摘要
目的观察叶下珠复方Ⅱ号对四氯化碳(CCl4)致小鼠急性肝损伤的保护作用,并探讨其作用机制。方法72只昆明小鼠(KM小鼠)随机分为正常组、模型组、叶下珠复方Ⅱ号高剂量组(6.04 g/kg)、中剂量组(3.02 g/kg)、低剂量组(0.604 g/kg)和联苯双酯组(150 mg/kg),给药7 d后,除正常组外,其余各组小鼠均按10 m L/kg腹腔注射0.12%CCl4大豆油溶液,16 h后取小鼠血清,检测丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)活性;取肝组织,观察肝组织病理改变,并检测超氧化物歧化酶(SOD)活性、还原性谷胱甘肽(GSH)和丙二醛(MDA)水平变化。结果与模型组比较,叶下珠复方Ⅱ号高、中剂量组可显著降低急性肝损伤小鼠血清ALT、AST活性(P<0.01或P<0.05),显著减轻肝组织病理改变,并提高肝组织SOD活性(P<0.01或P<0.05),降低肝组织MDA水平(P<0.01)。结论叶下珠复方Ⅱ号对CCl4诱导的小鼠急性肝损伤有较好的保护作用,其作用机制与抗脂质过氧化损伤有关。
Objective To determine the protective effect and mechanism of Compound Phyllanthus UrinsriaⅡ(CPUⅡ)on acute liver injury induced by carbon-tetrachloride(CCl4)in mice. Methods A total of 72 Kunming mice were randomly divided into 6 groups which were normal and model control groups(administration of normal saline solution),positive control(bifendate150 mg/kg),and high-(6.04 g/kg),medium-(3.02 g/kg)or low-dose(0.604 g/kg)CPUⅡgroups. After 7 days’ treatment,all mice except those of normal control were given an injection of CCl4(0.12%,10 ml/kg,i.p.). In 16 h later,all the animals were sacrificed and their serum samples and hepatic tissues were collected for testing serum levels of alanine aminotransferase(ALT)and aspartate aminotransferase(AST) for measuring pathological changes,activity of superoxide dismutase(SOD)and contents of malondialdehyde(MDA)and glutathione(GSH). Results Compared with the model group, high and medium dose CPUⅡtreatment resulted in significantly decreased serum ALT and AST levels(P〈0.01 or P〈0.05),alleviated hepatic morphological changes,enhanced SOD activity(P〈0.01 or P〈0.05),and reduced hepatic tissue MDA level(P〈0.01). Conclusion CPUⅡ exerts good protective effects on CCl4-induced acute liver injury in mice,whose mechanism is convinced to be associated with anti-lipid peroxidation.
出处
《中国热带医学》
CAS
2016年第8期766-769,共4页
China Tropical Medicine
基金
广东省重大科技专项(No.2012A080202009)
关键词
叶下珠复方Ⅱ号
四氯化碳
急性肝损伤
Compound Phyllanthus Urinsria Ⅱ
Carbon tetrachloride
Acute liver injury