Effect of Sinisan on Oxidative Stress in Cholestatic Hepatitis Rats Based on Nrf2/HO-1 Signaling Pathway
10.13422/j.cnki.syfjx.20240602
- VernacularTitle:基于Nrf2/HO-1信号通路探讨四逆散对胆汁淤积性肝炎大鼠氧化应激反应的影响
- Author:
Dan CAO
1
;
Qi CHEN
1
;
Xiaolu CHEN
1
;
Linzhen CHEN
1
;
Haiyan WANG
2
;
Juhui HAO
3
;
Wei ZHANG
4
;
Zhiqiang MA
1
Author Information
1. Beijing Key Laboratory for Quality Evaluation of Traditional Chinese Medicine，Beijing University of Chinese Medicine，Beijing 102488，China
2. Reproductive and Genetic Medical Center， Dalian Women and Children's Medical Group，Dalian 116000，China
3. School of Chinese Materia Medica，Beijing University of Chinese Medicine，Beijing 102488，China
4. The First Affiliated Hospital of Harbin Medical University，Harbin 150001，China
- Publication Type:Journal Article
- Keywords:
Sinisan;
cholestatic hepatitis;
oxidative stress;
nuclear factor erythroid 2 related factor 2 （Nrf2）;
heme oxygenase 1 （HO-1）
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2024;30(12):1-7
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveBased on the nuclear factor erythroid 2 related factor 2 （Nrf2）/heme oxygenase-1 （HO-1） signaling pathway， this paper explores the effect of Sinisan （SNS） on liver oxidative stress injury in cholestatic hepatitis rats and its mechanism. MethodThirty 6-week-old male SD rats were randomly divided into a control group， model group， low and high dose groups of SNS （2.5 and 5 g·kg-1） and ursodeoxycholic acid group （UDCA， 63 mg·kg-1）， with six rats in each group. Rats were administrated for seven consecutive days. On the 5th day， the control group was given olive oil of 10 mL·kg-1， and the other groups were given alpha-naphthalene isothiocyanate （ANIT） of 80 mg·kg-1. The serum biochemical indicator levels of cholestasis and the content of antioxidant factors in rat liver were detected by enzyme-linked immunosorbent assay （ELISA）. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in liver tissue. The relative mRNA and protein expressions of Nrf2， HO-1， and quinone oxidoreductase 1 （NQO1） in liver tissue were detected by real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot. ResultCompared with the control group， the model group showed a significant increase in the serum biochemical indicator levels of cholestasis and the content of antioxidant factors in liver tissue （P<0.01）. There were obvious pathological changes in the model group such as the disordered arrangement of hepatocytes， obvious congestion and necrosis in the portal area， infiltration of inflammatory cells， and destruction of the interlobular bile duct. The relative mRNA and protein expressions of Nrf2， HO-1， and NQO1 in liver tissue were significantly down-regulated in the model group （P<0.05， P<0.01）. Compared with the model group， the groups of SNS showed a significant decrease in the serum biochemical indicator levels of cholestasis and the content of antioxidant factors in liver tissue （P<0.01）， and the pathological liver injury was obviously improved. The necrotic area was reduced， and the infiltration of inflammatory cells was decreased. In addition， there was a small amount of extravasated blood in the interlobular vein. The relative mRNA and protein expressions of Nrf2， HO-1， and NQO1 in liver tissue were significantly up-regulated （P<0.05， P<0.01）. ConclusionSNS can significantly improve liver injury in cholestatic hepatitis rats， and its mechanism may be related to the inhibition of oxidative stress response mediated by the Nrf2/HO-1 signaling pathway.
