ±0.0050,0.2421 ±0.0097 and 0.2103 ±0.0103,respectively, which were significantly higher than those (0.1212±0.0079、0.1414±0.0058、0.1620±0.0081、0.1965±0.0103 、0.1715±0.0116) of control group (P＜0.05 or P＜0.01). The C Ⅲ levels of exposure group were (0.2559±0.0061、0.3249±0.0110、0.4171±0.0193、0.5441 ±0.0452、0.4751±0.0252), respectively, which were significantly higher than control group (0.2296±0.0121、0.2778±0.0116、0.3367±0.0269、0.3722±0.0214). The pC Ⅲ and C Ⅲ expression levels of exposure plus anti-TGF-β1 antibody group were significantly lower than those of control plus anti-TGF-β1 antibody group (P＜0.05 or P＜0.01).Conclusion AMs exposed to SiO2 can induce the elevated pC Ⅲ and C Ⅲ expression levels in HELF by TGF-β 1 to some extent.     

地塞米松预处理对大鼠光气吸入性肺损伤基质金属蛋白酶-9表达的影响

目的 探讨地塞米松对大鼠光气吸入性急性肺损伤(ALI)基质金属蛋白酶-9(MMP-9)表达的影响.方法 将SD大鼠随机分为3组:正常对照组(吸入与光气染毒组同等流量的空气)、光气染毒组(吸入8.33 mg/L的光气)、地塞米松预处理组(尾静脉注入2.5 mg/kg地塞米松1 h后,吸入8.33 mg/L的光气).染毒2 h后,收集支气管肺泡灌洗液(BALF)测定中性粒细胞细胞数、蛋白含量和肺湿/干重比(W/D).用放射免疫法测定各组血清和BALF中MMP-9水平.进行肺组织的病理学检查,用免疫组化法和实时定量聚合酶链反应(PCR)测定MMP-9表达的变化.结果 与染毒组比较,预处理组大鼠肺W/D、BALF中中性粒细胞数和蛋白含量明显降低,差异有统计学意义(P＜0.01).与染毒组[血清:(9.439±0.100)μg/L、BALF:(20.640±0.446)μg/L]比较,预处理组MMP-9含量[血清(4.799±0.043)μg/L、BALF:(15.052±0.029)μg/L]明显降低,差异有统计学意义(P＜0.01).与染毒组(2.789±0.282)比较,预处理组MMP-9mRNA的表达量(1.183±0.260)明显降低,差异有统计学意义(P＜0.01).染毒组肺泡壁明显充血、增厚,肺泡壁和肺间质内可见较多白细胞浸润以及肺泡结构破坏;预处理组肺泡结构较为清晰,肺泡壁稍增厚,伴少量炎性细胞浸润.正常对照组大鼠肺、支气管组织中MMP-9蛋白表达呈弱阳性,染毒组MMP-9蛋白表达呈强阳性,预处理组肺、支气管组织中MMP-9蛋白表达明显减弱.结论 地塞米松能有效地保护大鼠光气吸入性ALT,可能通过抑制MMP-9表达而达到肺保护作用.

