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目的探讨灯盏花素治疗糖尿病肾病(DN)的机制。方法大鼠随机分为正常对照组,糖尿病组和灯盏花素干预组,以链脲佐菌素复制糖尿病模型;采用放射免疫法检测神经肽Y含量,逆转录-聚合酶链反应(RT-PCR)和免疫组织化学方法分别检测肾皮质神经肽Y mRNA和Y2受体蛋白表达,大鼠血糖、尿白蛋白排泄率(UAER)、肾皮质Na+,K+-ATPase活性。结果灯盏花素干预组大鼠血糖〔(20.02±2.89)mmol/L〕、UAER〔(1.03±0.19)μg/min〕明显低于糖尿病组(P<0.01),血浆和肾皮质神经肽Y浓度分别为(4.453±0.245)ng/mL、(0.66±0.08)ng/mg,肾皮质Na+,K+-ATPase活性为(3.29±0.80)μmol Pi/mg.pro,明显低于糖尿病组(P<0.05);与糖尿病组比较,灯盏花素干预组大鼠肾皮质神经肽Y mRNA和Y2受体表达分别降低了30.2%,26.3%(P<0.05)。结论灯盏花素可通过下调肾皮质神经肽Y及Y2受体表达,抑制肾皮质Na+,K+-ATPase活性,改善DN。
Objective To investigate the mechanism of breviscapine in the treatment of diabetic nephropathy (DN). Methods The rats were randomly divided into normal control group, diabetic group and breviscapine intervention group, diabetic model was induced by streptozotocin, radioimmunoassay was used to detect neuropeptide Y content, RT-PCR ) And immunohistochemical methods were used to detect the expression of neuropeptide Y mRNA and Y2 receptor protein in renal cortex, blood glucose, urinary albumin excretion rate (UAER) and renal cortical Na +, K + -ATPase activity respectively. Results Compared with diabetic group (P <0.01), the plasma levels of neuropeptide Y in the breviscapine intervention group were significantly lower than those in the diabetic group [(20.02 ± 2.89) mmol / L〕 and UAER 〔(1.03 ± 0.19) (4.453 ± 0.245) ng / mL and (0.66 ± 0.08) ng / mg, respectively. The activity of Na + and K + -ATPase in renal cortex was (3.29 ± 0.80) μmol / ). Compared with diabetic group, the expression of neuropeptide Y mRNA and Y2 receptor in renal cortex decreased by 30.2% and 26.3% respectively (P <0.05) in breviscapine intervention group. Conclusion Breviscapine can improve the DN by down-regulating the expression of neuropeptide Y and Y2 receptors, inhibiting the activity of Na + and K + -ATPase in renal cortex.