Sheng-jiang powder ameliorates obesity-induced pancreatic inflammatory injury via stimulating activation of the AMPK signalling pathway in rats

被引:0
|
作者
Yi-Fan Miao [1 ]
Juan Li [1 ]
Yu-Mei Zhang [1 ]
Lv Zhu [1 ]
Huan Chen [1 ]
Ling Yuan [1 ]
Jing Hu [1 ]
Xiao-Lin Yi [1 ]
Qiu-Ting Wu [1 ]
Mei-Hua Wan [1 ]
Wen-Fu Tang [1 ]
机构
[1] Department of Integrative Medicine,West China Hospital,Sichuan University
基金
中国国家自然科学基金;
关键词
Obesity; Sheng-jiang powder; Adiponectin; Adenosine 5’-monophosphate-activated protein kinase; Pancreatic inflammatory injury;
D O I
暂无
中图分类号
R576 [胰腺疾病];
学科分类号
1002 ; 100201 ;
摘要
AIM To investigate the mechanisms by which Sheng-jiang powder(SJP) ameliorates obesity-induced pancreatic inflammatory injury.METHODS Sprague-Dawley rats were randomized into three groups: normal group(NG), obese group(HLG), or SJP treatment group(HSG). Obesity was induced by feeding a high-fat diet in the HLG and HSG, while the NG received standard chow. Rats were euthanized after 12 wk, and blood and pancreatic tissues were collected for histopathological analyses. Nuclear factor kappa-light-chain-enhancer of activated B cells(NF-κB) and transforming growth factor beta(TGF-β) expression, serum triglyceride and adiponectin levels, and apoptosis in pancreatic acinar cells were assessed. A high-fat AR42 J acinar cell injury model was established using very low-density lipoprotein(VLDL). AR42 J acinar cell culture supernatant, treated with different interventions, was applied to seven groups of pancreatic stellate cells(PSCs). The proliferation of PSCs and the expression of fibronectin and type I collagenase were assessed.RESULTS Compared with the NG, we found higher pathological scores for pancreatic tissues, lower serum adiponectin levels, higher expression levels of NF-κB in pancreatic tissues and TGF-β in pancreatic inflammatory cells, and increased apoptosis among pancreatic acinar cells for the HLG(P < 0.05). Compared with the HLG, we found reduced body weight, Lee’s index scores, serum triglyceride levels, and pathological scores for pancreatic tissues; higher serum adiponectin levels; and lower expression levels of NF-κB, in pancreatic tissue and TGF-β in pancreatic inflammatory cells for the HSG(P < 0.05). The in vitro studies showed enhanced PSC activation and increased expression levels of fibronectin and type I collagenase after SJP treatment. An adenosine 5‘-monophosphate-activated protein kinase(AMPK) inhibitor inhibited PSC activation.CONCLUSION SJP may ameliorate obesity-induced pancreatic inflammatory injury in rats by regulating key molecules of the adiponectin-AMPK signalling pathway.
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收藏
页码:4448 / 4461
页数:14
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