Abstract：

Objective To investigate the effects of dexamethasone on expression of matrix metalloproteinase-9 (MMP-9) in rats with acute lung injury induced by phosgene. Methods The rats were randomly divided into 3 groups: normal control group that consists of the rats with air exposure, phosgene group that consists of the rats with phosgene exposure and dexamethasone group that consists of the rats with phosgene exposure after 2.5 mg/kg dexamethasone being injected. Wet and dry ratio of the lung (W/D) was calculated, and leukocyte count and total protein content of bronchoalveolar lavage fluid (BALF) were recorded at 2 h after exposure. The concentrations of MMP-9 in the serum and BALF were measured by enzyme-linked immunosorbent assay. The pathologic changes of lung tissues were observed under light microscopy. The immunohistochemistry and the RT-PCR were used to detect the contents of MMP-9 in the lung tissue. Results Compared with phosgene group, the lung W/D, protein content and WBC count in of BALF dexamethasone group was significantly decreased (P＜0.01). MMP-9 levels of the serum and BALF in dexamethasone group were (4.799±0.043) μg/L and (15.052±0.029) μg/L, respectively, which were significantly lower than those [(9.439±0.100) and (20.640±0.446) μg/L] in phosgene group (P＜0.01). Compared with phosgene group (2.789±0.282), the expression level(1.183±0.260) of lung M MP-9 mRNA in dexamethasone group was significantly lower than that in phosgene group (P＜0.01).Histological experimental results showed the marked hyperemia and thickening of alveolar wallsand stroma cells infiltrating and more visible alveolar structure damage of alveolar walls in phosgene group while the alveolar structure and the alveolar walls were clear and slightly thickened with inflammatory cells in dexamethasone group. Immunohistochemical results showed that MMP-9 protein expression levels of lung and brochus tissues in normal control group and dexamethasone group were weakly positive, which in phosgene group were strongly positive. Conclusion Dexamethasone has a beneficial effects on acute lung injury induced by phosgene in rats due to the inhibiting MMP-9.     

吡非尼酮抗百草枯中毒小鼠肺纤维化的研究

目的 探讨吡非尼酮(PF)对百草枯(PQ)中毒小鼠肺纤维化的治疗作用,为临床治疗提供理论依据.方法 雄性ICR小鼠90只,随机分为正常对照组、PQ组、地塞米松组、25、50和100 mg/kgPF组,每组15只.正常对照组小鼠一次性空腹灌胃给予生理盐水,2 h后给予质量分数为1%羧甲基纤维素(CMC)灌胃,再每天定时空腹灌胃同等量CMC;PQ组、地塞米松组及各PF剂量组小鼠给予PQ100mg/kg一次性灌胃染毒,灌胃后2 h,再每天定时PQ组给予0.02ml/10 gCMC灌肠,PF组给予PF(25、50、100 mg/kg)和地塞米松(0.02 ml/10 g)灌胃,每天1次,共49 d.计算肺系数,HE染色,光学显微镜下观察肺组织病理改变;测定肺组织羟脯氨酸(HYP)含量,转化生长因子(TGF-β1)的mRNA表达水平、蛋白表达水平,支气管肺泡灌洗液(BALF)中的TGF-β1蛋白含量.结果 PQ组3 d生存率为53.33%,25、50、100 mg/kg PF组3 d生存率分别为46.67%、73.33%、86.67%,地塞米松组3 d生存率为80%,地塞米松组、50、100 mg/kg PF组3 d生存率明显高于PQ组和25 mg/kg PF组,差异有统计学意义(P＜0.05).25、50及100mg/kg PF组小鼠肺系数均明显低于PQ组,差异有统计学意义(P＜0.05).地塞米松组肺组织中HYP含量为(50.95±11.65)mg/g,25、50、100mg/kg PF组HYP含量分别为(44.52±9.48)、(43.27±6.01)、(40.82±5.90)mg/g,较PQ组[(74.27±3.68)mg/g]明显下降,差异均有统计学意义(P＜0.01).地塞米松组BALF中TGF-β1蛋白含量为(22.03±7.27)mg/ml,25、50、100 mg/kg PF组TGF-β1蛋白含量分别为(55.33±17.50)、(27.75±5.84)、(21.31±6.82)mg/ml,与PQ组[(52.52±15.51)mg/ml]相比,明显降低,差异有统计学意义(P＜0.01);100 mg/kg PF组肺组织TGF-β1mRNA表达水平与PQ组相比,明显下降,差异有统计学意义(P＜0.01)与PQ组比较,地塞米松组,50、100mg/kgPF组肺组织中TGF-β1蛋白表达下降,差异有统计学意义(P＜0.01).结论 PF可以减少百草枯中毒小鼠肺组织胶原沉积,减轻肺部纤维化程度.

