摘要
目的:研究金花茶多糖对四氯化碳(CCl_4)诱发的小鼠急性肝损伤的保护作用及其作用机制。方法:60只小鼠随机分为正常对照组、模型组、联苯双酯组(120 mg/kg)和金花茶多糖组(200 mg/kg,100 mg/kg,50 mg/kg)。除正常对照组及模型组外,各治疗组按20 ml/kg剂量灌胃给药,每天按时灌胃1次,共7天。末次给药后,除正常对照组外,其余组腹腔注射0.12%CCl_4花生油(10 ml/kg)建立急性肝损伤模型。禁食不禁水24 h后,眼球取血,收集肝脏。生化法测定血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)、丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性或含量;酶联免疫吸附法(ELISA)检测肝组织中肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)、白介素-6(IL-6)表达水平和一氧化氮(NO)含量;蛋白质印迹法(Western blot)检测肝组织NF-κB蛋白表达情况;HE染色肝切片,显微镜观察肝组织病理改变。结果:与CCl_4模型组相比,金花茶多糖剂量组(200mg/kg,100 mg/kg)小鼠血清中ALT、AST及MDA含量降低,SOD及GSH-Px的活性升高;肝组织中NO含量显著降低;肝组织中TNF-α、IL-1β、IL-6及NF-κB表达水平呈下降趋势;病理切片表明金花茶多糖剂量组(200 mg/kg,100 mg/kg)小鼠肝损伤显著减轻。而金花茶多糖50 mg/kg剂量组对CCl_4诱发的小鼠急性肝损伤无明显改善作用。结论:金花茶多糖对CCl_4诱导的小鼠急性肝损伤有明显的保护作用,其机制可能与抗氧化应激,清除自由基代谢产物,抑制脂质过氧化反应及抗炎有关。
Objective： To study the hepatoprotective effect and the related mechanisms of Camellia nitidissima polysaccharides on carbon tetraehlotide （CC14 ） induced acute hepatic injury in mice. Method： Sixty mice were randomly divided into normal group, model group, bifendate pills group（ 120 mg/kg） ,Camellia nitidissima polysaccharides groups （200 mg/kg, 100 mg/kg, 50 mg/kg）, 10 mice in each group. Except the normal control group and model group, the treatment groups were 20 ml/kg dose of oral administration,once a day for 7 days. After the last administration, in addition to the normal control group, the other groups were injected with 0.12% CCl4 peanut oil （ 10 ml/kg） to induce acute liver injury model. Fasting for 24 h, we collected the blood and collection liver, detected the activity or content of ALT, AST, MDA, SOD, GSH-PX and NO in blood or liver tissues; Used the ELISA to assay levels of TNF-α, IL- 6 and IL-1β in hver tissue; the NF-κB protein expression was detected by Western blot in liver tissue; the liver tissue pathological changes were observed by HE. Results： Compared with model group,the activities of ALT, AST and MDA in serums of Camellia nitidissima polysaccharide groups （200 mg/kg, 100 mg/kg） decreased, the activities of SOD and GSH-Px increased; NO content was significantly reduced in liver tissue; TNF-α, IL-1β, IL-6 and NF-κB content decreased in liver tissue ; The pathological sections showed that the hepatic injury of Camellia polysaccharide groups （200 mg/kg, 100 mg/kg）were relieved clearly. While the Camellia nitidissima polysaccharide group （50 mg/kg） on acute hepatic injury in mice caused by CCl4 had no significant improvement. Conclusion： The Camellia nitidissima polysaccharides have a good protective effect on the acute hepatic injury in mice induced by CCl4, and the mechanism may be associated with oxidative stress, free radical scavenging metabolites, inhibition of lipid peroxidation and anti-inflammation.
出处
《中药药理与临床》
CAS
CSCD
北大核心
2016年第6期117-120,共4页
Pharmacology and Clinics of Chinese Materia Medica
基金
国家自然科学基金(81360685)
广西科技攻关项目(桂科攻14124004-2-13)
广西自然科学基金(2014GXNSFBA118149)
广西壮族自治区卫生和计划生育委员会中医药科技专项(No.GZBZ16-15)
关键词
金花茶多糖
四氯化碳
急性肝损伤
氧化应激
polysaccharides of Camellia nitidissima（金花茶多糖）
carbon tetrachloride
acute hepatic injury
oxidative stress
