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作 者:魏长征[1] 吕晓云[1] 宋连猛 裴海霞[1] 张倩倩[1] 杨杰[1]
机构地区:[1]兰州大学基础医学院中西医结合研究所,甘肃兰州730000
出 处:《中国中医急症》2015年第6期984-987,共4页Journal of Emergency in Traditional Chinese Medicine
基 金:兰州市科技发展项目(No.2012-1-24)
摘 要:目的观察丹参酮ⅡA磺酸钠注射液对镉致肾损伤的保护作用并探讨其可能的作用机制。方法 40只Wistar大鼠随机分为空白组、模型组、亚硒酸钠组(0.05 mg/kg)、丹参酮低(4 mg/kg)、高(8 mg/kg)剂量组。镉染毒4周后,观察大鼠基本状况,检测大鼠血肌酐(Scr)、血尿素氮(BUN)、血清超氧化物歧化酶(SOD)、丙二醛(MDA)及其尿β2-微球蛋白(β2-MG)。于造模成功后,空白组、模型组给予腹腔注射0.9%氯化钠注射液,亚硒酸钠组给予腹腔注射亚硒酸钠溶液,丹参酮低、高剂量组分别给予4 mg/kg和8 mg/kg剂量丹参酮ⅡA磺酸钠注射液治疗。检测血液中的Scr、BUN、SOD、MDA、尿β2-MG含量,肾皮质、血、尿含镉量,肾脏皮质细胞凋亡率及Bax蛋白表达水平。结果染毒后模型组、亚硒酸钠组、丹参酮低剂量组、丹参酮高剂量组大鼠体质量、Scr、BUN、尿β2-MG、SOD及MDA与空白组差异有统计学意义(P<0.05或P<0.01)。采用丹参酮ⅡA-磺酸钠治疗后,丹参酮低剂量组、丹参酮高剂量组与模型组相比,血Scr、BUN、尿β2-MG、肾、血含镉量、MDA、SOD含量、肾脏皮质细胞凋亡率及Bax蛋白表达差异均有统计学意义(P<0.05或P<0.01)。结论丹参酮低、高剂量组对镉致肾脏损伤具有保护作用,其保护机制可能与抗氧化应激有关。Objective: To investigate the protective effect of Tanshinone Ⅱ A sulfonic acid sodium injection (STS) on Cadmium induced renal damage and its possible mechanism. Methods: 40 wistar rats were randomly divided into the sham group,model group,sodium selenite group(0.05 mg/kg),STS group(4 mg/kg),STS group(8 mg/kg). After exposed cadmium for 4 weeks,the basic condition of rats,Scr,BUN,SOD,MDA and 132-MG were observed. After the success of the modeling,the sham group and model group were intraperitoneally injected with 0.9% sodium chloride,while the sodium selenite group was intraperitoneally injected with Sodium selenite solu- tion,and the STS group (4 mg/kg and 8 mg/kg) was intraperitoneally injected with different doses of STS. At the end of the test, the Scr, BUN, SOD, MDA in the blood and 132-MG in the urine were detected. The cadmium con- tent in the Renal cortex,blood, urine and Bax were measured. Flow cytometry was used to measure Cell apoptosis in Renal cortex. Results: The basic condition,Scr,BUN,SOD,MDA, 132-MG in different groups had statistical differences. After compared with model group,in the STS group (4 mg/kg and g mg/kg) Scr,BUN ,β2-MG,cad- mium content, MDA , kidney Cell apoptosis and the expression of Bax protein were significantly reduced, and SOD increased significantly. Conclusions: Cadmium induced renal damage can be reduced by the STS group(4 mg/kg and 8 mg/kg). Its protection mechanism may be associated with the antioxidant abitity.
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