Abstract：

Objective To study the curative effects of pirfenidone (PF)on pulmonary fibrosis induced by paraquat (PQ) in mice and to provide the theoretical basis for clinical treatment. Methods Ninety adult healthy male ICR mice were randomly divided into six groups: control group, PQ group , 2 mg/kg Dexamethasone group, 25 mg/kg PF group, 50 mg/kg PF group and 100 mg/kg PF group, there were 15 mice in each group. The corresponding volume of normal saline was given to the each mouse in control group according to the weight, after 2 h 0.1% CMC was given to the each mouse of control group one time by intragastric administration, then the CMC was administrated at regular time until sacrifice. All mice for other 5 groups were exposed to 100 mg/kg PQ by intragastric administration. At 2 h after exposure to PQ, 0.02 ml/10 g dexamethasone and 25、50、100 mg/kg PF were given to mice for dexamethasone group and for 3 PF groups by intragastric administration each day for 49 days, respectively. The lung coefficient was calculated and pathological changes of lung tissue were observed by HE staining for each mouse. The hydroxyproline (HYP)level in lung tissue was measured for each mouse. The mRNA level of and the protein level of TGF-β1 in lungtissue for each mouse were determined, and the protein level of TGF-β1 in the bronchus-alveolus lavage fluid (BALF) of each mouse was detected. Results The survival rates on the 3rd day in PQ group, 3 PF groups and dexamethasone group were 53.33%, 46.67%, 73.33%, 86.67% and 80%, respectively. The survival rates on the 3rd day in dexamethasone group, 50 mg/kg and 100 mg/kg PF groups were significantly higher than those of PQ group and 25 mg/kg PF group (P＜0.05). The lung coefficients of 3 PF groups were significantly lower than that of the PQ group (P＜0.05). The lung tissue HYP levels of dexamethasone group and 3 PF groups were 50.95±11.65, 44.52±9.48, 43.27±6.01 and 40.82±5.90 mg/g respectively, which were significantly lower than that (74.27±3.68) of PQ group(P＜0.01 ). The TGF-β1 protein levels of BALF in dexamethasone group, 50 and 100 mg/kg PF groups were 22.03±7.27, 27.75±5.84 and 21.31 ±6.82 ng/ml respectively, which were significantly lower than that(52.52±15.51 ) ng/mlof PQ group(P＜0.01 ). The expression level of TGF-β1 mRNA in 100 mg/kg PF group decreased significantly, as compared with PQ group (P＜0.01). Conclusion PF could reduce the collagen deposition and pulmonary fibrosis induced by PQ in mice lungs.     

实验性糖尿病大鼠肺组织晚期糖基化终末产物、肺表面活性物质蛋白质A免疫组织化学分析

Objective To approach the changes of advanced glycosylated end products (AGEs),surfactant proteins A (SP-A) in the lung of experimental diabetic rats and their relationship. Methods 48 male SD rats were divided into diabetes mellitus (DM) group and control group, each group with 24 rats.The DM rat model was made by injecting streptozocin (60mg/kg) into caudal vein. The rats were killed and the lung was individually taken out at the end of 4, 12 and 20 weeks after the models were established. The changes of AGEs, SP-A in rats lung were observed with immunohistochemical assay and the images were analyzed( black is minimum of gray, white is maximum of gray ). Results We observed a great quantity of AGEs positive cells in the alveolar epithelial cells, bronchial mucosal epithelium, angio-endothelial cell and smooth muscle cells of the DM rats. The average gray (AG) was inferior to that of the controls(4weeks 93.92 ± 7.92 vs 104. 75 ± 8. 20; 12 weeks 76. 25 ± 6. 76 vs 93.50 ± 7.56; 20 weeks 47.63 ± 7.96 vs 142. 38 ± 19. 76; P ＜0. 05) and decreased with the DM course. In the 4 weeks DM rats, there were a few SP-A positive cells in the type Ⅱ alveolar epithelial cells, Clara cells and alveolar macrophage cells. In the 12 and 20 weeks DM rats, there were a great many CTGF and TGF-β1 positive cells. The AG was inferior to that of the controls( 12 weeks 75.63 ± 6. 70 vs 110. 50 ± 13.20;20 weeks 47.38 ± 4. 84 vs 97. 25 ± 9. 87; P ＜ 0. 01 ). Conclusion With the progress of diabetes, DM rats' pulmonary alveolar type Ⅱ cells injury appeared, that might be related with the deposition of AGEs.     

