TNF-α、IL-8在脂多糖致大鼠脑水肿中的表达

目的　探讨脂多糖 (lipopolysaccharide ,LPS)致大鼠脑水肿发生过程中 ,地塞米松作用下TNF α、IL 8表达水平的变化及相互关系。方法　利用LPS诱导大鼠脑水肿发生 ,测定脑组织含水量及伊文私蓝 (Evansblue,EB)含量 ,制备脑组织匀浆 ,ELISA法测IL 8含量 ,放射免疫法测TNF α含量。结果　LPS注入后LPS组和DXM组脑组织含水量和伊文思蓝含量均较NS组增高 (P <0 .0 5) ;LPS组TNF α和IL 8含量较NS组显著增高 (P <0 .0 1 ) ,但DXM组较LPS组显著降低 (P <0 .0 5) ;DXM组TNF α和IL 8含量在早期 (≤ 2 4h)较NS组增高 (P <0 .0 5) ,48h时则无显著差异 (P >0 .0 5)。LPS组脑组织含水量与EB含量 ,TNF α与脑组织含水量 ,IL 8与脑组织含水量 ,IL 8与EB含量均呈正相关 (r值分别为 0 .537,0 .42 3 ,0 .473 ,0 .831 ,P <0 .0 5)。结论　TNF α、IL 8参与了脂多糖诱导的脑水肿的发生、发展过程 ,早期应用糖皮质激素可以抑制炎性细胞因子的生成 ,减轻炎症反应与组织损伤。     

TNF-α、IL-8在脂多糖致大鼠脑水肿发生中的变化和意义

目的 :探讨肿瘤坏死因子 (TNF)、白细胞介素 8(IL 8)在脂多糖 (lipopolysaccharide ,LPS)致大鼠脑水肿发生中的变化及作用。方法 :LPS诱发大鼠脑水肿发生后 ,制备脑组织匀浆 ,ELISA法测定IL 8含量 ,放免法测定TNF α含量。结果 :LPS注入后TNF α、IL 8相继释放增加 ,与A组、NS组比较差异有非常显著性 (P <0 0 1 ) ,48h后仍维持较高水平 ,LPS组脑组织含水量与Evansblue(EB)含量 ,TNF α与脑组织含水量 ,IL 8与脑组织含水量 ,IL 8与EB含量均呈正相关 ,r值分别为 0 537、0 42 3、0 473、0 831。P <0 0 5。结论 :TNF α、IL 8与脑组织炎性损伤密切相关 ,介导了脂多糖导致脑水肿的发生、发展过程     

TNF—α、IL—8在多脂多糖致大鼠脑水肿发生中的变化和意义

目的：探讨肿瘤坏死因子（TNF）、白细胞介素－8（IL－8）在脂多糖（lipopolysaccharide,LPS)致大鼠脑水肿发生中的变化及作用。方法：LPS诱发大鼠脑水肿发生后，制备脑组织匀浆，ELISA法测定IL－8含量，放免法测定TNF－α含量。结果：LPS注入后TNF－α、IL－8相继释放增加，与A组、NS组比较差异有非常显著性（P＜0．01），48h后仍维持较高水平，LPS组脑组织含水量与Evans blue(EB)含量，TNF－α与脑组织含水量，IL－8与脑组织含水量，IL－8与EB含量均呈正相关，r值分别为0．537、0．423、0．473、0．831。P＜0．05。结论：TNF－α、IL－8与脑组织炎性损伤密切相关，介导了脂多糖导致脑水肿的发生、发展过程。     

