没食子儿茶素没食子酸酯对百草枯诱导SK-N-SH细胞凋亡的保护作用

目的探讨茶多酚中主要活性成分没食子儿茶素没食子酸酯(EGCG)对百草枯诱导人神经母细胞瘤细胞株SK-N-SH细胞凋亡的保护作用。方法培养的SK-N-SH细胞给予400μmol·L-1百草枯诱导细胞凋亡。实验分为6组:空白对照组、百草枯模型组、维生素E(10μmol·L-1)组和3个EGCG(1、5、10μmol·L-1)剂量组。以药物处理细胞2h后,加入百草枯,72h后MTT法检测细胞活力,取培养细胞上清液测定乳酸脱氢酶(LDH)漏出量,Hoechst 33258荧光染色法和流式细胞术检测细胞凋亡情况。结果与空白对照组相比,百草枯明显降低细胞活力(P<0.01),增加LDH漏出量(P<0.01),细胞膜结构不完整,出现空泡等凋亡现象,细胞凋亡发生率达到30.5%。EGCG处理后,显著提高细胞活力,减少LDH的漏出和降低细胞凋亡率(P<0.01),其中10μmol·L-1组的作用明显高于5μmol·L-1组或1μmol·L-1组(P<0.05或P<0.01)。结论EGCG具有抑制百草枯诱导的SK-N-SH细胞凋亡作用。     

葡萄籽原花青素对博莱霉素诱导的大鼠实验性肺纤维化的治疗作用

目的探讨葡萄籽原花青素(GSP)对大鼠肺纤维化的治疗作用及其机制。方法 45只SD雄性大鼠随机分为正常对照组(N组)、模型组(M组)、GSP组(G组),每组15只。M、G组大鼠气管内一次性注入博莱霉素生理盐水溶液0.2~0.3 m L(5 mg·kg~(-1))造模,N组气管内注射等容生理盐水。术后第2日开始,G组大鼠给予GSP生理盐水溶液0.1 m L·10 g~(-1)(500 mg·kg~(-1)·d~(-1))灌胃,M组和N组给予等容生理盐水,每日1次。给药7、14、28 d每组随机处死5只大鼠,取肺组织。观察肺组织病理变化,检测肺组织匀浆羟脯氨酸(HYP)含量,RT-q PCR法和Western blot法检测血管内皮生长因子(VEGF)及其受体1(VEGFR1)m RNA和蛋白质的表达。结果各时间点M组Ashcroft评分均高于N组(P<0.01)和G组(P<0.05),N组大鼠肺组织无明显病变,M组肺组织炎症反应和肺纤维化明显,G组各期肺泡炎症和纤维化程度均低于M组。各观察时点,M组大鼠肺组织HYP含量、VEGF和VEGFR1蛋白及m RNA表达均明显高于N组(P<0.01)。G组肺组织HYP含量、VEGF蛋白及m RNA表达均低于M组(P<0.05或P<0.01),给药7、14 d肺组织VEGFR1蛋白及m RNA表达低于M组(P<0.05),给药28 d与M组比较差异无显著意义(P>0.05)。结论 GSP能抑制大鼠肺纤维化,降低肺组织VEGF和VEGFR1蛋白和m RNA的表达可能为其作用机制之一。     

灯盏花素对实验性肺纤维化大鼠的干预作用

目的探讨灯盏花素对博莱霉素致肺纤维化大鼠肺组织细胞凋亡、Fas/FasL表达以及氧自由基的影响。方法48只大鼠随机分为对照组(16只)、模型组(16只)以及灯盏花素组(16只),气管内注入博莱霉素复制大鼠肺纤维化模型,次日灯盏花素组每日腹腔内注射灯盏花素注射液10mg.kg-1,于d7及d28每组分别处死8只大鼠,运用流式细胞仪测定肺纤维化大鼠肺组织细胞凋亡率、Fas/FasL表达,用TAB法测定肺组织匀浆丙二醛含量以及肺组织匀浆羟脯氨酸含量。结果炎症期和纤维化期大鼠肺组织细胞凋亡率增加,Fas/FasL表达增多,丙二醛及羟脯氨酸含量增高(P<0.01),而灯盏花素能明显降低肺组织的凋亡率,降低丙二醛及羟脯氨酸含量,下调Fas/Fasl的阳性表达。结论灯盏花素能减慢肺间质纤维化的进程,对肺间质纤维化有一定的保护作用。     

