Published online Oct 21, 2018. doi: 10.3748/wjg.v24.i39.4448
Peer-review started: July 9, 2018
First decision: August 25, 2018
Revised: September 12, 2018
Accepted: October 5, 2018
Article in press: October 5, 2018
Published online: October 21, 2018
To investigate the mechanisms by which Sheng-jiang powder (SJP) ameliorates obesity-induced pancreatic inflammatory injury.
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 AR42J acinar cell injury model was established using very low-density lipoprotein (VLDL). AR42J 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.
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.
SJP may ameliorate obesity-induced pancreatic inflammatory injury in rats by regulating key molecules of the adiponectin-AMPK signalling pathway.
Core tip: Obesity is a risk factor for non-alcoholic fatty pancreas disease and induces pancreatic inflammatory injury. Sheng-jiang powder (SJP) can ameliorate obesity-induced pancreatic inflammatory injury; however, the specific mechanisms remain unclear. This study demonstrates that SJP may inhibit the inflammatory response, prevent pancreatic fibrosis, promote pancreatic acinar cell repair, and ultimately ameliorate obesity-induced pancreatic inflammatory injury in rats by regulating the key molecules of the AMPK signalling pathway.