实验性糖尿病大鼠肺组织晚期糖基化终末产物、肺表面活性物质蛋白质A免疫组织化学分析

Objective To approach the changes of advanced glycosylated end products (AGEs),surfactant proteins A (SP-A) in the lung of experimental diabetic rats and their relationship. Methods 48 male SD rats were divided into diabetes mellitus (DM) group and control group, each group with 24 rats.The DM rat model was made by injecting streptozocin (60mg/kg) into caudal vein. The rats were killed and the lung was individually taken out at the end of 4, 12 and 20 weeks after the models were established. The changes of AGEs, SP-A in rats lung were observed with immunohistochemical assay and the images were analyzed( black is minimum of gray, white is maximum of gray ). Results We observed a great quantity of AGEs positive cells in the alveolar epithelial cells, bronchial mucosal epithelium, angio-endothelial cell and smooth muscle cells of the DM rats. The average gray (AG) was inferior to that of the controls(4weeks 93.92 ± 7.92 vs 104. 75 ± 8. 20; 12 weeks 76. 25 ± 6. 76 vs 93.50 ± 7.56; 20 weeks 47.63 ± 7.96 vs 142. 38 ± 19. 76; P ＜0. 05) and decreased with the DM course. In the 4 weeks DM rats, there were a few SP-A positive cells in the type Ⅱ alveolar epithelial cells, Clara cells and alveolar macrophage cells. In the 12 and 20 weeks DM rats, there were a great many CTGF and TGF-β1 positive cells. The AG was inferior to that of the controls( 12 weeks 75.63 ± 6. 70 vs 110. 50 ± 13.20;20 weeks 47.38 ± 4. 84 vs 97. 25 ± 9. 87; P ＜ 0. 01 ). Conclusion With the progress of diabetes, DM rats' pulmonary alveolar type Ⅱ cells injury appeared, that might be related with the deposition of AGEs.     

重建手术对膝关节内侧副韧带愈合的影响

Objective To provide histological evidence for clinic tendon reconstruction on severe medial collateral ligament injury in rabbits. Methods Medial collateral ligaments of two knee joints were completely incised to create own control model of MCL rupture. The operation group intimated the procedure of human being MCL reconstruction with semitendinous tendon. In the 4th,12th,16th,24th weeks, healing of MCL was observed by anatomy and the picrosirius-polarization method. Results In the 4th week, the MCL healing tissue of ex-periment group is more than control group. The average ratios of type Ⅲ collagen to Ⅰ, Ⅲ collagen in the experiment group [(0.263±0.075), (0.235±0.041), (0.210±0.045), (0.197±0.029)] were significantly lower than those in control group [(0.310±0.072), (0.286±0.045), (0.261±0.046), (0.236±0.043) ] in the 4th, 12th, 16th, 24th weeks, respectively (P < 0.05). Conclusions The semitendinons tendon reconstruction can improve MCL healing in early and middle period after injury.     

