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目的:研究醋炙降低甘遂乙酸乙酯部位对小鼠胃肠道氧化损伤的作用机制。方法:将小鼠分为空白对照组、甘遂组(256,160,100 g.kg-1)、醋甘遂组(256,160,100 g.kg-1),灌胃给药7 d后,取小鼠胃、肠匀浆测定乳酸脱氢酶(LDH)活力、超氧化物歧化酶(SOD)活力、丙二醛(MDA)和谷胱甘肽(GSH)含量。取胃、肠组织进行HE染色,光镜观察其组织形态学改变。结果:空白对照组小鼠体重无明显减轻,大便性状正常,甘遂和醋甘遂各剂量组出现体重明显减轻和大小便失禁,但与甘遂组比较,醋甘遂各剂量组体重减轻较少,泻下作用有所缓和。与空白对照组比较,甘遂各剂量组胃肠SOD活力、GSH含量明显降低,MDA含量、LDH活力明显增高(P<0.05,P<0.01);与甘遂组比较,醋甘遂各剂量组胃肠SOD活力、GSH含量明显增高,MDA含量、LDH活力明显降低(P<0.05,P<0.01)。与空白对照组比较,甘遂各剂量组胃肠黏膜损伤显著加重(P<0.05,P<0.01);与甘遂组比较,醋甘遂各剂量组胃肠黏膜损伤显著减轻(P<0.05,P<0.01)。结论:醋炙能明显降低甘遂乙酸乙酯部位对小鼠胃肠道的氧化损伤,为后续进一步探讨甘遂醋炙减毒机制提供了一定的依据。
OBJECTIVE: To investigate the mechanism of vinegar-induced lowering of gastrointestinal oxidative damage in mice induced by ethyl acetate. Methods: The mice were divided into blank control group, Kansui group (256,160,100 g.kg-1) and Kadsura group (256,160,100 g.kg-1) The activity of lactate dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH) were determined by homogenization. The stomach and intestine tissue were stained with HE, and their morphological changes were observed with light microscope. Results: The body weight of the blank control group had no obvious weight loss and the stool traits were normal. The body weight of each dose group of Kansui and Valsurgan was significantly reduced and incontinence was relieved. Compared with Kansuishan group, Less, diarrhea effect has been eased. Compared with the blank control group, the activity of SOD and the content of GSH and the content of MDA and the activity of LDH in each dose group were significantly increased (P <0.05, P <0.01); Compared with the Kansui group, The activities of SOD and GSH in the gastrointestinal tract were significantly increased, and the contents of MDA and LDH were significantly decreased (P <0.05, P <0.01). Compared with the control group, the damage of gastrointestinal mucosa in each dosage group of Kansui significantly increased (P <0.05, P <0.01) P <0.01). CONCLUSION: Vinegar Sunburn can obviously reduce the oxidative damage to the gastrointestinal tract of mice induced by ethyl acetate of Kansui root, which will provide a basis for further study on the mechanism of Sunitinase reduction.