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目的:研究合欢皮总皂苷对小鼠呼吸系统的毒性及机制。方法:以昆明小鼠为受试对象,实验随机分为生理盐水对照组、合欢皮总皂苷低剂量致毒组(7.5 mg/kg)、合欢皮总皂苷高剂量致毒组(750 mg/kg),灌胃给药14d后,气管插管术,生物信号记录系统记录呼吸的频率和幅值。取肺组织,HE染色观察病理形态的变化,生化法测定肺组织SOD和GSH-Px活性,末端标记法(TUNEL法)检测肺组织细胞凋亡,免疫组织化学法检测肺组织COX-1、COX-2基因蛋白的表达。结果:合欢皮总皂苷致毒剂量对小鼠呼吸频率和幅值无显著影响;肺组织病理变化明显,其SOD、GSH-Px活性与生理盐水组比较致毒组肺组织SOD和GSH-Px的活性显著降低,与低剂量致毒组比较高剂量致毒组SOD活性显著降低而GSH-Px活性无显著差异;与对照组比较,致毒组肺间质及支气管黏膜上皮细胞凋亡数目增多,COX-2表达增加,COX-1表达无显著改变。结论:致毒剂量合欢皮总皂苷对小鼠呼吸频率和肺通气量无明显影响,对呼吸系统的毒性主要表现在促使支气管黏膜上皮细胞凋亡、肺组织的氧化损伤及炎症反应。
Objective: To study the toxicity and mechanism of total Hesperidin in respiratory system of mice. Methods: Kunming mice were used as experimental subjects. The rats were randomly divided into three groups: saline control group, Hopshurium total saponin low dose group (7.5 mg / kg), Hopshine saponins high dose group (750 mg / kg) ), 14d after intragastric administration, tracheal intubation, biological signal recording system to record the frequency and amplitude of respiration. The changes of pathological changes were observed by HE staining. The activities of SOD and GSH-Px in lung tissue were determined by biochemical methods. The apoptosis of lung tissue was detected by TUNEL method. The expressions of COX-1, COX -2 gene protein expression. Results: The total dose of HGH had no significant effect on the respiratory rate and amplitude of the mice. The pathological changes of the lungs were obvious. The activities of SOD and GSH-Px in the lung tissue of the poisoned rats were significantly higher than those in the saline group Compared with the control group, the activity of SOD in the high-dose group was significantly decreased and the activity of GSH-Px was no significant difference. Compared with the control group, the number of apoptotic cells in lung interstitial and bronchial epithelial cells increased, COX-2 expression increased, COX-1 expression did not change significantly. CONCLUSION: The total dose of alfalfa does not affect the respiratory rate and pulmonary ventilation in mice. The toxicity to respiratory system is mainly caused by the apoptosis of bronchial epithelial cells, the oxidative damage of lung tissue and the inflammatory reaction.