α黑素细胞刺激素保护内毒素休克小鼠的免疫学机制研究

为研究α黑素细胞刺激素 (α MSH)对内毒素休克小鼠发挥保护作用的免疫学机制 ,将BALB/c小鼠经腹腔注射 (ip)LPS5 0 μg/kg和D 半乳糖胺 (D Gal) 90 0mg/kg建立内毒素休克模型后 ,在不同时间给予α MSHip后观察小鼠的存活率 ;用MTT法测定小鼠血清中IL 1、TNF α、IL 6的含量 ;用Griess试剂测定血清中NO的含量。腹腔巨噬细胞 (MΦ)膜表面免疫相关分子以流式细胞仪检测。结果是给予LPS前 1h、同时和后 1hα MSH 2 5mg/kgip可以明显提高内毒素休克小鼠的存活率 ,其中以给予LPS 1h后注射α MSH疗效最佳 ,能显著降低血清中IL 1、TNF α含量 (P <0 0 0 1) ,增加IL 6的产生 (P <0 0 5 ) ,抑制LPS引起的腹腔MΦ高表达CD14、CD40、CD5 4及CD86分子。因此 ,α MSH降低TNF α、IL 1及NO的含量 ,抑制MΦ膜表面CD14、CD5 4、CD40及CD86的表达 ,在其抗内毒素休克效应中起重要作用。     

大鼠胰岛β细胞损伤中IL-18的作用研究

新生Wistar大鼠离体胰岛与细胞因子孵育后 ,观测胰岛素释放和一氧化氮 (NO )生成的变化 ,并用逆转录 聚合酶链反应 (RT PCR )观察IL 18受体信号链 (IL 18Rβ )mRNA的表达水平。结果表明 :(1) 0 6 2 5～ 10nmol/L基因重组小鼠 (rm )IL 18孵育胰岛 2 4h后 ,对累积的和葡萄糖刺激的胰岛素释放以及NO生成均无显著效应 ;(2 ) 2 0 0U/ml基因重组大鼠 (rr)γ干扰素 (IFN γ )或 2 5 0U/ml基因重组人 (rh )肿瘤坏死因子 α (TNF α)单独存在对胰岛素释放和NO生成均无明显效应 ,也不能促使 10nmol/LrmIL 18对胰岛素释放和NO生成产生影响 ;(3) 2 0 0U/mlrrIFN γ +2 5 0U/mlrhTNF α或 15pg/mlrhIL 1β均明显促进NO生成和抑制胰岛素释放 ,而 10nmol/LrmIL 18则不影响IFN γ +TNF α或IL 1β的上述效应 ;(4 )即使经IL 1β和 (或 )IFN γ +TNF α或IL 12孵育后 ,大鼠胰岛素瘤 (RIN )细胞或离体大鼠胰岛仍未见IL 18RβmRNA的表达。提示IL 18在细胞因子所致胰岛β细胞损伤中不发挥直接作用 ,原因是IL 18受体在胰岛 β细胞中不表达。     

TNBS诱发大鼠结肠炎P选择素的表达及其与TNF-α、IL-8的相关性研究

目的 :研究P 选择素在三硝基苯磺酸 (TNBS)诱发的大鼠结肠炎组织中的表达、循环血中血小板膜表面含量的变化及其与组织TNF α和血清IL 8表达的相关性 ,探讨其在结肠炎发生发展中的作用及血栓并发症形成的可能机制。方法 :用TNBS 乙醇灌肠制作大鼠结肠炎模型 ,分别在制模后 2 4小时、1周和 2周取心脏血 ,放射免疫法测定P 选择素的含量 ,ELISA夹心法检测IL 8的含量 ,免疫组化法分析P 选择素及TNFα在病变部位的表达。结果 :与正常对照组比较 ,P 选择素在结肠组织炎症的各个时间点均有表达 ,阳性表达率大于 5 0 %。血小板膜表面P 选择素在灌肠后 2 4小时未见升高 ,第 1、2周明显升高(P <0 0 1)。血清IL 8含量及TNFα表达曲线变化情况相似 ,在 2 4小时升高最为明显 ,随着病程延长而下降。P 选择素与IL 8在同期炎症中呈正相关 ,而与TNF α无线性相关。结论 :P 选择素在结肠炎症早期介导局部的炎症反应 ,晚期仍然是维持炎症、血栓形成的重要因素之一。P 选择素含量升高和表达增强与IL 8呈正相关 ,与TNF α无线性相关。     

