Journal Article

Preventive effects of 1,25-（OH）2VD3 against ConAinduced mouse hepatitis through promoting vitamin D receptor gene expression

Xu-dong HU Shi-li JIANG Cheng-hai LIU Yi-yang HU Cheng LIU Ming-yu SUN Gao-feng CHEN Ping LIU

2010

Overview

Aim： To investigate the immunosuppressive effects of 1,25-dihydroxyvitamin D3 （1,25-（OH）2VD3） on concanavalin A （ConA）-induced hepatitis and elucidate the action mechanism. Methods： Female BALB/C mice were intravenously administered ConA （20 mg/kg） to induce acute immunological liver injury. Liver damage was evaluated in respect to serum alanine transaminase （ALT） level and liver histological changes. The proliferation of splenocytes was measured by using [^3H]-thymidine incorporation. The cytokine level in the cultured splenocyte supernatant was determined by using enzyme-linked immunosorbent assays （ELISAs）. The percentage of different splenic T cell subtypes was analyzed by using flow cytometry. The expression of splenic vitamin D receptor （VDR） mRNA and protein was detected by using real-time qRT-PCR and Western blot, respectively. Results： 1,25-（OH）2VD3 （2.5 pg/kg, ip） significantly decreased the serum ALT levels and markedly attenuated the histological liver damage. The beneficial effect of 1,25-（OH）2VD3 was associated with： （i） inhibition of CD4^＋ T cell activation; （ii） reduction of interferon-y （IFN- Y） and elevation of both 1L-4 and IL-5 in supernatants of cultured splenocytes; and （iii） elimination of activated T cells by increasing VDR mRNA and protein expression in the spleen. Conclusion： 1,25-（OH）2VD3 had a significant protective effect against ConA-induced hepatitis, and its mechanism of action was associated with down-regulation of T cell-mediated immunity and up-regulation of VDR gene expression.

• Subject: 丙氨酸转氨酶 / 受体基因 / 基因表达调控 / 维生素D3 / 脾细胞增殖 / 预防作用