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作 者:赵林[1] 王志学[1] 齐芳华[1] 牟林茂[1] 李安源[1] ZHAO Lin WANG Zhi-xue QI Fang-hua MU Lin-mao LI An-yuan(Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China)
出 处:《中国中医基础医学杂志》2017年第6期787-790,共4页JOURNAL OF BASIC CHINESE MEDICINE
基 金:山东省中医药科技发展计划项目(2007-124)
摘 要:目的:研究宁肾颗粒对Ig A肾病(Ig AN)大鼠系膜细胞(Ms C)凋亡的影响。方法:32只SD大鼠按随机数字表法分为空白对照组、模型组、宁肾颗粒低剂量和高剂量组并复制Ig AN模型,造模后药物干预4周分别给予生理盐水,生理盐水,低、高剂量(12g/kg·d、24g/kg·d)宁肾颗粒。干预后,检测尿红细胞计数、24 h尿蛋白、系膜区病理、Ms C的凋亡率、皮质Bax蛋白表达。结果:与空白对照组比较,模型组的尿红细胞计数和24 h尿蛋白定量均有增高,系膜区病理损害加重,Ms C凋亡率、皮质区Bax蛋白表达均降低;较模型组,宁肾颗粒低剂量和高剂量组尿红细胞计数和蛋白定量均减少,宁肾颗粒高剂量组系膜区病理损害减轻、MsC凋亡率、Bax蛋白表达均升高。结论:宁肾颗粒可减轻Ig AN模型大鼠的血尿、蛋白尿,其作用机制可能与上调Bax蛋白表达促进Ms C凋亡,进而抑制Ms C异常增殖有关。Objective: To research the effects of Ningshen Granule on apoptosis of mesangial cells (MsC) in rats with IgA nephropathy. Methods Thirty-two rats were randomly divided into normal control group, model group, Ningshen granula low-dose and high-dose groups (12 and 24 g/kg). The IgA nephropathy rats were established by lipopolysaccharide, bovine serum albumin and carbon tetrachloride. After the models were established, the rats of the four groups were administrated in the morning and evening on every day for consecutive 4 weeks. After the above treatment, red blood cell count of urine, 24 hours urine protein quantity, MsC apoptosis rate were detected. Expression of Bax protein of renal cortex tissue was detected by Western blot. Results: Compared with the control group, the red blood cell count of urine, 24 hours urine protein quantity, MsC apoptosis rate and the expression of Bax protein were significantly increased. Compared with the model group, the red blood cell count of urine and 24 hours urine protein quantity of the rats in Ningshen granula low- dose and high-dose groups were decreased. Compared with the model group, the MsC apoptosis rate and the expression of Bax protein in Ningshen granula high-dose group were decreased significantly. Conclusion: Ningshen granula could relieve the hematuria and albuminuria, and its mechanism may be related to up-regulation the expression of Bax protein in MsC, enhancement the apoptosis and inhibited the proliferation of MsC.
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