碘化钠对人甲状腺上皮细胞TNF-α、IL-1β分泌的影响

为研究碘化钠 (NaI)对人甲状腺上皮细胞 (TEC )分泌细胞因子TNF α和IL 1β的影响 ,以探讨碘在GD病 (GD )发病中的可能机制 ,取手术切除的GD病患者甲状腺组织和甲状腺腺瘤患者瘤旁正常甲状腺组织 ,进行细胞培养。以不同浓度的NaI (10 8～ 10 3 mol/L )刺激单层培养的甲状腺细胞 ,采用放射免疫测定技术测定刺激前后甲状腺细胞培养上清液中细胞因子TNF α和IL 1β的含量。同时以透射电镜观察NaI刺激后甲状腺细胞的形态学改变。结果 :(1)正常甲状腺细胞能分泌少量的TNF α和IL 1β。GD的甲状腺细胞TNF α和IL 1β的分泌量与正常TEC相比显著增加 (P <0 0 1) ;(2 )当NaI浓度为 10 8～10 3 mol/L时 ,正常人甲状腺细胞TNF α、IL 1β的分泌量与 0mol/L组相比无显著性差异 (P >0 0 5 ) ;透射电镜示正常甲状腺细胞无损伤型改变 ;(3)当NaI浓度为 10 6～ 10 3 mol/L时 ,GD甲状腺细胞TNF α的分泌量显著增加 (P <0 0 5 ) ;当NaI浓度为 10 8～ 10 3 mol/L时 ,GD甲状腺细胞IL 1β的分泌量显著增加 (P <0 0 5 )。NaI浓度超过 10 6mol/L时 ,透射电镜示GD甲状腺细胞出现损伤型改变。表明高浓度的碘不仅造成GD甲状腺细胞的直接损伤 ,而且可以增加甲状腺细胞细胞因子TNF α和IL 1β的分泌 ,特别是在GD甲状腺细     

咪唑安定保护家兔心肌缺血再灌注损伤机制的研究

目的 :观察咪唑安定对家兔心肌缺血 /再灌注期血清和心肌TNF α、IL 6的影响 ,探讨其保护作用机制。方法 :利用结扎 /开放左冠状动脉左前降支 ,结扎 30min/开放 1 80min建立心肌缺血 /再灌注模型。 2 4只家兔随机分为三组 (每组 8只 ) :假手术对照组 (A组 ) ,未予心肌缺血处理 ;缺血再灌注组 (B组 )于缺血前 5min(I0 )、缺血 30min(I1 )、再灌注 1h(R1 )和 3h(R2 )取颈内静脉血 ,并于实验结束后取心肌组织匀浆 ,分别测定IL 6和TNF α浓度 ;咪唑安定组(C组 )缺血前 2 0min静脉注射咪唑安定 0 .75mg/kg(人等效剂量 ) ,以每小时 0 .4mg/kg持续泵入 ,取血样时点和检测指标均同B组。结果 :C组血清TNF α在I1 和R1 时升高 ,R2 时降低 ,IL 6在R2 时升高 ,但在各时点均较B组相应值低 (P <0 .0 1或 0 .0 5 ) ,心肌组织TNF α、IL 6水平亦低于B组 (P <0 .0 5 ) ,但较A组明显升高 (P <0 .0 1 ) ;B组TNF α在I1 时点显著升高 ,IL 6在R1 和R2 时点持续升高 ,心肌组织中TNF α和IL 6含量明显增加 ,同A组和C组比差异有高度显著性。结论 :在心肌缺血再灌注损伤中 ,咪唑安定通过抑制心肌组织和血清TNF α和IL 6的合成或释放 ,从而对心肌组织有保护作用。     

热休克反应对大鼠感染性脑水肿细胞因子和一氧化氮的 …

为研究ＩＬ－１β－、ＴＮＦ－α及ＮＯ在感染性脑水肿时的变化和热休克反应对它们的影响，探讨热休克反应对大鼠感染性脑水中的保护作用是否与其有关，本实验采用ＥＬＩＳＡ法和Ｇｒｉｅｓｓ法分别检测各组大鼠脑组织均浆中ＩＬ－１β－、ＴＮＦ－α及ＮＯ的含量，大鼠分３组：①正常对照组（ＮＳ）；②感染性脑水肿组（ＰＢ）；③热休克处理组（ＨＳ＋ＰＢ）。每组又分为４ｈ、８ｈ、２４ｈ三个时间点。结果显示：与ＮＳ组比较，４     

