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作 者:邢丽[1] 柏林[1] 禹程远[1] 邸波[1] 解汝娟[1]
机构地区:[1]哈尔滨医科大学附属第一医院肾内科,150001
出 处:《实用医学杂志》2010年第14期2485-2487,共3页The Journal of Practical Medicine
基 金:黑龙江省科技厅重点攻关项目(编号:GC07C35301);黑龙江省教委基金(编号:11511187)
摘 要:目的:观察大鼠IgA肾病模型中小管间质的损害,并应用替米沙坦对其进行干预,研究其保护作用及可能机制。方法:运用牛血清白蛋白(BSA)+脂多糖(LPS)+四氯化碳(CCl4)。方法:建立IgA肾病模型,设立正常对照组、IgA模型组、替米沙坦治疗组,实验前后进行相关生化指标的测定,光学显微镜观察肾脏组织形态改变;免疫组化观察各组TGF-β1、α-SMA表达;RT-PCR检测TGF-β1、MCP-1变化。结果:模型组尿蛋白量增高,治疗组则有所降低(1.59±0.18vs14.14±1.99vs1.88±0.09),差异具有统计学意义;实验前后模型组肾功能改变显著,治疗组前后变化无统计学意义;模型组大鼠肾脏组织存在不同程度的系膜细胞增生及间质炎细胞浸润,而治疗组上述变化减轻;免疫组化及RT-PCR显示TGF-β1、α-SMA及MCP-1在正常组肾小管及间质中微量表达,模型组高表达,治疗组表达减少。结论:IgA肾病存在肾小管间质的损伤;替米沙坦可减少IgA肾病大鼠尿蛋白的排泄,抑制炎症及纤维化因子的表达,对IgA肾病小管间质的损伤起保护作用。Objective To explore the effect of telmisartan on tubulointerstitial injury in rat model of IgA nephropathy. Methods The rat model of IgA nephropathy was established by using bovine serum albumin, lipopoly- saccharide, and carbon tetrachloride. SD rats were randomly divided into control group, IgA model group, and telmisartan group. The related biochemical indicators were measured before and after the experiment. The morphologic changes in renal tissues were observed microscopically. Expressions of TGF-β1 and α-SMA were determined by immunohistochemistry and expressions of TGF-β1 and MCP-1 were detected using RT-PCR. Results As compared with the control group 24-hour urine protein was increased markedly in IgA model group, but lowered in telmisartan group ( 1.59 ± 0.18 vs. 14.14 ± 1.99 vs. 1.88 ± 0.09). Renal function changed significantly in the model group but did not differ significantly in the treatment group. As compared with IgA model group, mesangial cell proliferation and inflammatory cell infiltration was notably alleviated in the treatment group.Immunohistochemistry and RT-PCR showed TGF- β1, α-SMA, and MCP-1 expressed mildly in the tubule and interstitium in the control group and highly in the model group but downregulated in telmisartan group. Conclusions IgA nephropathy has tubulointerstitial injury. Telmisartan can decrease urine protein excretion and suppress inflammation and the expression of fibrosis factors, playing a protective role in tubulointerstitial injury in IgA nephropathy.
关 键 词:肾小球肾炎 IGA 血管紧张素受体拮抗剂 小管间质损伤
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