• 吡非尼酮抑制转化生长因子β1诱导肺成纤维细胞胶原合成的实验研究
  • Protective effect of Xuebijing injection on liver injury in severe acute pancreatitis and its effect on the expression of hepatic signal transduction and activator of transcription (p-STAT3)
  • 周俊平.吡非尼酮抑制转化生长因子β1诱导肺成纤维细胞胶原合成的实验研究[J].内科急危重症杂志,2019,25(5):410-412
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    DOI:10.11768/nkjwzzzz20190517
    中文关键词:  吡非尼酮  肺成纤维细胞  p38MAPK  胶原  TGF-β1
    英文关键词:Severe acute pancreatitis  Acute liver injury  Xuebijing  P-STAT3 signaling pathway
    基金项目:基金项目:湖北省教育厅科研项目 (No:B2016116)
    作者单位E-mail
    周俊平 枣庄矿业集团中心医院 2738920058@qq.com 
    摘要点击次数: 1956
    全文下载次数: 3031
    中文摘要:
          目的: 探讨吡非尼酮对转化生长因子β1(TGF-β1)诱导的肺成纤维细胞胶原合成的影响及机制。方法 : 以人胚胎肺成纤维MRC-5细胞为研究对象,用p38丝裂原活化蛋白激酶(p38MAPK)信号抑制剂SB203580和吡非尼酮处理TGF-β1诱导的肺成纤维细胞,MTT检测细胞增殖, Western blot检测细胞中Ⅲ型胶原酶(Col Ⅲ)、I型胶原酶(ColⅠ)蛋白表达和p38MAPK磷酸化水平。结果: TGF-β1诱导处理后的肺成纤维细胞增殖能力升高,细胞中Col Ⅲ、ColⅠ和p38MAPK磷酸化水平升高。吡非尼酮处理可以降低TGF-β1诱导的肺成纤维细胞增殖能力,减少细胞中Col Ⅲ、ColⅠ和p38MAPK磷酸化蛋白表达。p38MAPK信号抑制剂SB203580处理具有协同吡非尼酮降低TGF-β1诱导的肺成纤维细胞增殖和表达蛋白Col Ⅲ、ColⅠ及p38MAPK磷酸化水平的作用。结论: 吡非尼酮通过抑制p38MAPK信号,从而抑制TGF-β1诱导的肺成纤维细胞胶原合成。
    英文摘要:
          Objective: To investigate the effect of Xuebijing on severe acute pancreatitis (SAP) -associated acute liver injury in the rats and explore the underlying mechanisms. Methods: Male Sprague-Dawley (SD) rats (n=60) were randomly divided into sham-operated group (n=20), SAP model group (n=20), and treatment group (n=20). SAP model was induced by retrograde injection of 5% sodium taurocholate (1 mL/kg) into the biliopancreatic duct. The rats in Xuebijing treatment group were intraperitoneally injected with 4 mL/kg Xuebijing. The rats were sacrificed at 12 h (n=10) and 24 h (n=10) after the treatment. The levels of serum ALT and AST were determined by the puncture through inferior vena cava. The serum levels of TNF-α and IL-6 were examined by ELISA, and the protein levels of p-STAT3 in the liver were evaluated by Western blotting. Results: As compared with sham-operated group,the levels of serum ALT, AST, IL-6 and TNF-α in SAP model group were significantly increased, and those in Xuebijing treatment group were significantly decreased as compared with those in model group. Meanwhile, the phosphorylation levels of p-STAT3 were significantly increased in model group as compared with sham-operated group. The rats in Xuebijing treatment group had lower phosphorylation levels of STAT3. Conclusion: Xuebijing exerts a protective effect on pancreatitis-associated acute liver injury in the rats possibly via inhibiting p-STAT3 signaling pathway.