摘要
目的 探讨 3 磷酸甘油醛脱氢酶 (G3PD)的修饰蛋白 (MP)对庆大霉素诱导的老年急性肾功能衰竭 (ARF)大鼠肾小管修复以及肾功能改善的影响。 方法 将老年鼠及青年鼠各分成 3组 ,即正常组、模型组和MP组。庆大霉素腹腔注射 ( 14 0mg·kg-1 ·d-1 ) ,连续 7d ,制备大鼠ARF模型。采用镉还原比色法检测一氧化氮 (NO) ,采用硫代巴比妥酸法和羟胺法分别测定丙二醛 (MDA)和超氧化物歧化酶 (SOD) ,苦味酸法测定血肌酐 (Scr)。同时 ,光镜、电镜观察肾组织学改变。 结果 老年MP组与老年模型组相比 ,NO含量明显升高〔血清 ( 94 2 9± 7 68) μmol/L与 ( 70 14± 5 53 ) μmol/L ,肾脏( 5 94± 1 3 6) μmol/g组织与 ( 3 62± 1 11) μmol/g组织 ,均为P <0 0 1〕 ;青年MP组与青年模型组相比 ,NO同样明显升高。另外 ,老年、青年MP组与各自模型组相比 ,MDA降低 ,SOD升高 ,同时Scr下降 (均为P <0 0 1) ;光镜、电镜显示肾脏病理改变减轻。 结论 MP可以升高老年及青年ARF大鼠的NO含量 ,减轻肾脏病理变化 ,改善肾功能。
Objective To study whether G3PD modifier protein (MP) could repair tubular epidermal cell(TEC) and ameliorate renal functions in aged rats with gentamycin induced acute tubular necrosis(ATN). Methods Aged and young rats were randomly divided into 3 groups, namely aged and young normal groups, aged and young model groups and the aged and young MP groups. The animal models of acute renal failure (ARF) were induced by gentamycin (140 mg·kg -1 ·d -1 , ip×7 d). Nitric oxide (NO) concentration was determined by Cd activated cadmium reduction method, malonaldehyde(MDA) with thiobarbituric acid test, superoxide dismutase(SOD) with hydroxylamine test, serum creatinine (Scr) with picric acid method, and the renal histology was observed by light and electron microscopy. Results NO was significantly higher in the aged MP group than that in the aged model group 〔serum: (94.29±7.68)μmol/L vs (70.14±5.53)μmol/L, P <0.01; kidney: (5.94±1.36)μmol/g vs (3.62±1.11)μmol/g, P <0.01〕. Both the young MP group and the young model group showed the same results as the aged ones. As compared with the aged and young model groups, MDA, Scr of the aged and young MP ones reduced while their SOD increased( P <0.01). LM and EM showed a lighter renal pathological change. Conclusions MP increases the NO concentration of the aged ARF rats as the young ones, and reduces the renal pathological changes, and ameliorates the renal functions.
出处
《中华老年医学杂志》
CAS
CSCD
北大核心
2002年第3期206-209,共4页
Chinese Journal of Geriatrics
基金
卫生部科学研究基金资助项目 ( 96 1 2 1 1 )
