Hepatology research : the official journal of the Japan Society of Hepatology · 2011
Effect of the regulation of retinoid X receptor-α gene expression on rat hepatic fibrosis.
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Wang Zheng, Xu Jiapeng, Zheng Yongchao, Chen Wei, Sun Yongwei, Wu Zhiyong, Luo Meng
Аннотация
AIM: To study the effect of retinoid X receptor-α (RXR-α) expression on rat hepatic fibrosis.
METHODS: 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.
RESULTS: 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).
CONCLUSION: The increased RXR-α gene expression inhibited HSC activation and proliferation and the degree of hepatic fibrosis.
METHODS: 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.
RESULTS: 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).
CONCLUSION: The increased RXR-α gene expression inhibited HSC activation and proliferation and the degree of hepatic fibrosis.