急性胰腺炎患者血清TNF-α、IL-6和IL-8含量测定

研究血清TNF α、IL 6和IL 8在急性胰腺炎 (AP )发生发展中的作用和临床意义。采用双抗体夹心ELISA法测定 41例AP患者及正常对照组 40例血清TNF α、IL 6、IL 8和C 反应蛋白 (CRP )水平。结果显示 ,重症急性胰腺炎 (SAP )和轻症急性胰腺炎 (MAP )血清TNF α、IL 6、IL 8和CRP水平较正常对照组明显增高 (P <0 0 5 ) ,SAP组又较MAP组增高 (P <0 0 5 )。2 7例MAP患者血清TNF α、IL 6、IL 8和CRP水平在治疗后 3d已有下降 ,7d降至正常水平。 14例SAP患者血清TNF α、IL 6、IL 8和CRP水平在治疗后 7d明显降低 ,2 1d仍未降至正常水平。血清中TNF α、IL 6和IL 8可能与AP的严重程度相关 ,在临床上联合检测血清TNF α、IL 6、IL 8和CRP可用于AP的病情严重程度判定和观察治疗后疗效及病情恢复的情况     

Natural polyamine inhibits mouse skin inflammation and macrophage activation

Objective

Natural polyamines are some of the most abundant polycationic molecules in eukaryotic cells, regulating gene expression. Polyamines have been reported to possess anti-inflammatory activities in many model inflammation systems. However, there is no report on their role in 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced dermal edema.

Methods

Mouse ear edema was induced by TPA. Edema biopsies were investigated using H&E staining. Levels of nitric oxide (NO) were determined using the Griess reaction. Tumor necrosis factor α (TNFα) and interleukin (IL)-1β levels in cell supernatants were measured by TNFα and IL-1β ELISA kits.

Results

Spermidine and spermine caused significant decreases in ear thickness, water content, and neutrophil infiltrations in comparison with negative control (p < 0.05). External polyamines reduced the levels of inflammatory mediators such as NO, TNFα, and IL-1β in lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophages. Spermine had a higher inhibitory effect on the production of cytokines such as IL-1β and TNFα in LPS-stimulated murine macrophages compared to other polyamines.

Conclusion

Our findings clearly demonstrated that polyamines are involved in the anti-inflammatory effect by reducing dermal edema thickness and other inflammatory mediators like NO and cytokines in a dose-dependent manner.     

TNF gene cluster deletion abolishes lipopolysaccharide-mediated sensitization of the neonatal brain to hypoxic ischemic insult

In the current study, we explored the role of TNF cluster cytokines on the lipopolysaccharide (LPS)-mediated, synergistic increase in brain injury after hypoxic ischemic insult in postnatal day 7 mice. Pretreatment with moderate doses of LPS (0.3?μg/g) resulted in particularly pronounced synergistic injury within 12?h. Systemic application of LPS alone resulted in a strong upregulation of inflammation-associated cytokines TNFα, LTβ, interleukin (IL) 1β, IL6, chemokines, such as CXCL1, and adhesion molecules E-Selectin, P-Selectin and intercellular adhesion molecule-1 (ICAM1), as well as a trend toward increased LTα levels in day 7 mouse forebrain. In addition, it was also associated with strong activation of brain blood vessel endothelia and local microglial cells. Here, deletion of the entire TNF gene cluster, removing TNFα, LTβ and LTα completely abolished endotoxin-mediated increase in the volume of cerebral infarct. Interestingly, the same deletion also prevented endothelial and microglial activation following application of LPS alone, suggesting the involvement of these cell types in bringing about the LPS-mediated sensitization to neonatal brain injury.     