表没食子儿茶素没食子酸酯对博莱霉素所致大鼠肺纤维化的干预作用及其机制研究

目的观察表没食子儿茶素没食子酸酯(EGCG)对实验性大鼠肺纤维化的干预作用及可能的作用机制。方法大鼠随机分为正常对照组、模型组、醋酸泼尼松组和EGCG大、中、小剂量组。通过气管内注入博莱霉素(BLM)复制大鼠肺纤维化模型,于造模后d 2各治疗组开始给药,给药后d7、14、28处死大鼠,取肺组织,观察形态学变化,并测定生化指标。结果EGCG能减少实验性肺纤维化大鼠肺组织中胶原沉积及降低肺系数(P<0.05,P<0.01),提高T-AOC、SOD水平(P<0.05,P<0.01),减轻肺部的病理损害。结论EGCG对BLM诱导产生的大鼠肺纤维化有一定的抑制作用。     

表没食子儿茶素没食子酸酯对亚硫酸盐诱导的心肌细胞氧化损伤的抑制作用

<正>绿茶常被称为是天然的抗氧化剂,含有很多种酚类物质,其中以表没食子儿茶素没食子酸酯(EGCG)含量最高且生物活性最强。流行病学调查和实验室研究表明,EGCG具有清除自由基、抗氧化、抗癌、抗肿瘤等功效[1-2],如在日本     

博莱霉素致大鼠肺纤维化胶原表达的研究

目的：探讨博莱霉素致大鼠肺间质纤维化肺组织前胶原I和前胶原III mRNA及蛋白质变化的意义。方法：大鼠随机分为经气管内一次性灌注生理盐水为正常对照组,灌注搏莱霉素分为博莱霉素3天组,7天组,14天组,30天组,分子杂交和免疫组化方法测定肺组织的前胶原I,前胶原III的mRNA和蛋白质表达。结果：博莱霉素7天组前胶原I,前胶原III的mRNA高于正常对照组（P＜0．01）,14天组达到峰值水平,博莱霉素30天组的前胶原I mRNA仍高于正常对照组（P＜0．01）,而前胶原III的mRNA水平与正常对照组。结论：博莱霉素致肺纤维化时,前胶原基因转录水平的升高,引起的胶原合成加速是肺间质胶原积聚的主要原因。     

Effects of epigallocatechin-3-gallate combined with ascorbic acid and glycerol on the stability and uric acid-lowering activity of epigallocatechin-3-gallate