急性二氧化碳中毒大鼠不同氧疗效果评价

目的 研究急性二氧化碳中毒大鼠应用不同氧疗的效果,以筛选急性二氧化碳中毒现场最佳氧疗技术.方法 健康雄性SD大鼠60只,随机分为正常对照组、二氧化碳染毒组、高压氧治疗组(压力为2 ATA、氧浓度100%)、高浓度常压吸氧治疗组(氧浓度50%)、低浓度常压吸氧治疗组(氧浓度33%).以二氧化碳吸入制作急性二氧化碳中毒大鼠模型,给予不同方式氧疗后,检测各组大鼠动脉血pH、氧分压(PO2)和二氧化碳分压(PCO2),取肺组织和脑组织,观察病理变化.结果 二氧化碳染毒组动脉血pH(7.31±0.06)和PO2[(68.50±15.02)mm Hg]比正常对照组[pH(7.42±0.02)和PO2(92.83±8.27)mm Hg]低,PCO2[(71.66±12.10)mm Hg]比正常对照组[(48.25±2.59)mm Hg]高,差异均有统计学意义(P＜0.05);高压氧治疗组、高浓度常压吸氧治疗组、低浓度常压吸氧治疗组动脉血pH(分别为7.37±0.02、7.39±0.03、7.38±0.02)和PO2[分别为(82.25±12.98)、(84.75±11.24)、(83.75±16.77)mm Hg]比二氧化碳染毒组高,PCO2[分别为(52.25±4.95)、(51.75± 4.82)、(52.66±5.61)mm Hg]比二氧化碳染毒组低,差异均有统计学意义(P＜0.05);各氧疗组动脉血pH、PO2和PCO2与正常对照组的差异无统计学意义(P＞0.05);各氧疗组之间动脉血pH、PO2和PCO2的差异无统计学意义(P＞0.05).病理大体解剖可见,二氧化碳染毒组大鼠肺脏可见大面积点、片状淤血,高浓度和低浓度常压吸氧治疗组的大鼠肺脏淤血情况较染毒组有所减轻,高压氧治疗组大鼠肺脏外观未见明显异常.光学显微镜下可见,二氧化碳染毒组大鼠肺组织出现弥漫性出血和渗出,高浓度和低浓度常压吸氧治疗组大鼠的肺组织出血和渗出情况较染毒组有所减轻,高压氧治疗组大鼠肺组织仅有轻微的出血和渗出.各组动物脑组织大体解剖和光学显微镜下所见没有区别,均未见明显出血、水肿、细胞变性和坏死.结论 急性二氧化碳中毒大鼠给予高压氧治疗后肺脏病理改变明显好于高浓度和低浓度常压吸氧治疗组,高浓度和低浓度常压吸氧治疗组治疗效果无明显差异,但血气分析结果和肺脏病理较染毒组有所好转,建议有条件的医疗单位可以尽早给予高压氧治疗,在无高压氧治疗设施的情况下,早期吸氧也是应急救治的良好措施.

Abstract：

Objective To study therapeutic effects by using different oxygen therapies in rats with acute carbon dioxide poisoning, to select the best oxygen therapy technology for patients with acute carbon dioxide poisoning on the spot. Methods Sixty healthy male Sprague-Dawley rats were randomized into normal control group, carbon dioxide exposure group, hyperbaric oxygen treatment group (pressure 2 ATA,FiO2100% ),high concentration of atmospheric oxygen treatment group (FiO250%),low concentration of atmospheric oxygen treatment group(FiO233%). After treated with different oxygen in rats with acute carbon dioxide poisoning, arterial pH, PO2 and PCO2 of rats were detected, in addition observe pathological changes of lung tissue and brain tissue. Results The arterial pH (7.31±0.06) and PO2 [(68.50±15.02)mm Hg] of carbon dioxide exposure group were lower than those of control group [pH (7.42±0.02) and PO2(92.83±8.27)mm Hg],PCO2[(71.66±12.10)mm Hg] was higher than that of control group[(48.25±2.59)mm Hg](P＜0.05);the arterial pH (hyperbaric oxygen treatment group 7.37 ±0.02, high concentration of atmospheric oxygen treatment group 7.39±0.03, low concentration of atmospheric oxygen treatment group 7.38±0.02) and PO2 of oxygen treatment groups [hyperbaric oxygen treatment group, high concentration of atmospheric oxygen treatment group, low concentration of atmospheric oxygen treatment group were (82.25±12.98), (84.75±11.24),(83.75 ±16.77)mm Hg, respectively] were higher than that of carbon dioxide exposure group,PCO2 [hyperbaric oxygen treatment group, high concentration of atmospheric oxygen treatment group, low concentration of atmospheric oxygen treatment group were ( 52.25±4.95 ), ( 51.75 ±4.82 ), ( 52.66±5.61 ) mm Hg,respectively] was lower than that of carbon dioxide exposure group (P＜0.05);there was no significant difference of the arterial pH, PO2 and PCO2 between oxygen treatment groups and control group (P＞0.05);there was no significant difference of the arterial pH, PO2 and PCO2 among oxygen treatment groups (P＞0.05). There was large area of bleeding of lungs in rats with carbon dioxide poisoning,the bleeding of lungs in rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment was better than the rats with carbon dioxide poisoning,there was no abnormal appearance of lungs in rats with hyperbaric oxygen treatment. The light microscope observation showed that there were diffuse bleeding and exudation of lungs in rats with carbon dioxide poisoning, the bleeding and exudation of lungs in rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment were better than the rats with carbon dioxide poisoning, there were only minor bleeding and exudation of lungs in rats with hyperbaric oxygen treatment. There was no difference of brain in anatomy and microscopy among all groups, there were no significant bleeding, edema, cell degeneration and necrosis.Conclusions Lung pathology in acute carbon dioxide poisoning rats with hyperbaric oxygen treatment is better than the rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment, there is no significant difference of effect between high concentration of atmospheric oxygen treatment group and low concentration of atmospheric oxygen treatment group,however,the results of blood gas analysis and lung pathology than the exposure group improved, so qualified medical unit for hyperbaric oxygen therapy as soon as possible, hyperbaric oxygen treatment facilities in the absence of circumstances,the emergency treatment of early oxygen is also a good measure.     

