Di'ao Xinxuekang alleviates non-alcoholic steatohepatitis in mice by up-regulating Nrf2/HO-1 signaling pathway.
10.19540/j.cnki.cjcmm.20211115.401
- Author:
Guo-Ying LI
1
;
Wen-Jing CHEN
2
;
Bu-Yun JIA
1
;
Xiang HE
1
;
Dan-Dan WANG
1
;
Guang-Liang CHEN
3
Author Information
1. College of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine Hefei 230012, China.
2. First Affiliated Hospital, Anhui University of Chinese Medicine Hefei 230601, China.
3. College of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine Hefei 230012, China Anhui Province Key Laboratory of Chinese Medicinal Formula Hefei 230012, China.
- Publication Type:Randomized Controlled Trial, Veterinary
- Keywords:
Di′ao Xinxuekang;
Nrf2/HO-1 signaling pathway;
inflammation;
non-alcoholic steatohepatitis;
oxidative stress
- MeSH:
Animals;
Drugs, Chinese Herbal;
Inflammation/metabolism*;
Lipids;
Liver;
Mice;
NF-E2-Related Factor 2/metabolism*;
Non-alcoholic Fatty Liver Disease/metabolism*;
Oxidative Stress;
Signal Transduction;
Superoxide Dismutase/metabolism*;
Tumor Necrosis Factor-alpha/metabolism*
- From:
China Journal of Chinese Materia Medica
2022;47(9):2491-2499
- CountryChina
- Language:Chinese
-
Abstract:
The present study investigated the therapeutic effect and mechanism of Di'ao Xinxuekang(DXXK) on non-alcoholic steatohepatitis(NASH) in mice. Sixty-five C57 BL/6 J mice were randomly divided into a normal group and an experimental group for model induction with the high-fat diet for 16 weeks. Then the mice in the experimental group were randomly divided into a model group, an atorvastatin group(4 mg·kg~(-1)·d~(-1)), and high-(200 mg·kg~(-1)·d~(-1)), medium-(60 mg·kg~(-1)·d~(-1)), and low-dose(20 mg·kg~(-1)·d~(-1)) DXXK groups, with 10 mice in each group. Drugs were administered by gavage for eight weeks. Serum lipid, liver lipid, serum alanine aminotransferase(ALT), aspartate aminotransferase(AST), malondialdehyde(MDA), superoxide dismutase(SOD), and glutathione reductase(GSH-Px) were determined. Interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) were measured by enzyme-linked immunosorbent assay(ELISA). The liver index was calculated. The liver pathological change and lipid accumulation were observed by HE and oil red O staining. The liver ultrastructure was observed by the transmission electron microscope. The mRNA and protein expression of nuclear factor-erythroid 2 related factor 2(Nrf2) and heme oxygenase-1(HO-1) was detected by real-time fluorescence-based quantitative PCR and Western blot, respectively. The results showed that compared with the normal group, the model group displayed serum lipid and liver lipid metabolism disorders, elevated transaminase, lipid deposition, steatosis, and inflammation, suggesting that the NASH model in mice was properly induced. Compared with the model group, the DXXK groups showed decreased serum lipid, liver lipid, ALT, AST, MDA, IL-1β, and TNF-α, increased SOD and GSH-Px, alleviated hepatic steatosis, ballooning, and inflammation, and up-regulated Nrf2 and HO-1 gene and protein expression. In conclusion, DXXK can significantly alleviate NASH in mice, which is related to the inhibition of oxidative stress and inflammatory damage by up-regulating the Nrf2/HO-1 signaling pathway.