ContextEpigallocatechin-3-gallate (EGCG) is unstable and easily oxidized, which limits its applications. Ascorbic acid (Vc) is a natural antioxidant.ObjectiveThe effects of EGCG combined with Vc and glycerol on stability and uric acid-lowering activity of EGCG were examined.Materials and methodsEGCG (aqueous solution), EGCG + Vc (aqueous solution), EGCG (glycerol solution) and EGCG + Vc (glycerol solution) were prepared and incubated under different conditions in vitro. The recovery rate of EGCG was calculated by HPLC. Kunming mice were randomly divided into normal control group, model group, allopurinol (5 mg/kg), EGCG (10 mg/kg), EGCG + Vc (both 10 mg/kg), EGCG (10 mg/kg) + glycerol (60%), and EGCG (10 mg/kg) + Vc (10 mg/kg) + glycerol (60%) (n = 6). Allopurinol was injected intraperitoneally to mice, others were administered intragastrically to (2 cases) mice. All mice were continuously administrated for 7 days, once a day.ResultsEGCG recovery rates of EGCG group and EGCG + Vc + glycerol group respectively reached to 32.34 ± 1.86% and 98.90 ± 0.64% when they were incubated for 4 h at 80 °C. EGCG recovery rates reached to 91.82 ± 5.13% (incubated for 6 h at pH 8) and 88.85 ± 2.63% (incubated for 4 h in simulated intestinal fluid) when EGCG incubated with Vc and glycerol. Compared with the model group, UA values of EGCG + Vc + glycerol group reduced by 43.49% while EGCG group reduced by 25.63%. The activities of xanthine oxidase (XOD, 31.41 U/gprot) and adenosine deaminase (ADA, 10.05 U/mgprot), and the mRNA expression levels of glucose transporter 9 (GLUT9, 1.03) and urate transporter 1 (URAT1, 0.44) in EGCG + Vc + glycerol group were notably lower than those of EGCG group (38.12 U/gprot, 13.16 U/mgprot, 1.54, and 0.55). The mRNA expression levels of ATP-binding cassette superfamily G member 2 (ABCG2, 1.39) and organic anion transport 1/2 (OAT1/2, 2.34, 2.53) in EGCG + Vc + glycerol group were notably higher than those of EGCG group (0.57, 1.13, and 1.16).Discussion and conclusionsOur findings suggest that when EGCG used in combination with Vc and glycerol could effectively increase its biology activities and can be generalized to the broader pharmacological studies. This sheds light on the development and application of EGCG in the fields of food and medicine.     

七叶皂苷钠对博莱霉素致大鼠肺纤维化的干预作用的研究

目的探讨七叶皂苷钠对实验性大鼠肺纤维化的保护作用。方法 50只清洁级Wistar雄性大鼠采用数字随机法分为空白对照组、盐水对照组、模型组和治疗组。模型组和治疗组采用博莱霉素诱导大鼠肺纤维化模型。治疗组造模后第2天起给予七叶皂苷钠5mg/kg腹腔注射,连续7d。造模后第7、14、28天随机处死大鼠,留取肺组织,检测各组大鼠肺组织中转化生长因子(TGF)-β1表达的变化。结果模型组大鼠肺组织中TGF-β1表达量高于空白对照组、盐水对照组及治疗组,第28天与治疗组比较差异无统计学意义(P>0.05),余各时间点与空白对照组、盐水对照组及治疗组比较差异均有统计学意义(P<0.01,P<0.05)。结论七叶皂苷钠能明显抑制博莱霉素致肺纤维化大鼠早期肺组织TGF-β1的过高表达。     

博莱霉素诱导的肺纤维化动物模型评价及应用研究进展

特发性肺纤维化(IPF)是一种发病原因不明的严重损伤性肺部疾病,缺乏理想的治疗药物。在临床上肿瘤患者使用博莱霉素治疗后,少数患者出现肺纤维化病变。目前博莱霉素已被广泛用于制备IPF动物模型。本文对博莱霉素诱导肺纤维化动物模型的研究现状进行总结,并与临床IPF的作用机制、病理变化等进行对比评价,以期对IPF发病机制研究和药物研发有所帮助。     

Anti-angiogenic activity and intracellular distribution of epigallocatechin-3-gallate analogs

Angiogenesis, a process of construction of new blood capillaries, is crucial for tumor progression and metastasis. Our previous studies demonstrated that a component of green tea, epigallocatechin-3-gallate (EGCG), suppressed angiogenesis and subsequent tumor growth. In this study, to elucidate the detailed mechanism of the anti-angiogenic effect of EGCG and to enhance the antiangiogenic activity of EGCG, we designed and synthesized EGCG derivatives and examined their biological effect and intracellular localization in human umbilical vein endothelial cells (HUVECs). EGCG derivatives aminopentyl dideoxyEGCG and aminopentyl dideoxygallocatechin-3-gallate (cis-APDOEGCG and trans-APDOEGCG) had an enhanced inhibitory effect on the proliferation when used at more than 30 μM. To elucidate antiangiogenic effect of EGCG, we used a 1 μM concentration for subsequent experiments where no effect on proliferation was observed. These EGCG derivatives showed a stronger inhibitory effect on migration, invasion, and tube formation by HUVECs than the non-derivatized EGCG. Furthermore, the derivatives induced a change in the distribution of F-actin and subsequent morphology of the HUVECs. Next, we synthesized fluorescent TokyoGreen-conjugated EGCG derivative (EGCG-TG) and observed the distribution in HUVECs under a confocal laser scanning microscope. Abundant fluorescence was observed in the cells after a 3-h incubation, and was localized in mitochondria as well as in cytoplasm. These results suggest that EGCG was incorporated into the HUVECs, that a portion of it entered into their mitochondria.     

