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作 者:陈靖[1] 顾勇[1] 张健[1] 朱蔚钰 林善锬[1]
出 处:《中华肾脏病杂志》2000年第5期287-290,共4页Chinese Journal of Nephrology
基 金:卫生部基金!(96-2-127)
摘 要:目的观察钙通道阻滞剂硝苯地平和活性维生素 D制剂罗钙全对尿毒症患者外周血单个核细胞(PBMC)上甲状旁腺素(PTH)受体基因表达的影响。方法30例非糖尿病常规血液透析患者随机分成硝苯地平组、罗钙全组和安慰剂组,治疗8周。应用逆转录-聚合酶链反应(RT-PCR)方法检测用药前后PBMC上PTH受体mRNA表达。结果硝苯地平治疗能使尿毒症患者PBMC上PTH受体<mRNA的低表达显著上调(0.1436±0.0500比0 3584±0.0400,P<0. 001),但仍未达到正常组水平(0.6837±0.0300,P<0.001)。罗钙全治疗可明显纠正低钙、高磷和高PTH血症,对PTH受体mRNA表达也有一定上调作用(0.1472±0.0100比0.2192±0.0200,P<0.001)。结论硝苯地平和罗钙全均能部分纠正尿毒症患者PTH受体基因表达的异常。Objective To investigate the effects of calcium channel blocker (nifedipine)and 1, 25 (OH) 2VitD3 (calcitriol) on the mRNA expression of PTH receptor in PBMC of uremic patients. Methods Thirty non-diabetic uremic patients undergoing maintenance hemodialysis were divided into the following groups: (1) nifedipine group; (2) calcitriol group; (3) placebo group. The level of PTH receptor mRNA was measured by semi-quantitative RT-PCR method at the end of 8th week. Results The down-regulation of PTH receptor in PBMC was observed in all patients before treatment, and there was no difference among three groups. After 8-week treatment, the levels of PTH receptor mRNA expression(PTH receptor I. O. D/ beta-actin I. O. D) were significantly increased in nifedipine group(from 0. 1436 ± 0. 0500 to 0. 3584 ± 0. 0400, P < 0. 001 ) and in calcitriol group(from 0. 1472 ± 0. 0100 to 0. 2192 ± 0. 0200, P < 0. 001 ), but still lower than that in normal group(0. 6837 ± 0. 0300, P < 0. 001 ). Placebo therapy produced no change. Conclusion Both calcium channel blocker and 1, 25 (OH) 2VitD3 could up-regulate PTH receptor mRNA expression in PBMC of uremic patients.
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