丹参酮IIA磺酸钠对阿霉素肾病大鼠肾损伤的干预机制研究

Research on Intervention Mechanism of Tanshinone Type IIA Sulfonate of Adriamycin Nephrosis Rats Kidney Injury

目的:观察丹参酮IIA磺酸钠对阿霉素肾病大鼠24 h尿蛋白定量,血浆黏度,病理组织形态、肾组织PAI-1、TGF-β1的影响,并探讨其作用机理。方法:SD雄性大鼠随机分为空白组,模型组、阳性药对照组、丹参酮ⅡA低剂量组、丹参酮ⅡA高剂量组。采用阿霉素尾静脉注射,复制阿霉素肾病模型。造模3周后各给药组分别给予相应剂量药物腹腔注射。给药2周后检测24 h尿蛋白定量、全血黏度、血浆黏度、病理组组形态、肾组织TGF-β1、PAI-1的含量表达。结果:丹参酮IIA磺酸钠可以降低阿霉素肾病大鼠24 h尿蛋白定量,降低血浆黏度,肾组织TGF-β1、PAI-1的表达明显增强,与模型对照组比较有显著性差异(P<0.05)。结论:丹参酮IIA磺酸钠可降低阿霉素肾病降低24 h尿蛋白定量、改善病理组织损伤、可能与抑制肾组织TGF-β1、PAI-1的表达有关。

Objective ： To observe the effects of tanshinone type IIA sulfonate of adriamycin nephrosis rats quantitative 24 h urine protein, blood plasma viscosity, histopathologic morphology, kidney tissues TGF - 1 and PAI - 1 and to explore its mechanism. Methods： SD male rats were randomly divided into blank group, model group, positive control group, tanshinone Ⅱ A low dose group, tansbinone Ⅱ A high dose group. Adriamycin nephrosis model was established by injection of adriamycin the tail intravenous,3 weeks after injection, each dose group were given corresponding doses of intraperitoneal injection of drugs. 2 weeks later, test the 24 hours urinary protein quantitative,pathological way form, kidney tissues TGF - 1 and PAI - 1 expressions. Results ： Tansbinone type IIA sulfonate can reduce adriamycin nephrosis rats 24 hours urinary protein quantitative, improve blood viscosity, kidney tissues PAI- 1 and TGF - β1 expressions and compared with model control group there was significant difference （P 〈 0.05）. Conclusion ： Tanshinone type IIA sulfonate may be by reducing the 24 h urine protein quantitative and improving pathological tissue damage and inhibiting kidney tissues TGFβ - 1 and PAI- 1 to treat adriamycin nephropathy.