Protective effects of epigallocatechin-3-gallate against lead-induced oxidative damage

A positive association of lead exposure with clinical cardiovascular outcomes has been identified. Epigallocatechin-3-gallate (EGCG) is one of the active polyphenols in green tea, it has not been reported as an antioxidant against lead toxicity. This study was carried out to investigate whether EGCG could protect the ventricular myocytes of rats against lead-induced oxidative damage. Isolated ventricular myocytes were exposed to lead and/or EGCG, then activities of superoxide dismutase (SOD), catalase (CAT), and malondialdehyde (MDA) and the levels of hydroxyl radical (OH(·)), hydrogen peroxide (H(2)O(2)), and superoxide anion (O(2) (·-)) were measured. The results showed that lead induced a significant decrease of SOD and CAT activities, while the levels of MDA increased significantly. Increases in intracellular OH(·), O(2) (·-), and H(2)O(2) were found as well. These processes were concentration-dependent and statistically significant different when compared to 2.0 μM lead exposure. The activity of SOD and CAT increased while the levels of MDA and reactive oxygen species (ROS) decreased after treatment with EGCG. While there were progressive benefits with increasing EGCG concentrations, there was no statistical significance at a 30 μg/mL dose when compared with the control. These results will provide more evidence for lead toxicity to tissue, cell, and biological macromolecule.     

雾化吸入粉防己碱对博来霉素致肺纤维化大鼠的药效作用

目的 探讨雾化吸入粉防己碱对博来霉素诱导肺纤维化大鼠模型的药效作用。方法 将100只SD大鼠随机分为对照组、假手术组、模型组、粉防己碱（5 mg·mL^-1）雾化10、30 min（单次实际给药剂量为0.072、0.220 mg·^kg-1）组,每组10只,并采用气管注入博来霉素方法制备大鼠肺纤维化模型,造模24 h后雾化给药。连续给药第14、28 d,观察大鼠肺系数、肺功能,HE染色后观察肺组织病理,Masson染色后观察胶原纤维变化,天狼星红染色检测大鼠肺组织中I型与III型胶原纤维;并采用Western blotting检测肺组织中波形蛋白（Vimentin）、α-平滑肌肌动蛋白（α-SMA）和转化生长因子-β1（TGF-β1）表达;酶联免疫吸附（ELISA）法检测大鼠肺组织中羟脯氨酸（HYP）和纤连蛋白（FN）含量。结果 粉防己碱雾化后中位粒径为2.98 μm;给药28 d时效果更优,与模型组比较,雾化30 min组的气道阻力显著降低（P＜0.05）,肺顺应性显著升高（P＜0.05）,肺系数显著降低（P＜0.05）;肺泡炎症评分、肺纤维化评分显著降低（P＜0.05）,I型和III型胶原纤维明显减少; Vimentin和TGF-β 1的表达显著下调（P＜0.01）;显著下调HYP和FN的水平（P＜0.05）。结论 雾化吸入粉防己碱具有抗大鼠肺纤维化作用,其中雾化给药28 d效果更优。     

