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刺五加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。

Acanthopanax 3-Methyladenine Ameliorates Sodium Taurocholate-Induced Severe Acute Pancreatitis by Inhibiting the Autophagic Pathway in Rats.

作者信息

Wang Xiaohong, Zhou Guoxiong, Liu Chun, Wei Ronglong, Zhu Shunxing, Xu Yuefen, Wu Mengjie, Miao Qing

机构信息

Department of Gastroenterology, Danyang People's Hospital, Danyang 212300, China.

Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong 226001, China.

出版信息

Mediators Inflamm. 2016;2016:8369704. doi: 10.1155/2016/8369704. Epub 2016 Dec 28.

DOI:10.1155/2016/8369704
PMID:28115794
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5225378/
Abstract

. To observe the therapeutic effects of Acanthopanax and 3-methyladenine against severe acute pancreatitis (SAP). . 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-B) 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. . There was no significant difference in mortality between SAP group and both treatment groups ( > 0.05). Serum amylase levels, protein, and mRNA expression levels of nucleus NF-B 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 ( < 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. . 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.

摘要

观察刺五加和3 - 甲基腺嘌呤对重症急性胰腺炎(SAP)的治疗效果。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。采用酶联免疫吸附测定法(ELISA)测定血清淀粉酶水平;分别通过蛋白质免疫印迹法(Western blot)和定量实时聚合酶链反应(quantitative real-time PCR)检测胰腺组织中核因子κB(NF-κB)p65、轻链3II(LC3-II)、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;术后3、12和24小时观察胰腺的死亡率和病理变化。SAP组与两个治疗组的死亡率无显著差异(P>0.05)。两个治疗组术后12和24小时的血清淀粉酶水平、核NF-κB p65、LC3-II和Beclin-1的蛋白和mRNA表达水平、PI3K-III的mRNA表达水平以及胰腺病理评分均显著低于SAP组(P<0.05或0.01)。两个治疗组胰腺腺泡细胞在术后12和24小时的自噬体和自噬溶酶体数量均少于SAP组。刺五加和3 - 甲基腺嘌呤对大鼠SAP具有相似的治疗效果。其机制可能是通过抑制胰腺腺泡细胞的异常自噬激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1b9/5225378/1629451d784d/MI2016-8369704.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1b9/5225378/4db229733e2f/MI2016-8369704.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1b9/5225378/4147142a9135/MI2016-8369704.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1b9/5225378/1629451d784d/MI2016-8369704.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1b9/5225378/4db229733e2f/MI2016-8369704.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1b9/5225378/afc96d1e6614/MI2016-8369704.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1b9/5225378/204183519f27/MI2016-8369704.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1b9/5225378/3caf76eef3dd/MI2016-8369704.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1b9/5225378/4147142a9135/MI2016-8369704.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1b9/5225378/1629451d784d/MI2016-8369704.006.jpg

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