白细胞介素-1β及肿瘤坏死因子-α对脑损伤后胶质细胞c-fos mRNA表达的影响

本研究用分子杂交技术观察了白细胞介素-1β及肿瘤坏死因子-α对脑损伤后及培养的胶质细胞c-fosmRNA表达的影响。结果发现：脑损伤后损伤周围组织c-fosmRNA表达圣动态变化：1h后增加170％．12h后增加30％，24h后增加130％。发现白细胞介素-1β和肿瘤坏死因子-α能显著增加脑损伤后12h及24hc-fosmRNA的表达；当培养的胶质细胞中加入此二者后1hc-fosmRNA表达明显增加，12h后有所下降。又发现同时加入此二者时，c-fosRNA表达增加更加显著。以上结果提示；白细胞介素-1β和肿瘤坏死因子-α能影响脑损伤后胶质细胞c－fosmRNA的表达，它们对胶质细胞的作用可能与c-fos基因有关。     

Intracranial injection of recombinant stromal-derived factor-1 alpha (SDF-1α) attenuates traumatic brain injury in rats

Objective

This study was conducted to investigate the role of stromal-derived factor-1 alpha (SDF-1α) in a secondary brain injury after traumatic brain injury (TBI) in rats, and to further elucidate its underlying regulatory mechanisms.

Materials and methods

Male Sprague–Dawley rats underwent TBI for 30 min, and then received intracranial injections of recombinant SDF-1α, SDF-1α antibody, or saline as a vehicle control. At 24 h after TBI, brain tissues from the experimental animals were subjected to histology, immunohistochemistry, quantitative real-time polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA), and western blot analyses.

Results

TBI-induced brain edema and blood–brain barrier disruption were ameliorated by post-injury injections of SDF-1α. TBI-induced neuronal degradation and apoptosis, accompanied by increased cleaved caspase-3, cleaved PARP and Bax, and decreased Bcl-2 were found to be attenuated by SDF-1α injection. Nitric oxide (NO) and inducible nitric oxide synthase (iNOS) levels decreased in SDF-1α treated animals after TBI. SDF-1α repressed inflammatory responses by inhibiting the expression of pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6. However, neutralizing the effect of SDF-1α with its antibody abolished these therapeutic alterations in TBI animals. Importantly, SDF-1α attenuated the brain lesion by affecting the ERK and NF-κB signaling pathways after mechanical head trauma in rats.

Conclusions

SDF-1α ameliorates mechanical trauma-induced pathological changes via its anti-apoptotic and anti-inflammatory action in the brain.     

Vitexin alleviates interleukin‐1β‐induced inflammatory responses in chondrocytes from osteoarthritis patients: Involvement of HIF‐1α pathway

It has been reported that vitexin has anti‐inflammatory effects in osteoarthritis (OA) rats. However, the effects of vitexin on interleukins‐1β (IL‐1β)‐stimulated OA patient‐derived chondrocytes have not been reported. The purpose of this study was to investigate the anti‐inflammatory effects of vitexin on IL‐1β‐stimulated human osteoarthritis chondrocytes and to reveal the involvement of hypoxia‐inducible factor 1α (HIF‐1α) pathway. Enzyme‐linked immunosorbent assay, quantitative real‐time PCR and Western blotting assays were employed. ELISA results demonstrated that the proinflammatory cytokine levels of interleukins‐6 (IL‐6) and tumour necrosis factor α (TNF‐α) in the serum and synovial fluid and HIF‐1α level in the synovial fluid were significantly elevated in OA patients compared to normal healthy subjects. Moreover, the Western blotting results indicated that the protein expression of HIF‐1α was significantly higher in the cartilage tissues of OA patients. OA patient‐derived chondrocytes were stimulated by IL‐1β and treated with different concentration of vitexin for 24 hours. Vitexin showed no cytotoxicity and increased the survival of chondrocytes under IL‐1β stimulation. Vitexin suppressed IL‐1β‐induced production of NO and prostaglandin E2 (PGE₂) in chondrocytes culture. The treatment of vitexin significantly inhibited IL‐1β‐induced expressions of proinflammatory cytokine levels of IL‐6, TNF‐α, matrix metalloproteinase (MMP)‐1, MMP‐3 and MMP‐13. Furthermore, Western blotting results demonstrated that HIF‐1α is involved in vitexin's protective effects on IL‐1β‐stimulated injuries in OA patient‐derived chondrocytes. Our study demonstrates that vitexin alleviates IL‐1β‐induced inflammatory responses in chondrocytes from osteoarthritis patients, which may be attributed partly to the inhibition of HIF‐1α pathway.     

