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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 effect of tanshinone IIA sulfonate on 24 h urinary protein, plasma viscosity, histopathology, renal tissue PAI-1 and TGF-β1 in rats with adriamycin-induced nephropathy and its mechanism. Methods: SD male rats were randomly divided into blank group, model group, positive control group, tanshinone Ⅱ A low dose group and tanshinone Ⅱ A high dose group. Using doxorubicin tail vein injection, copy adriamycin nephropathy model. Three weeks after modeling, each administration group was given the corresponding dose of intraperitoneal injection. After 2 weeks of administration, 24 h urinary protein, whole blood viscosity, plasma viscosity, pathological group morphology and expression of TGF-β1 and PAI-1 in renal tissue were detected. Results: Tanshinone IIA sulfonate reduced the 24 h urinary protein in rats with adriamycin-induced nephropathy, and decreased the plasma viscosity. The expression of TGF-β1 and PAI-1 in renal tissue was significantly increased compared with the model control group (P <0.05). CONCLUSION: Sodium tanshinone IIA sulfonate can reduce the quantification of 24 h urinary protein in adriamycin-induced nephropathy and improve the pathological tissue injury, which may be related to the inhibition of the expression of TGF-β1 and PAI-1 in renal tissue.