丹参注射液与异甘草酸镁抗肝纤维化的临床对比研究

Objective To observe the change of liver function and liver fibrosis indexes of the chronic hepatitis B patients that were treated by Danshen injection(DI) and magnesium isnglyeyrrhizinate(MI). Methods 80 chronic hepati-tis B patients based on the conventional treatment were randomly divided into D1 group(40 patients) and MI group(40 pa-tients). The two groups were used with DI and MI injection for 30 days respaetively and then,the levels of liver function and serum hepatic fibrosis(HA, LN, Ⅳ -C) were detected and compared before and after treatment. Results Treatment by DI and MI could both improve liver function significantly, the effect of Ml group was better than DI group(P < 0.05). Moreover, in improving serum hepatic fibrosis, the effect of DI group was better than MI group (P < 0.05). Conclusions The efficacy of the improvement to hepatic fibrosis DI is better than MI, while in improvement of liver function MI is superior to DI.     

丹参注射液与异甘草酸镁抗肝纤维化的临床对比研究

Objective To observe the change of liver function and liver fibrosis indexes of the chronic hepatitis B patients that were treated by Danshen injection(DI) and magnesium isnglyeyrrhizinate(MI). Methods 80 chronic hepati-tis B patients based on the conventional treatment were randomly divided into D1 group(40 patients) and MI group(40 pa-tients). The two groups were used with DI and MI injection for 30 days respaetively and then,the levels of liver function and serum hepatic fibrosis(HA, LN, Ⅳ -C) were detected and compared before and after treatment. Results Treatment by DI and MI could both improve liver function significantly, the effect of Ml group was better than DI group(P < 0.05). Moreover, in improving serum hepatic fibrosis, the effect of DI group was better than MI group (P < 0.05). Conclusions The efficacy of the improvement to hepatic fibrosis DI is better than MI, while in improvement of liver function MI is superior to DI.     

丹参注射液与异甘草酸镁抗肝纤维化的临床对比研究

Objective To observe the change of liver function and liver fibrosis indexes of the chronic hepatitis B patients that were treated by Danshen injection(DI) and magnesium isnglyeyrrhizinate(MI). Methods 80 chronic hepati-tis B patients based on the conventional treatment were randomly divided into D1 group(40 patients) and MI group(40 pa-tients). The two groups were used with DI and MI injection for 30 days respaetively and then,the levels of liver function and serum hepatic fibrosis(HA, LN, Ⅳ -C) were detected and compared before and after treatment. Results Treatment by DI and MI could both improve liver function significantly, the effect of Ml group was better than DI group(P < 0.05). Moreover, in improving serum hepatic fibrosis, the effect of DI group was better than MI group (P < 0.05). Conclusions The efficacy of the improvement to hepatic fibrosis DI is better than MI, while in improvement of liver function MI is superior to DI.