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目的: 研究淫羊藿苷对糖尿病大鼠睾丸病变的改善,并初步讨论其可能的作用机制。方法: 采用链脲佐菌素(40 mg·kg-1)尾静脉注射建立糖尿病大鼠模型。实验分为3组:正常组、模型组和淫羊藿苷组。淫羊藿苷组给予淫羊藿苷溶液80 mg·kg-1·d-1灌胃。12周末处死各组大鼠,测血清葡萄糖和睾酮含量,睾丸组织中特异性酶琥珀酸脱氢酶(SDH)、酸性磷酸酶(ACP)、γ-谷氨酰转肽酶(γ-GT)及乳酸脱氢酶(LDH)活性; HE染色,置光镜下观察睾丸组织病理变化;免疫组化法测定转化生长因子β1 (TGF-β1)和Ⅳ型胶原蛋白酶的表达。结果: 与正常对照组比较,模型组血清葡萄糖水平上升和睾酮水平下降;睾丸组织特异性酶活性降低;病理学检测可见生精上皮层变薄,各级生精细胞减少;TGF-β1和Ⅳ型胶原蛋白酶表达增加。淫羊藿苷组明显改善上述指标(P<0.01)。结论: 淫羊藿苷对糖尿病所致的睾丸损伤有明显的保护作用,其机制可能与促进睾酮释放、抑制睾丸Ⅳ型胶原蛋白酶及TGF-β1表达有关。  相似文献   
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目的 研究淫羊藿苷对D-半乳糖致小鼠睾丸病变的影响.方法 雄性小鼠皮下注射D-半乳糖200 mg/kg连续30 d造成睾丸病变.从第31天起分别灌胃给予淫羊藿苷50,100 mg/kg,1次/d干预,连续20 d.结果 与正常对照组比较,睾丸、附睾、精囊腺重量指数下降;睾丸组织超氧化物歧化酶(SOD)含量明显下降,丙二醛(MDA)含量明显升高;血清睾酮下降,乳酸脱氢酶(LDH)、酸性磷酸酶(ACP)及谷氨酰转肽酶(γ-GT)活力降低;病理学检测可见生精上皮层变薄,各级生精细胞减少.淫羊藿苷50,100 mg/kg组上述现象明显改善(P<0.05).结论 淫羊霍苷对D-半乳糖致雄性小鼠睾丸损伤有明显的改善作用,其机制可能与其促进睾酮释放和抗氧化有关.  相似文献   
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Objective:To Investigate whether total triterpene acids(TTAs),isolated from Corpus Fructus,attenuates renal function by reducing oxidative stress and down-regulating the expression of transforming growth factor β_1(TGF-β_1).Methods:Diabetes was induced by an injection of streptozotocin(40 mg/kg intravenously).Thirty rats were randomly divided into three groups:control group,diabetic model group and TTAs treatment group(50 mg/kg,intragastrically)administrated for 8 weeks from 5th to 12th week.All rats were anaesthetized and then were killed to remove kidneys.The renal function and redox enzyme system parameters were tested.Glomerular morphology was observed by a light microscopy.Immunohistochemistry and Western blot assays were employed to determine the protein levels of TGF-β_1.Results:TTAs attenuated the levels of urinary protein,serum creatinine and blood urea nitrogen,although it did not significantly reduce the level of glucose.In addition,TTAs decreased the malondialdehyde while increased superoxide dismutase,catalase and glutathione peroxide activities in diabetic rats.The renal pathological changes in TTAs treatment group were ameliorated.Furthermore,TTAs also ameliorated the expression of TGF-β_1.Conclusion:TTAs improved renal function via reducing oxidative stress and down-regulation the expression of TGF-β_1 in diabetic rats.  相似文献   
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