血栓通注射液抗博来霉素致大鼠肺纤维化药效学研究

目的 研究血栓通注射液抗博来霉素诱导肺纤维化模型大鼠的药效学。方法 将180只SD大鼠随机分为假手术组、模型组、吡非尼酮（阳性药,50 mg · kg^-1）组和血栓通注射液低、中、高剂量（注射液原液1、2、4 mL·kg^-1）组,每组30只,采用气管内注射博来霉素方法制备肺纤维化大鼠模型,于造模24 h后各给药组ip给药,并分别在造模7、14、28 d取材。观察大鼠一般状态、体质量、肺系数;应用DSI/BUXCO监测系统检测肺功能指标潮气量、气道阻力及肺顺应性变化;进行HE与Masson染色,光镜下观察肺组织病理变化;并采用酶联免疫吸附法（ELISA）检测大鼠肺组织中I型胶原（COL-Ⅰ）和纤维黏连蛋白（FN）的水平。结果 通过对大鼠的一般情况观察,发现给予血栓通注射液后,肺纤维化模型大鼠的活动和精神状态均有改善。与模型组比较,吡非尼酮组、血栓通注射液组大鼠体质量显著增加（P＜0.01、0.001）,大鼠肺系数显著降低（P＜0.05、0.01、0.001）。肺功能结果显示,与模型组比较,造模7 d时血栓通注射液中剂量显著上调动态肺顺应性（P＜0.01）;造模14 d时血栓通注射液高剂量显著降低气道阻力（P＜0.05）和上调动态肺顺应性（P＜0.01）;造模28 d时吡非尼酮和血栓通注射液中剂量均显著上调动态肺顺应性（P＜0.01）。HE及Masson结果显示,吡非尼酮组、血栓通注射液组的肺纤维化程度明显轻于模型组。ELISA结果显示,与模型组比较,造模7 d时吡非尼酮组、血栓通注射液高剂量组大鼠肺组织中的FN显著降低（P＜0.01、0.001）,吡非尼酮组COL-Ⅰ水平显著降低（P＜0.001）;造模14 d时吡非尼酮组和血栓通注射液中、高剂量组大鼠肺组织中的COL-Ⅰ水平显著降低（P＜0.05、0.01）,吡非尼酮组FN显著降低（P＜0.05）;造模28 d时吡非尼酮组和血栓通注射液中、高剂量组大鼠肺组织中的COL-Ⅰ、FN水平显著降低（P＜0.05、0.01、0.001）。结论 血栓通注射液可改善肺纤维化模型大鼠肺功能与肺部形态学病变,降低肺组织中COL-Ⅰ和FN水平,对肺纤维化大鼠产生保护作用。     

Regulation of urokinase plasminogen activator by epigallocatechin-3-gallate in human fibrosarcoma cells

(-)-Epigallocatechin-3-gallate (EGCG), a main flavanol of green tea, potently suppressed the urokinase-type plasminogen activator (uPA) expression in human fibrosarcoma HT 1080 cells. EGCG induced not only the suppression of the uPA promoter activity but also the destabilization of uPA mRNA. EGCG inhibited the phosphorylation of extracellular signal-regulated kinases 1 and 2 (Erk-1/2) and P38 mitogen-activated protein kinase (MAPK), but not the phosphorylation of c-jun N-terminal kinase (JNK) and Akt. Specific inhibitors of Erk-1/2 (2'-amino-3'-methoxyflavone, PD98059) and P38 MAPK (pyridinylimidazole, SB203580) were found to suppress the uPA expression and the uPA promoter activity. However, the specific inhibitors did not affect the uPA mRNA stability. These results suggest that EGCG could regulate the uPA expression by at least two different mechanisms: EGCG may inhibit the Erk-1/2 and P38 MAPK, leading to suppression of the uPA promoter activity, and EGCG may destabilize the uPA mRNA in an Erk-1/2- and p38 MAPK-independent way.     

