健脾清化方对慢性肾功能衰竭高脂血症大鼠肾组织氧自由基和转化生长因子β1 mRNA表达的影响

目的观察健脾清化方对慢性肾功能衰竭高脂血症大鼠肾组织氧自由基和转化生长因子β1(trans-forminggrowthfactorβ1,TGFβ1)mRNA表达的影响。方法模型组和健脾清化方治疗组大鼠予以高脂饲料喂养结合5/6肾切除法,建立慢性肾功能衰竭高脂血症大鼠模型,并分别予以蒸馏水和健脾清化方灌胃干预8周。干预结束后,检测正常对照组、模型组和健脾清化方治疗组大鼠24h尿蛋白定量及血尿素氮、肌酐、胆固醇、甘油三酯、高密度脂蛋白和低密度脂蛋白的水平;并检测各组大鼠肾组织超氧化物歧化酶的活性及丙二醛和游离脂肪酸的含量。采用RT-PCR技术检测各组大鼠肾组织TGFβ1mRNA的表达水平。结果模型组大鼠24h尿蛋白定量及血尿素氮、肌酐、胆固醇、甘油三酯、高密度脂蛋白和低密度脂蛋白水平均较正常对照组明显升高;肾组织超氧化物歧化酶活性较正常对照组明显下降;肾组织丙二醛、游离脂肪酸含量及TGFβ1mRNA表达水平则较正常组对照组明显升高,差异均有统计学意义。健脾清化方治疗组上述指标则均较模型组有不同程度的改善,差异有统计学意义。结论健脾清化方可减少慢性肾功能衰竭高脂血症大鼠24h尿蛋白定量,改善其肾功能,其作用机制与改善脂质代谢紊乱、调节氧化-抗氧化系统及降低肾组织TGFβ1的表达相关。

Effects of Jianpi Qinghua Recipe on oxygen radicals and transforming growth factor β1 in renal tissue in a rat model of chronic renal failure with hyperlipidemia

OBJECTIVE: To evaluate the effects of Jianpi Qinghua Recipe (JPQHR) on oxygen radicals and transforming growth factor beta1 (TGFbeta1) in renal tissue in a rat model of chronic renal failure with hyperlipidemia. METHODS: Chronic renal failure with hyperlipidemia was induced in rats in untreated group and JPQHR-treated group by 5/6 nephrectomy and high fat diet. Then the rats in these two groups were fed distilled water and JPQHR respectively for eight weeks. The rats in normal control group received no specific interventions. After eight weeks of treatment, the levels of 24 h urine protein (Upr), blood urea nitrogen (BUN) and serum creatinine (Cr), cholesterol (Ch), triglycerides (TG), high-density lipoprotein (HDL) and low-density lipoprotein (LDL) of rats in these three groups were examined. The activity of superoxide dismutase (SOD), contents of malondialdehyde (MDA) and non-esterified fatty acids (NEFA) and expression level of TGFbeta1 mRNA in renal tissue of rats in each groups were also determined. RESULTS: The levels of 24 Upr, BUN and serum Cr, Ch, TG and LDL in the JPQHR-treated group were significantly lower than those in the untreated group. The contents of MDA and NEFA and the expression level of TGFbeta1 mRNA in the JPQHR-treated group were also significantly lower than those in the untreated group, while the activity of SOD was significantly increased in the JPQHR-treated group as compared with that in the untreated group. CONCLUSION: The results indicate that JPQHR can improve the renal function of rats with chronic renal failure and hyperlipidemia by regulating lipid metabolism, maintaining balance between prooxidants and antioxidants and reducing expression of TGFbeta1 mRNA in renal tissue.