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作 者:钱玲梅[1] 刘峰[2] 倪毓辉[2] 郭锡熔[2]
机构地区:[1]南京医科大学第一附属医院,210029 [2]南京医科大学儿科医学研究所
出 处:《江苏医药》2008年第7期700-702,共3页Jiangsu Medical Journal
基 金:国家自然科学基金(30371502);江苏省自然科学基金(BK2001120)
摘 要:目的探讨抵抗素(resistin)及其结合多肽(RBP)对大鼠肝细胞糖原合成的影响。方法体外培养大鼠BRL肝细胞,分为空白对照组、抵抗素(60ng/ml)干预组、RBP(1nmol/L)干预组和抵抗素(60ng/ml)+RBP(1nmol/L)联合干预组,培养2h后筹集细胞,以蒽酮法检测胞内糖原含量,并采用RT-PCR法检测IRS2、SOCS3、GLUT2等基因mRNA的表达变化。结果与空白对照组比较,抵抗素干预组糖原含量显著下降,但RBP干预组则无显著差异;与抵抗素干预组相比,抵抗素+RBP联合干预组糖原含量明显升高。各干预组BRL细胞中GLUT2基因的mRNA水平无显著差异。抵抗素干预组SOCS3 mRNA水平显著上调、IRS2 mRNA水平显著下调;但两者在抵抗素+RBP联合干预组则无明显变化。结论RBP能拮抗抵抗素抑制肝细胞糖原合成的作用,但对正常肝细胞糖原合成功能无明显影响。Objective To investigate the effects of resistin and resistin binding peptide (RBP) on the glycogen synthesis of BRL hepatocytes in rats. Methods BRL cells were cultured in vitro and respectively treated with resistin (60 ng/ml,group R) ,RBP (1 nmol/L,group RBP) , resistin (60 ng/ ml) plus RBP (1 nmol/L) (group RR) ,or without intervention as the control (group C) for 2 hours. Glycogen content was detected. The expressions of glucose transporter 2 (GLUT2), IRS2 and SOCS3 gene mRNA were detected by RT-PCR. Results The glycogen content was significantly lower in group R than that in group C,which was not remarkably different between group RBP and group C, but was higher in group RR than that in group R. There was no significant difference in the GLUT2 mRNA level among the four groups. The expression of SOCSs mRNA was upregulated and that of IRS2 mRNA was downregulated in group R, which was not significantly changed in group RR. Conclusion RBP can antagonize the effects of resistin on the glycogen synthesis in BRL cells.
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