Found programs:
Authors:Wang Lingmei; Guan Shihe; Zhang Hao
Keywords:chronic hepatitis B;vitamin D;vitamin D receptor
DOI:10.19405/j.cnki.issn1000-1492.2020.06.012
〔Abstract〕 Objective To analyze the expression levels of vitamin D(Vit D), liver vitamin D receptor(VDR) in patients with chronic hepatitis B(CHB) and its correlations with liver function and hepatitis B virus(HBV) serological indicators, and further explore whether Vit D can exert antiviral effects in vitro. Methods The serum levels of Vit D were measured in 81 untreated CHB patients and 40 healthy subjects. The expression of VDR in liver tissue was analyzed by immunohistochemistry. HBV-related parameters(HBsAg, HBeAg, HBV DNA) in cell culture supernatants and the protein expressiones(VDR, IRF-9, MxA) in cells were detected after HepG2.2.15 cellswere treated with Vit D alone or in combination with IFN-α. Results The serum Vit D level in CHB group was lower than that in healthy controls( HC) group( P<0. 05). The serum Vit D level was positively correlated with albumia( ALB)( r = 0. 339,P = 0. 002),negatively correlated with HBV DNA viral load( r =-0. 274,P =0. 013),correlated with e atigen status( P<0. 05),no correlation with alanine aminotransferase( ALT) 、aspartate aminotransferase( AST) 、total bilirubin( TBIL) 、alkaline phosphatase( ALP) 、gamma-glutamyl transferase( GGT),HBsA g and HBc Ab. Also,the expression levels of Vit D and VDR were related to the severity of CHB. The expression levels of Vit D in serum and VDR in liver tissue of severe CHB patients were lower than those of mild and moderate CHB patients. The expression of VDR,JAK-STAT signal transduction molecules IRF-9 and downstream antiviral protein Mx A in the Vit D combination with IFN-α group were higher and the secretion of HBV-related antigens was lower than those in the blank group and the single treatment group. Conclusion There may be a decline in the function of the Vit D/VDR signaling pathway in patients with CHB. Vit D may play a synergistic IFN-α antiviral effect by increasing the VDR expression and thereby enhancing the IFN-JAK-STAT signaling pathway.