甘露醇对脂多糖致小鼠脑水肿治疗的多参数评估

本研究采用脂多糖(LPS)诱导细胞因子建立小鼠脑水肿模型,评估不同作用时间(2、4、12、24 h)甘露醇对小鼠脑水肿的治疗效果.观察实验前后脑水含量差异,测定细胞因子含量(IL-1β、AQP4、TNF-α),再研究脑组织光学内源信号变化规律,最后基于这些参数分析甘露醇对脂多糖致小鼠脑水肿治疗效果.LPS组脑含水量低于...     

灵芝活性多糖GLIS对正常和荷瘤小鼠骨髓巨噬细胞的激活作用

为研究灵芝活性多糖GLIS对正常和荷瘤小鼠巨噬细胞的激活作用,用灵芝活性多糖GLIS刺激体外培养的正常和荷瘤小鼠的巨噬细胞,检测GLIS刺激后巨噬细胞分泌至培养基中的TNF-α、IL-1β和NO的含量,以及小鼠巨噬细胞对乳胶颗粒的吞噬率的变化,并检测GLIS刺激的巨噬细胞对肿瘤细胞的抑制作用,同时研究灵芝活性多糖GLIS组成的糖和蛋白部分对活性的影响。结果显示经灵芝活性多糖GLIS刺激后,能显著刺激巨噬细胞分泌TNF-α和IL-1β,并产生大量的NO。小鼠巨噬细胞对乳胶颗粒的吞噬功能也明显的增强,且荷瘤小鼠的巨噬细胞对GLIS的敏感度要优于正常小鼠,GLIS中的糖部分对它的活性作用起主要作用。该研究表明,灵芝活性多糖GLIS对正常和荷瘤小鼠巨噬细胞均具有明显的激活作用。     

Apocynin降低1型糖尿病小鼠心肌组织炎症因子的表达

目的： 探讨NADPH氧化酶抑制剂apocynin对1型糖尿病小鼠心肌组织IL-1β、IL-18、TNF-α和COX-2表达的影响及其机制研究。方法: C57小鼠腹腔注射STZ建立1型糖尿病动物模型,44只8周龄雄性小鼠分为对照组（sham,n=6）、apocynin对照组（Apo,n=6）、1型糖尿病组（STZ,n=16）及1型糖尿病apocynin治疗组(STZ+Apo,n=16)。实验于8周末结束,运用超声心动图检测小鼠心脏功能,以实时定量RT-PCR技术测定心肌组织IL-1β、IL-18、TNF-α和COX-2 mRNA表达,以Western blotting检测心肌组织磷酸化Akt表达。结果: 1型糖尿病小鼠心脏功能降低伴随心肌组织IL-1β、IL-18、TNF-α和COX-2 mRNA表达增加,STZ+Apo组小鼠心脏功能增高伴随心肌组织IL-1β、IL-18、TNF-α和COX-2 mRNA表达减少;1型糖尿病小鼠心肌组织磷酸化Akt显著减少,STZ+Apo组心肌组织磷酸化Akt明显增加。结论: Apocynin提高1型糖尿病小鼠心脏功能伴随显著减少心肌组织IL-1β、IL-18、TNF-α和COX-2 mRNA的表达,其机制可能与增加心肌组织磷酸化Akt表达密切相关。     

