Paeoniflorin attenuates CLP-induced acute liver injury by activating Nrf2/Υ-GCS in rats

被引:0
|
作者
Zhou, Lifang [1 ]
Peng, Huiyun [2 ]
Li, Shuangjie [1 ]
机构
[1] Hunan Childrens Hosp, Dept Hepatopathy, Changsha 410007, Hunan, Peoples R China
[2] Univ South China, Hengyang, Hunan, Peoples R China
关键词
Paeoniflorin; acute liver injury; cecal ligation and puncture; NF-E2-related factor 2; EXPERIMENTAL SEPSIS; OXIDATIVE STRESS; SYSTEMIC INFLAMMATION; SEPTIC SHOCK; NRF2; CELLS; PATHWAY; NANOPARTICLES; DYSFUNCTION; REGULATOR;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Objective: Acute liver injury (ALI) is a common and serious complication of sepsis. The imbalance between oxidation and anti-oxidation plays an important role in sepsis-induced ALI. Recent studies suggest that paeoniflorin (PF) may serve as an antioxidant. Nrf2-ARE signal pathway is known as an important anti-oxidative system. This study aimed to investigate the protective effects of PF on sepsis-induced ALI in which the role of Nrf2 was explored. Methods: Rats were randomly divided into 3 groups: sham group, sepsis group and PF group (n=12 per group). Sepsis was induced by cecal ligation and puncture (CLP). In PF group, rats were intraperitoneally rejected with PF at 90 mg/kg following CLP. The survival was determined within 48 h. At 6 h after treatment, the serum alanine aminotransferase (ALT), MDA content and SOD activity were measured and the liver was harvested for the Western blot assay and real time PCR of Nrf2 and Upsilon-GCS expressions. Results: Our results indicated that the survival rate within 48 h increased significantly, the serum ALT and malondialdehyde (MDA) reduced markedly, the serum superoxide dismutase (SOD) activity increased remarkably and the mRNA and protein expressions of nucleus Nrf2 and Upsilon-GCS in the liver were increased significantly in PF group as compared to sepsis group. Conclusion: Our findings suggest that PF is able to protect against sepsis induced ALI via modulating Nrf2 signaling pathway.
引用
收藏
页码:15935 / 15941
页数:7
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