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目的:探讨长期大量给予益母草醇提组分致大鼠肾毒性的病理损伤机制。方法:按45 d毒性实验方法,进行益母草醇提组分高、中、低剂量组的肾组织病理学检查;检测大鼠血清丙二醛(MDA)、超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)以及总巯基(-SH)的含量和活性。结果:病理组织学检查发现,益母草醇提组分高、中、低剂量组均可见不同程度的肾小管损伤,且损伤程度随剂量增加而加重,与空白组相比有明显差异;血清酶学检测发现,益母草醇提组分可导致MDA、总-SH含量增加,SOD,GSH-Px活性下降,GSH含量降低,上述变化随剂量的增加而逐渐加重,与空白组相比有明显差异。结论:氧化损伤机制可能是益母草导致肾毒性病理损伤的机制之一。
Objective: To investigate the mechanism of pathological damage induced by long-term large-dose administration of alcohol extract from Motherwort in rats. Methods: The pathological examination of kidney in high, middle and low dose of Leonurus extract was performed by 45-day toxicity test. Serum malondialdehyde (MDA), superoxide dismutase (SOD) Prototype glutathione (GSH), glutathione peroxidase (GSH-Px) and total thiol (-SH) content and activity. Results: Histopathological examination showed that renal toxicity was found in all the groups of high, medium and low dose of alcohol extract of Motherwort, and the degree of injury increased with the increase of dose, which was significantly different from that of the blank group. Serum enzyme The results showed that the fraction of alcohol extracted from motherwort could lead to the increase of MDA, the content of total-SH, the decrease of the activity of SOD and GSH-Px and the decrease of the content of GSH. The above changes gradually increased with the increase of dosage. Conclusion: The mechanism of oxidative damage may be one of the mechanisms by which Motherwort causes renal toxicity pathological damage.