Published online Dec 21, 2017. doi: 10.3748/wjg.v23.i47.8334
Peer-review started: September 22, 2017
First decision: October 10, 2017
Revised: October 20, 2017
Accepted: November 14, 2017
Article in press: November 14, 2017
Published online: December 21, 2017
Processing time: 90 Days and 0.6 Hours
Previous studies have shown that the pathological changes of liver fibrosis, which refer to a series of pathogenic factors and pathological changes in the pathogenesis of a variety of liver diseases, could be reversed. In the past decade, numerous studies demonstrated that NF-E2-related factor 2 (Nrf2) as a transcription factor plays as an important role against oxidative stress in normal liver cells. Morin possesses biological properties, including antioxidant, anti-inflammatory, anti-apoptosis, and anticancer activities. To our knowledge, in vivo investigation of the effect of morin on the Nrf2 signaling pathway and Nrf2 expression in a CCl4-induced liver fibrosis model has not been reported previously.
Previous studies demonstrated that morin protected acute liver damage and ameliorated liver fibrosis induced by CCl4, and morin inhibited proliferation and induced apoptosis of activated hepatic satellate cells by suppressing the Wnt/β-catenin and the NF-kB signaling pathways. However, there is no molecular evidence about the effects of morin on the Nrf2 signaling pathway.
The purpose of this study was to investigate whether morin can reduce hepatic fibrosis by inducing the expression of Nrf2 and its downstream antioxidant enzymes in a rat model of CCl4-induced hepatic fibrosis.
Twenty male Sprague-Dawley rats were randomly divided into four groups: control group, morin group, carbon tetrachloride (CCl4) group, and morin + CCl4 group. At the end-point of the experimental period, serum AST, ALT, and ALP were measured, and the liver specimens were obtained for pathological assessment. α-SMA, collagen I, collagen III, NF-E2-related factor 2 (Nrf2), heme oxygenase (HO-1), and quinone oxidoreductase 1 (NQO1) were analyzed by real-time PCR and Western blot methods using frozen liver specimens.
Rats in the morin + CCl4 group had less hyperplasia of fiber tissues, minimal inflammatory cells, and less body weight loss with favorable liver enzyme measurements compared to rats treated with CCl4 only. Additionally, morin-treated rats had significantly lower mRNA and protein expression of α-SMA, collagen I, and collagen III, but significantly higher mRNA and protein expression of Nrf2, HO-1, and NQO1 compared to rats treated with CCl4 only (P < 0.05).
Our study showed that morin could play a protective role by inducing the expression of Nrf2 and its downstream antioxidant factors (HO-1 and NQO1) and reducing the expression of α-SMA, collagen I, and collagen III in a rat model of CCl4-induced hepatic fibrosis.
Although further studies are required, out study demonstrated that morin could effectively alleviate chronic liver damage by activation of the Nrf2 pathway.