论文部分内容阅读
目的：研究庆大霉素（ＧＭ）引起大鼠急性肾功能衰竭（ＡＲＦ）后，人参总皂甙（ＧＳ）能否减轻ＧＭ的进一步肾损害，促进肾小管的修复。方法：雄性Ｗｉｓｔａｒ大鼠３２只随机分成３组：正常对照组（Ⅰ组）腹腔注射生理盐水７ｄ，模型组（Ⅱ组）腹腔注射ＧＭ７ｄ，在随后７ｄ中自由饮水，ＧＳ治疗组（Ⅲ组）腹腔注射ＧＭ７ｄ后，给予ＧＳ灌胃７ｄ。结果：ｄ１５显示Ⅱ组中血肌酐水平、血清和肾皮质匀浆中丙二醛（ＭＤＡ）含量均比Ⅰ、Ⅲ组显著升高（Ｐ＜００１），同时血清和肾皮质匀浆中超氧化物歧化酶（ＳＯＤ）活性比Ⅰ、Ⅲ组显著下降（Ｐ＜００１）；但Ⅲ组血肌酐升高与Ⅰ组无显著性差异，血清和肾皮质匀浆中ＭＤＡ升高与ＳＯＤ下降较Ⅰ组有显著性差异（Ｐ＜００１）。病理检查Ⅲ组也比Ⅱ组损害轻、修复快。结论：反应性氧代谢产物（ＲＯＭ）的增多及肾脏抗氧化能力的下降参与了大鼠ＧＭ肾损害，ＧＳ能通过清除ＲＯＭ减轻肾损害，促进肾小管及肾功能的恢复。
OBJECTIVE: To investigate whether ginsenosides (GS) can reduce the further renal damage of GM and promote the repair of renal tubules after gentamicin (GM) induces acute renal failure (ARF) in rats. METHODS: Thirty-two male Wistar rats were randomly divided into three groups: normal control group (group I) was intraperitoneally injected with normal saline for 7 days, model group (group II) was intraperitoneally injected with GM7d, followed by free drinking water for 7 days, and GS treatment group (group III). After intraperitoneal injection of GM7d, GS was given for 7 days. RESULTS: D15 showed that serum creatinine levels, malondialdehyde (MDA) content in serum and renal cortex homogenate were significantly higher in group II than in groups I and III (P < 0.01), and serum and renal cortex homogenates were hyperactive. The activity of SOD was significantly lower than that of group I and III (P<001). However, there was no significant difference in serum creatinine between group III and group I. The level of MDA and SOD in serum and renal cortex homogenates were not significantly different. The drop was significantly different from that of group I (P<001). Pathological examination in group III was also milder than that in group II and repaired quickly. Conclusion: The increase of reactive oxygen metabolites (ROM) and the decrease of renal antioxidation ability are involved in the damage of GM kidney in rats. GS can reduce renal damage by clearing ROM and promote the recovery of renal tubules and renal function.