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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 protective effect of Camellia polysaccharides on acute liver injury induced by carbon tetrachloride (CCl 4) in mice and its mechanism. Methods: Sixty mice were randomly divided into normal control group, model group, bifendate group (120 mg / kg), and Jinhuacha polysaccharide group (200 mg / kg, 100 mg / kg, 50 mg / kg). In addition to the normal control group and model group, each treatment group by gavage 20 ml / kg dose, daily gavage once a day for a total of 7 days. After the last administration, except the normal control group, the other groups were injected intraperitoneally with 0.12% CCl 4 peanut oil (10 ml / kg) to establish acute liver injury model. Fasting can not help but after 24 h, the eye blood, collecting the liver. The activity or content of serum ALT, AST, MDA, SOD and GSH-Px in serum were determined by biochemical method The levels of TNF-α, IL-1β, IL-6 and nitric oxide (NO) in liver tissue were detected by enzyme linked immunosorbent assay (ELISA) The protein expression of NF-κB in liver tissue was detected by Western blot. The liver sections were stained with HE and the pathological changes of liver were observed with microscope. Results: Compared with the CCl 4 model group, the serum levels of ALT, AST and MDA were decreased and the activities of SOD and GSH-Px were increased in the groups of 200 mg / kg and 100 mg / kg. NO The levels of TNF-α, IL-1β, IL-6 and NF-κB in hepatic tissue showed a decreasing trend. The pathological sections showed that the hepatic Injury significantly reduced. The Golden Flower tea polysaccharide 50 mg / kg dose group of CCl 4 -induced acute liver injury in mice had no significant effect. CONCLUSION: Camellia polysaccharides can protect CCl_4-induced acute liver injury in mice and its mechanism may be related to anti-oxidative stress, clearance of free radical metabolites, inhibition of lipid peroxidation and anti-inflammation.