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作 者:杨筱瑶 王亦薇[1] 施中凯[2] YANG Xiaoyao;WANG Yiwei;SHI Zhongkai(Department of Science and Education,Heilongjiang Provincial Hospital,Harbin Heilongjiang 150036,China;Department of Radioimmunoassay Laboratory)
机构地区:[1]黑龙江省医院科教部,黑龙江哈尔滨150036 [2]黑龙江省医院放射免疫特检科,黑龙江哈尔滨150036
出 处:《中国继续医学教育》2018年第29期156-158,共3页China Continuing Medical Education
基 金:2016年哈尔滨市应用技术研究与开发项目(2016RAXYJ091);黑龙江省卫生和计划生育委员会科研课题(2016-506)
摘 要:目的探索黄葵胶囊对糖尿病肾病大鼠TGF-β_1、α-SMA、ILK表达的影响。方法将SD大鼠分为正常对照组、糖尿病肾病组和黄葵处理组三组,用链脲佐菌素将SD大鼠诱导为糖尿病肾病模型。通过检测血清肌酐、尿素氮、24小时尿蛋白水平及TGF-β_1、α-SMA、ILK表达水平来评价黄葵胶囊的治疗效果和潜在的分子机制。用HE染色来判断肾脏的病理改变,用q RT-PCR方法来评估TGF-β_1、α-SMA及ILK的表达水平。结果黄葵胶囊可以改善大鼠血清肌酐、尿素氮、24小时尿蛋白水平和一般状态,同时可延缓恶化的肾脏改变。HE染色显示黄葵胶囊可改善糖尿病大鼠的肾脏病理改变,包括肾脏纤维化等。q RT-PCR结果显示黄葵胶囊可以抑制TGF-β_1、α-SMA及ILK的表达。结论黄葵胶囊可能通过抑制TGF-β_1、α-SMA及ILK表达水平,降低血清肌酐、尿素氮和尿蛋白,实现其对糖尿病肾病的治疗效果。Objective To investigate the effects of Huangkui capsule on the expression of TGF-β1, α-SMA and ILK in the kidney tissues of diabetic nephropathy. Methods SD rats were divided into three groups normal control group, untreated DN group and HKC-treated DN group. The therapeutic effects and underlying molecular mechanism of HKC on DN rats induced by streptozotocin were evaluated by levels of serum creatinine, blood urea nitrogen, 24-hour urinary protein and expression of TGF-β1, α-SMA and ILK. Pathological changes of kidney tissues were observed by hematoxylin-eosin (HE) staining. Moreover, quantitative real-time polymerase chain reaction (qRT-PCR) were applied to detect the changes of TGF-β1, α-SMA and ILK. Results Our results showed that, the rats treated with HKC had an improved general state and reduced creatinine, blood urea nitrogen and 24-hour urinary protein levels. The deterioration of renal function was delayed due to treatment with HKC. We utilized HE staining to observe that HKC can improve histopathological fndings in the kidney tissues of DN rats, including kidney fbrosis. Results of qRT-PCR also showed that HKC can inhibited the expressions of TGF-β1, α-SMA and ILK in the rats model of DN. Conclusion Our present fndings demonstrate that HKC inhibited the expression of TGF-β1, α-SMA and ILK reduced creatinine, blood urea nitrogen and 24-hour urinary protein, which may account for the therapeutic efects on DN.
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