地塞米松对肺纤维化大鼠肺组织超微结构的影响

目的:探讨地塞米松对肺纤维化大鼠肺组织氧自由基和超微结构的影响。方法:SD大鼠经气管内灌注博莱霉素诱导肺纤维化,随后每日注射地塞米松3.33mg·kg- 1干预。于注药后d 2 9处死。通过HE染色和透射电镜观察显微结构的变化,并通过测定肺组织超氧化物歧化酶(SOD )、丙二醛(MDA)来评价干预效果。结果:地塞米松组与博莱霉素组相比,肺组织SOD下降,MDA升高,肺纤维化程度减轻。结论:地塞米松能减轻大鼠肺纤维化,部分机制与抗氧化有关。     

昆布多糖对博来霉素诱导的大鼠肺间质纤维化的影响

目的 观察昆布多糖对博来霉素诱导的大鼠肺间质纤维化的影响。方法 通过气管注射博来霉素复制大鼠肺纤维化模型，不同浓度昆布多糖（25，50，100mg·mL^-1）灌胃给药，在造模的第0，3，7，14，28天测肺羟脯氨酸含量。结果 博来霉素造模第7，28天时，昆布多糖中、高剂量组大鼠肺羟脯氨酸含量与模型组比较有显著性差异（P〈0．05）；第14天时与模型组比较，高剂量组有显著性差异（P〈0．05）。结论 昆布多糖能抑制博来霉素诱导的大鼠肺间质纤维化。     

泛素-蛋白酶体抑制剂对大鼠肺纤维化的影响

目的:探讨泛素-蛋白酶体抑制剂MG-132对大鼠肺纤维化的影响。方法:45只SD大鼠随机分成对照组、模型组、干预组和治疗组。模型组和干预、治疗组大鼠气管内滴入博来霉素(5mg.kg-1)建立肺纤维化动物模型,对照组以等量生理盐水气管内滴入。干预组于第造模后第1天起给予MG-132腹腔内注射(0.1mg.kg-1.d-1),模型组和对照组注射等量生理盐水;治疗组于造模后第28天起给予MG-132(0.1mg.kg-1.d-1)腹腔内注射。于不同时间点测肺系数、肺组织行病理学检查及肺组织羟脯氨酸(HYP)含量测定。结果:干预组及治疗组肺系数及肺组织HYP含量各时间点均低于模型组(P<0.01,P<0.05),肺泡炎的程度也轻于模型组;虽然干预组和治疗组肺纤维化程度均明显重于对照组,但干预组28d和治疗组肺纤维化较模型组轻。结论:泛素-蛋白酶体抑制剂MG-132对大鼠肺纤维化有一定的干预、治疗作用。     

Skin delivery of epigallocatechin-3-gallate (EGCG) and hyaluronic acid loaded nano-transfersomes for antioxidant and anti-aging effects in UV radiation induced skin damage

The present work attempts to develop and statistically optimize transfersomes containing EGCG and hyaluronic acid to synergize the UV radiation-protective ability of both compounds, along with imparting antioxidant and anti-aging effects. Transfersomes were prepared by thin film hydration technique, using soy phosphatidylcholine and sodium cholate, combined with high-pressure homogenization. They were characterized with respect to size, polydispersity index, zeta potential, morphology, entrapment efficiency, Fourier Transform Infrared Spectroscopy (FTIR), Differential Scanning Calorimetry (DSC), X-ray Diffraction (XRD), in vitro antioxidant activity and ex vivo skin permeation studies. Cell viability, lipid peroxidation, intracellular ROS levels and expression of MMPs (2 and 9) were determined in human keratinocyte cell lines (HaCaT). The composition of the transfersomes was statistically optimized by Design of Experiments using Box–Behnken design with four factors at three levels. The optimized transfersome formulation showed vesicle size, polydispersity index and zeta potential of 101.2?±?6.0?nm, 0.245?±?0.069 and ?44.8?±?5.24?mV, respectively. FTIR and DSC showed no interaction between EGCG and the selected excipients. XRD results revealed no form conversion of EGCG in its transfersomal form. The optimized transfersomes were found to increase the cell viability and reduce the lipid peroxidation, intracellular ROS and expression of MMPs in HaCaT cells. The optimized transfersomal formulation of EGCG and HA exhibited considerably higher skin permeation and deposition of EGCG than that observed with plain EGCG. The results underline the potential application of the developed transfersomes in sunscreen cream/lotions for improvement of UV radiation-protection along with deriving antioxidant and anti-aging effects.     

