PKC抑制剂LY333531对阿霉素肾病小鼠肾组织氧化应激的影响

发布时间：2018-10-20 15:49

【摘要】：目的探讨PKC抑制剂LY333531对阿霉素肾病小鼠肾组织氧化应激的影响。方法建立小鼠阿霉素肾病模型,24只小鼠随机分成对照组、阿霉素肾病组和LY333531 10 mg/(kg·d)灌胃治疗组,每组8只。阿霉素肾病组和LY333531治疗组一次性尾静脉注射阿霉素(10 mg/kg),建立小鼠阿霉素肾病模型,对照组注射等量生理盐水;阿霉素注射后第5天、出现蛋白尿时,LY333531治疗组予LY333531 10 mg/(kg·d)灌胃,阿霉素肾病组和对照组予等量溶媒灌胃。2周时处死小鼠。处死前留取血尿标本检测尿蛋白、尿肌酐和血生化。观察肾脏病理,并检测肾组织和尿中丙二醛(MDA)含量及肾组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)与谷胱甘肽过氧化物酶(GSH-PX)活性。结果 LY333531可明显抑制阿霉素肾病小鼠尿蛋白排泄。与对照组相比,阿霉素肾病组肾组织及尿MDA含量明显增加(P0.05,P0.01),肾组织SOD、CAT、GSH-PX活性明显下降(P0.05,P0.01);与阿霉素肾病组比较,LY333531治疗组肾组织及尿MDA含量明显降低(P0.05),肾组织SOD、CAT、GSHPX活性显著增高(P0.05)。结论 LY333531对阿霉素肾病小鼠肾脏有明显保护作用,其机制可能部分与抑制肾组织氧化应激有关。
[Abstract]:Objective to investigate the effect of PKC inhibitor LY333531 on oxidative stress in renal tissue of adriamycin nephropathy mice. Methods A model of adriamycin nephropathy was established in mice. Twenty-four mice were randomly divided into control group, adriamycin nephropathy group and LY333531 10 mg/ (kg d) group with 8 rats in each group. Adriamycin nephropathy model was established in mice in adriamycin nephropathy group and LY333531 treatment group by single tail vein injection of doxorubicin (10 mg/kg), the control group was injected with the same amount of normal saline, and the LY333531 group was given LY333531 10 mg/ (kg d) intragastric perfusion on the 5th day after adriamycin injection. The doxorubicin nephropathy group and the control group were given the same amount of solvent intragastric perfusion, and the mice were killed at 2 weeks. Urine protein, urine creatinine and blood biochemistry were collected before execution. The contents of malondialdehyde (MDA) in kidney and urine and the activities of superoxide dismutase (SOD),) catalase (CAT) and glutathione peroxidase (GSH-PX) in renal tissue were observed. Results LY333531 could significantly inhibit urinary protein excretion in adriamycin nephropathy mice. Compared with the control group, the content of MDA in renal tissue and urine was significantly increased (P0.05, P0.01), the activity of SOD,CAT,GSH-PX in renal tissue was decreased significantly (P0.05P0.01) in the group of doxorubicin nephropathy, and the content of MDA in kidney and urine in the group treated with LY333531 was significantly lower than that in the group of doxorubicin nephropathy (P0.05), and the activity of SOD,CAT,GSHPX in renal tissue was significantly increased (P0.05). Conclusion LY333531 has obvious protective effect on kidney of adriamycin nephropathy mice, and its mechanism may be related to the inhibition of oxidative stress in renal tissue.
【作者单位】：云南省第一人民医院肾内科;
【基金】：云南省科技计划项目(编号:2008CD045)
【分类号】：R965

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