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目的探讨葡萄籽原花青素(GSP)对氯化镉(CdCl2)诱导大鼠肝氧化损伤的保护作用。方法 40只SPF级SD大鼠,雌雄各半,随机分为对照组(腹腔注射生理盐水和灌胃生理盐水)、染镉组(腹腔注射1.5 mg/kg的CdCl2和灌胃生理盐水)、GSP低、中、高剂量干预组(均腹腔注射1.5 mg/kg CdCl2,同时分别灌胃20、40、80 mg/kg GSP),采用硫代巴比妥酸法和单细胞凝胶电泳技术(SCGE)分别检测肝细胞中丙二醛(MDA)的含量和DNA损伤情况。结果染镉组肝细胞MDA含量和细胞彗尾长、Olive尾矩均明显高于对照组,表明1.5 mg/kg CdCl2可引发大鼠肝脏出现明显的脂质过氧化损伤。GSP抑制染镉大鼠肝细胞MDA的产生,呈明显的剂量-效应关系,GSP低、中、高剂量组MDA清除率分别为12.74%、24.22%、43.65%。GSP低、中、高剂量干预组中肝脏细胞的彗尾长、Olive尾矩均低于染镉组的,表明GSP具有一定抑制DNA损伤和促进DNA修复的生物学作用。结论 GSP对镉致肝组织脂质过氧化和DNA损伤有一定的保护作用。
Objective To investigate the protective effect of grape seed proanthocyanidins (GSP) on liver injury induced by cadmium chloride (CdCl2) in rats. Methods Forty Sprague-Dawley (SD) SD rats were randomly divided into control group (intraperitoneal injection of normal saline and intragastric administration of normal saline), cadmium-exposed group (intraperitoneal injection of 1.5 mg / kg CdCl2 and intragastric administration of saline), GSP Low, medium and high dose intervention groups (all intraperitoneal injection of 1.5 mg / kg CdCl2, while gavage 20,40,80 mg / kg GSP), using thiobarbituric acid method and single cell gel electrophoresis (SCGE ) Were detected liver malondialdehyde (MDA) content and DNA damage. Results The content of MDA, the length of tail and the tail of Olive tail were all significantly higher than those of the control group, indicating that 1.5 mg / kg CdCl2 could induce obvious lipid peroxidation injury in rat liver. GSP inhibited the production of MDA in hepatocytes of cadmium-exposed rats, showing a dose-response relationship. The clearance rate of MDA in GSP low, medium and high dose groups was 12.74%, 24.22% and 43.65%, respectively. GSP low, medium and high dose intervention group liver cells comet tail length, Olive tail moment were lower than the cadmium group, indicating that GSP has a certain inhibition of DNA damage and promote DNA repair biological role. Conclusion GSP can protect liver from lipid peroxidation and DNA damage induced by cadmium.