没食子儿茶素没食子酸酯对MPP~+诱导大鼠PC12细胞凋亡的拮抗作用

目的探讨没食子儿茶素没食子酸酯(EGCG)对MPP+诱导大鼠PC12细胞凋亡的拮抗作用。方法培养PC12细胞给予MPP+(900μmol.L-1)诱导细胞凋亡,实验分为6组:空白对照组、MPP+组、维生素E(10μmol.L-1)组和EGCG高(100μmol.L-1)、中(50μmol.L-1)、低(10μmol.L-1)剂量组。药物处理0.5h后,加入MPP+损伤细胞,4h后取细胞测定乳酸脱氢酶(LDH)漏出量,MTT法检测细胞活力,Hoechst33342荧光染色法和流式细胞术检测细胞凋亡,透射电镜观察凋亡细胞线粒体形态结构改变。结果MPP+处理后,细胞活力下降,LDH漏出量增加,细胞凋亡率增加,线粒体肿胀,出现空泡和嵴断裂等细胞凋亡征象。维生素E和不同剂量EGCG处理后,明显提高细胞活力,降低LDH漏出和细胞凋亡率,并减少MPP+引起的线粒体结构损伤。结论EGCG具有抑制MPP+诱导的大鼠PC12细胞凋亡作用,其作用与保护细胞线粒体结构的完整性有关。     

复方苦参注射液抗博来霉素致大鼠肺纤维化药效学研究

目的 探讨复方苦参注射液对博来霉素诱导肺纤维化模型大鼠的影响及相关机制。方法 将120只SD大鼠随机分为对照组、假手术组、模型组及复方苦参注射液低、中、高剂量（注射液原液1、2、4 mL·kg^-1）组,每组20只,采用气管内注射博来霉素方法制备肺纤维化大鼠模型,造模24 h后给药组ip复方苦参注射液,第14、28天取材。观察大鼠一般状态、肺系数、肺功能、肺组织病理变化,并采用酶联免疫吸附法（ELISA）检测大鼠血清中肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）的水平,进一步检测肺组织中羟脯氨酸（HYP）、丙二醛（MDA）和超氧化物歧化酶（SOD）表达量的变化。结果 大鼠的一般情况观察发现,与假手术组比较,模型组大鼠食量及饮水量均有所下降,精神萎靡,毛色暗淡发黄,同时模型组大鼠出现拱背及口唇、爪甲及尾尖均呈现紫黯现象,部分大鼠出现口鼻出血,呼吸困难现象。给予复方苦参注射液后,肺纤维化模型大鼠的活动和精神状态均有改善作用。与假手术组比较,模型组大鼠体质量明显降低（P<0.01、0.001）,肺系数显著增加（P<0.001）,肺功能指标潮气量下降（P<0.001）,气道阻力升高（P<0.001）,动态肺顺应性降低（P<0.001）,肺组织发生纤维化、炎细胞浸润等明显损伤,血清中TNF-α和IL-1β水平显著升高（P<0.001）,肺组织中HYP水平显著升高（P<0.001）,而SOD活性则显著下降（P<0.001）,MDA水平有增加趋势。与模型组比较,复方苦参注射液低、中剂量组大鼠体质量显著增加（P<0.05、0.001）,大鼠肺系数显著降低（P<0.05、0.001）,潮气量显著上调（P<0.001）,气道阻力显著降低（P<0.01、0.001）,动态肺顺应性显著上调（P<0.01、0.001）,大鼠肺组织纤维化程度明显减轻,血清中TNF-α水平降低（P<0.01、0.001）,肺组织中HYP含量显著降低（P<0.01）,SOD活性则显著升高（P<0.05、0.01、0.001）,MDA有下调趋势,但差异不显著。结论 复方苦参注射液可改善肺纤维化模型大鼠肺功能与肺部形态学病变,降低血清中TNF-α水平,以及下调肺组织中HYP含量与提高SOD活性,减轻炎性反应并增加抗氧化能力,对肺纤维化大鼠产生保护作用。