Effect of the regulation of retinoid X receptor‐α gene expression on rat hepatic fibrosis

To study the effect of retinoid X receptor-α (RXR-α) expression on rat hepatic fibrosis. Rat hepatic fibrosis was induced by CCl(4) , and the rats were randomly divided into an early-phase hepatic fibrosis group (2 weeks) and a sustained hepatic fibrosis group (8 weeks). They were then divided into four groups (normal control, hepatic fibrosis, negative control and RXR-α groups). A recombinant lentiviral expression vector carrying the rat RXR-α gene was injected into the rats to induce RXR-α expression by intraportal infusion, hepatic tissue pathological examination was performed, and hydroxyproline content was detected. Hepatic stellate cells (HSC) were cultured in vitro, an RXR-α lentivirus vector was used to activate HSC, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) activation was assayed to detect HSC proliferation. In vivo experiments indicated that in the sustained hepatic fibrosis group, there were significant differences in the hydroxyproline content, and expression of RXR-α, α-smooth muscle actin (α-SMA) and type I collagen (P < 0.01). However, in the early-phase hepatic fibrosis group, hydroxyproline content and the protein level of RXR-α showed no significant difference compared with the normal control group (P > 0.05). In vitro studies revealed that expression of RXR-α significantly inhibited expression of α-SMA and type I collagen in activated HSC (P < 0.01), as well as HSC proliferation (P < 0.01). The increased RXR-α gene expression inhibited HSC activation and proliferation and the degree of hepatic fibrosis.