Protective effects of heme oxygenase-1 against severe acute pancreatitis via inhibition of tumor necrosis factor-α and augmentation of interleukin-10

BMC Gastroenterology

Research Article

Ning Han¹  Xiao-bin Dong¹  Fei-hu Zhang¹  Hao Zhao¹  Li Kong¹  Kai-liang Fan¹  Yu-han Sun² 

[1] Department of Emergency Center, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jingshi Road No.16369, 250011, Jinan, Shandong Province, China;Department of Traditional Chinese Medicine, Jinan Municipal Organs Hospital, Jianguoxiaojingsan Road No.35, 250001, Jinan, Shandong Province, China;

关键词: Heme oxygenase-1;    Severe acute pancreatitis;    Oxidative stress;    Tumor necrosis factor-α;    Interleukin-10;   

DOI  :  10.1186/s12876-017-0651-4

 received in 2017-01-11, accepted in 2017-07-31,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundHeme oxygenase-1 (HO-1) is an inducible defense gene which plays a significant role in inflammation. HO-1 protects cells and tissues through the mechanism of anti-oxidation, maintaining microcirculation and anti-inflammation. The aim of the current study is to investigate the role of HO-1 on systemic inflammatory response in severe acute pancreatitis (SAP).MethodsForty male Sprague-Dawley (SD) rats were randomly assigned into four groups: control group (n = 10); SAP group (n = 10), SAP model was induced by retrograde injection of 3% sodium taurocholate through pancreatic duct; HO-1 stimulation group (n = 10), SD rats were injected 75 μg/kg hemin intraperitoneally 30 min after induction of SAP; HO-1 inhibition group (n = 10), SD rats were injected 20 μg/kg Zinc porphyrin (Zn-PP) intraperitoneally 30 min after induction of SAP. After 24 h of SAP establishment, tissues were collected for HO-1, tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) mRNA expression, and blood samples were collected for cytokines and biochemical measurements. Meanwhile, the histopathological changes of pancreas and liver tissues were observed.ResultsThe expression of HO-1 mRNA and protein were significantly induced by SAP in rat pancreas and liver. Hemin treatment significantly decreased oxidative stress and TNF-α in plasma and tissues, while the IL-10 was significantly increased. Pancreas and liver injury induced by SAP was markedly attenuated by Hemin treatment. Moreover, inhibition of HO-1 expression by Zn-PP administration aggravated the injury caused by SAP.ConclusionsInduction of HO-1 in early SAP may modulate systemic inflammatory response and prevent pancreas and nearby organs such as liver injury through inhibition of TNF-α and augmentation of IL-10.

【 授权许可】

CC BY   
© The Author(s). 2017