穿心莲内酯对肺纤维化大鼠BALF中细胞因子和肺组织Ⅰ、Ⅲ型胶原mRNA表达的影响

目的:探讨穿心莲内酯灌胃对博来霉素(BLM)致肺纤维化大鼠支气管肺泡灌洗液(BALF)中TNF-α、TGF-β1浓度和肺组织Ⅰ、Ⅲ型胶原mRNA表达的影响。方法:取健康雄性SD大鼠90只,随机分为生理盐水(NS)组、BLM组、泼尼松(Pred)组、不同剂量穿心莲内酯组(即穿A组62.5mg/kg、穿B组125 mg/kg、穿C组250 mg/kg),各组大鼠15只,分别气管内灌注BLM(BLM组、Pred组、穿A组、穿B组、穿C组)或NS(NS组)后,每天给予NS(NS组、BLM组)、Pred(Pred组)或穿心莲内酯(穿A组、穿B组、穿C组)灌胃,各组分别于气管内灌注药物后第7、14、28天处死大鼠5只。用HE、Masson染色观察肺泡炎症和纤维化改变;实时荧光定量逆转录-聚合酶链反应检测肺组织Ⅰ、Ⅲ型胶原mRNA表达;酶联免疫吸附试验测定BALF中TNF-α、TGF-β1浓度;同时监测肾功能指标血尿素氮(BUN)、肌酐(Cr)及肝功能指标血丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)。结果:肝肾功能监测显示:不同剂量穿心莲内酯组、NS组、BLM组、Pred组所监测的AST、ALT、BUN、Cr比较,差异无统计学意义(P>0.05)。NS组大鼠肺组织未发现肺泡间隔水肿、炎性细胞浸润和纤维化形成。BLM组第7天时肺泡腔内可见大量炎性细胞浸润,第14天时肺泡炎仍存在,但炎症细胞明显减少,肺泡间隔内成纤维细胞明显增多,肺泡结构破坏,肺泡隔增宽,第28天时炎症较前减轻,肺纤维化程度加重,部分肺泡腔消失,形成严重纤维化。穿A组病理形态改变与BLM组相似。Pred组、穿B组、穿C组大鼠第7天有较多的炎症细胞浸润及局部聚积,第14天和第28天的纤维化病理改变均较BLM组、穿A组明显减轻。NS组各个时间点BALF中TGF-β1、TNF-α含量均明显低于同时间点BLM组、Pred组、穿A组、穿B组、穿C组BALF中的浓度(P<0.05)。BLM组3个时间点BALF中TGF-β1、TNF-α含量较Pred组、穿B、穿C组高(P<0.05)。与BLM组比较,穿A组BALF中TGF-β1、TNF-α含量无统计学意义。NS组各个时间点肺组织Ⅰ、Ⅲ型胶原mRNA表达均明显低于同时间点BLM组、Pred组、穿A组、穿B组、穿C组肺组织中的表达(P<0.05)。BLM组3个时间点Ⅰ、Ⅲ型胶原mRNA表达较Pred组、穿B组、穿C组高(P<0.05)。与BLM组比较,穿A组肺组织Ⅰ、Ⅲ型胶原mRNA表达无统计学差异。结论:穿心莲内酯灌胃可减轻BLM致肺纤维化大鼠肺泡炎和肺纤维化程度,降低肺组织Ⅰ、Ⅲ型胶原mRNA表达,降低BALF中TNF-α、TGF-β1浓度,且对肝肾无明显毒副作用。     

探讨醒脑灌肠液对心肺复苏后大鼠脑损伤及IL-33/ST2信号通路的影响

目的:研究醒脑灌肠液对心肺复苏后大鼠脑损伤及IL-33/ST2信号通路的影响,以探讨醒脑灌肠液对心肺复苏后大鼠的脑保护作用及机制。方法:SD大鼠随机分为假手术组、模型组、醒脑灌肠液低剂量(5 mL/kg)组、醒脑灌肠液中剂量(10 mL/kg)组、醒脑灌肠液高剂量(20 mL/kg)组和乌司他丁组,每组12只,除假手术组,其它各组建立大鼠心肺复苏模型,并相应给予醒脑灌肠液和乌司他丁治疗。7 d后所有大鼠进行神经功能缺损评分;处死大鼠检测脑组织含水量;以苏木精-伊红(HE)染色检测各组大鼠脑组织病理性变化;以超氧化物歧化酶(SOD)和丙二醛(MDA)检测试剂盒分别检测脑组织中SOD和MDA水平;以酶联免疫吸附法(ELISA)检测血清中S100钙结合蛋白β亚基(S100β)和神经元特异性烯醇化酶(NSE)含量及脑组织中白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)水平;以Western blot法检测脑组织白细胞介素33(IL-33)和生长刺激表达基因2蛋白(ST2)表达。结果:与假手术组相比,模型组大鼠脑组织出现组织结构紊乱,局灶出血,神经元核收缩、凋亡等病理改变;神经功能缺...