摘要
目的:观察人参皂苷Rg1对四氯化碳(carbon tetrachloride,CCl4)所致小鼠急性肝损伤的保护作用,并探讨其相关机制。方法:80只昆明小鼠被随机分为生理盐水组、CCl4模型组、人参皂苷Rg1低(10 mg·kg-1)、中(20 mg·kg-1)和高(40 mg·kg-1)剂量组,每组16只。在3个不同的人参皂苷Rg1剂量组通过使用不同剂量的人参皂苷Rg1灌胃给药连续7 d后,一次性腹腔注射CCl40.1 m L·10 g-1建立小鼠急性肝损伤模型。在造模后的30 min后各选取小鼠6只,分离并培养枯否氏细胞(Kupffer cells,KCs),测定KCs中核转录因子(nuclear factor-κappa B,NF-κB)活性的变化;在腹腔注射CCl416 h后测定血清中丙氨酸氨基转移酶(alanine aminotransferase,ALT)和天冬氨酸氨基转移酶(aspartate transaminase,AST)的活性以及肿瘤坏死因子α(tumor necrosis factorα,TNF-α)、白细胞介素-6(interleukin 6,IL-6)的含量;测定肝组织中的超氧化物歧化酶(superoxide dismutase,SOD)活力和丙二醛(malondialdehyde,MDA)含量,并观察肝组织病理学变化。结果:病理切片表明人参皂苷Rg1各治疗组小鼠肝损伤不同程度减轻;与CCl4模型组相比较,各治疗组小鼠血清ALT、AST活性和TNF-α、IL-6的含量均有不同程度的降低;肝组织匀浆中SOD活力不同程度升高;MDA含量不同程度降低。在KCs中,CCl4模型组NF-κB活性显著增高,人参皂苷Rg1能够浓度依赖性的降低NF-κB活性。结论:人参皂苷Rg1对CCl4所致小鼠急性肝损伤具有保护作用,其机制可能与阻止抗氧化酶活性降低、提高抗脂质过氧化作用以及抑制KCs中NF-κB活性、降低小鼠血清TNF-α、IL-6的含量等有关。
Objective： To investigate the protective effects of Ginsenoside Rg1 on the acute hepatic injury induced by carbon tetrachloride（CCl4） in mice, and detect its related mechanisms. Methods： Eighty mice were randomly divided into the normal saline group, CCl4 model group, and Ginsenoside Rg1 low, medium and high dosage group（10 mg·kg^-1, 20 mg·kg^-1 and40 mg·kg^-1 of Ginsenoside Rg1）（16 mice each group）. The acute hepatic injury model in mice were established using disposable intraperitoneal injection with 0.1 mL·10 g^-1 of CCl4 after different dosages of Ginsenoside Rg1 injecting into mice for 7 days. Six mice from each group were selected after 30 min of making model. Kupffer cells（KCs） were isolated and cultured, the activites of nuclear factor-κappa B（NF-κB） in which were determined. The activites of alanine aminotransferase（ALT）, aspartate aminotransferase（AST）, and serum levels of tumor necrosis factor（TNF）- α and interleukin（IL）-6 were detected. The activites of superoxide dismutase（ SOD） and content of malondialdehyde（ MDA） were observed, and the histopathological change of liver tissue was measured after 16 h of intraperitoneal injection with CCl4. Results：The pathological sections showed that the varying degrees alleviation of liver injury was identified in each treatment group.Compared with the CCl4 model group, among the each treatment group, the activities of ALT and AST and contents of TNF-αand IL-6 in serum of decreased significantly to various degrees, the activities of SOD in liver homogenate significantly enhanced, the content of MDA also increased obviously at different degrees. In KCs, the activities of NF-κB in CCl4 model significantly increased, the Ginsenoside Rg1 could increase the activities of NF-κB in a dose dependent manner. Conclusions：The Ginsenoside Rg1 can protect CCl4-induced hepatic injury in mice, the mechanism may be related to prevent the activities decreasing of anti-oxidative enzyme, inhibit the activities of NF-κB in KCs by increasing the effects of anti-lipid-peroxidation, and decrease the serum contents of TNF-α and IL-6.
出处
《南通大学学报（医学版）》
2016年第4期260-264,共5页
Journal of Nantong University(Medical sciences)
基金
安徽省自然科学基金青年基金资助项目(1508085QH151)
安徽省教育厅重点项目(KJ2015A147)
