NADPH oxidase participates in pancreatic injury in rats with acute hypertriglyceridemic pancreatitis by regulating Akt/GSK3 β pathway
10.3760/cma.j.issn.1671-0282.2019.12.008
- VernacularTitle: NADPH氧化酶通过调节Akt/GSK3β通路参与高脂血症性急性胰腺炎大鼠胰腺损伤
- Author:
Xiaojia YANG
1
;
Kailiang ZHAO
1
;
Man LI
1
,
2
;
Chenyang WANG
1
,
2
;
Qianying HE
1
,
2
;
Weixing WANG
1
Author Information
1. Department of General Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China
2. Key Laboratory of Hubei Province for Digestive System Disease, Wuhan 430060, China
- Publication Type:Journal Article
- Keywords:
Hypertriglyceridemia;
Acute pancreatitis;
Pancreatic injury;
NADPH oxidase;
Oxidative stress
- From:
Chinese Journal of Emergency Medicine
2019;28(12):1501-1506
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the aggravation of pancreatic tissue injury in rats with acute hypertriglyceridemic pancreatitis and the possible role of NADPH oxidase (NOX).
Methods:Thirty SPF rats were randomly (random number)divided into five groups: N group, H group, NLAP group, HLAP group and HAPO group. AMY, TG, TC and FFA levels were detected. The pathological changes of pancreas were observed under light microscope and the ultrastructural changes of pancreatic acinar cells were observed by TEM. Serum levels of MDA, SOD, IL-1β, TNF-α and LDH were detected. The expression of NOX4, p-Akt and p-GSK3β in pancreas was detected by immunofluorescence, and the expression of NF-κB and TNF-α in pancreas was detected by immunohistochemistry.
Results:Intraperitoneal injection of P-407 could significantly increase the levels of serum TG, TC and FFA in rats. After acute pancreatitis induced by L-Arg, the levels of serum AMY in the NLAP and HLAP groups were significantly increased, while Apocynin could significantly decrease the level of serum AMY. Compared with the NLAP group, the pathological injury of pancreatic tissue in the HLAP group was more serious, the level of inflammatory mediators was significantly increased, and the cell necrosis was more serious. After inhibiting NOX, the activation of Akt/GSK3β pathway was regulated and the pancreatic injury was improved.
Conclusion:In HTGP, NOX aggravates pancreatic injury by regulating the activation of Akt/GSK3 β pathway. Inhibition of NOX expression can play a protective role in pancreas injury of HTGP..
