首页> 美国卫生研究院文献>Mediators of Inflammation >Acanthopanax versus 3-Methyladenine Ameliorates Sodium Taurocholate-Induced Severe Acute Pancreatitis by Inhibiting the Autophagic Pathway in Rats
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Acanthopanax versus 3-Methyladenine Ameliorates Sodium Taurocholate-Induced Severe Acute Pancreatitis by Inhibiting the Autophagic Pathway in Rats

机译:刺五加与3-甲基腺嘌呤通过抑制大鼠自噬途径改善牛磺胆酸钠诱导的重症急性胰腺炎

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摘要

Objectives. To observe the therapeutic effects of Acanthopanax and 3-methyladenine against severe acute pancreatitis (SAP). Methods. Sodium taurocholate-induced SAP rats were equally randomized into a SAP group, an Acanthopanax group, and a 3-methyladenine group. Serum amylase levels were determined by ELISA; protein and mRNA expression levels of nucleus nuclear factor kappa B (NF-κB) p65, light chain 3II (LC3-II), and Beclin-1 and mRNA expression levels of Class III phosphatidylinositol 3-kinase (PI3K-III) in pancreas tissue were detected by Western blot and quantitative real-time PCR, respectively; mortality and pathological change of the pancreas were observed at 3, 12, and 24 h after operation. Results. There was no significant difference in mortality between SAP group and both treatment groups (P > 0.05). Serum amylase levels, protein, and mRNA expression levels of nucleus NF-κB p65, LC3-II, and Beclin-1 protein, mRNA expression levels of PI3K-III, and pathological score of the pancreas in both treatment groups were significantly lower than those in SAP group at 12 and 24 h after operation (P < 0.05 or 0.01). The number of autophagosomes and autophagolysosomes of pancreatic acinar cells in both treatment groups was smaller than that in SAP group at 12 and 24 h. Conclusions. Acanthopanax and 3-methyladenine had similar therapeutic effects against SAP in rats. The mechanism may be through inhibiting abnormal autophagy activation of pancreatic acinar cells.
机译:目标。观察刺五加和3-甲基腺嘌呤对严重急性胰腺炎(SAP)的治疗作用。方法。将牛磺胆酸钠诱导的SAP大鼠随机分为SAP组,刺五加组和3-甲基腺嘌呤组。通过ELISA测定血清淀粉酶水平;胰腺组织中核仁因子κB(NF-κB)p65,轻链3II(LC3-II)和Beclin-1的蛋白和mRNA表达水平以及III类磷脂酰肌醇3-激酶(PI3K-III)的mRNA表达水平分别通过蛋白质印迹和实时定量PCR检测;术后3、12、24h观察胰腺的死亡率和病理变化。结果。 SAP组与两个治疗组之间的死亡率无显着差异(P> 0.05)。两个治疗组的血清淀粉酶水平,核NF-κBp65,LC3-II和Beclin-1蛋白的蛋白质和mRNA表达水平,PI3K-III的mRNA表达水平以及胰腺的病理学评分均显着低于那些治疗组。 SAP组术后12和24 h(P <0.05或0.01)。两个处理组的胰腺腺泡细胞自噬体和自噬体的数量在12和24h时均小于SAP组。结论。刺五加和3-甲基腺嘌呤对大鼠的SAP具有相似的治疗作用。其机制可能是通过抑制胰腺腺泡细胞的异常自噬激活。

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