论文部分内容阅读
目的:探讨二至丸不同提取部位对抗大鼠酒精性肝损伤的作用及机制。方法:将二至丸水提液依次用不同溶剂萃取,经干燥后得到石油醚、乙酸乙酯、正丁醇和萃余液4个部位浸膏,加水溶解配制溶液。取70只雄性Wistar大鼠随机分为7组,空白对照组,模型组,阳性药硫普罗宁肠溶片组(60 mg·kg-1),二至丸水提液石油醚、乙酸乙酯、正丁醇萃取部位和萃余液4个部位组(15.12 g·kg-1),造模同时连续ig给药28 d。以乙醇灌胃法连续28 d建立酒精性肝损伤模型,末次给药24 h后,所有大鼠采用颈动脉采血,分离血清检测血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、乙醇脱氢酶(ADH)、甘油三酯(TG)、血清内毒素、肿瘤坏死因子α(TNF-α)、干扰素γ(IFN-γ)、白细胞介素18(IL-18)的活性和肝匀浆超氧化物歧化酶(SOD)、丙二醛(MDA),观察肝脏病理形态学改变。结果:与空白对照组相比,模型组血清ALT,AST,ADH,TG,血清内毒素,TNF-α,IFN-γ及IL-18活性明显升高,有显著性差异(P<0.01),表明模型制备成功;各给药组ALT,AST,ADH,TG指标的升高被显著抑制,与模型组相比有差异(P<0.01或P<0.05)。与空白对照组相比,模型组肝匀浆中MDA含量明显升高,SOD活性下降(P<0.01),与模型组相比硫普罗宁、二至丸水提液石油醚部位组和乙酸乙酯部位组MDA的升高被显著抑制(P<0.01或P<0.05);与模型组相比,硫普罗宁、乙酸乙酯组、正丁醇组和萃余液组SOD的下降被明显抑制(P<0.01或P<0.05)。通过病理学切片观察,各给药组均一定程度能显著改善肝组织的病理变化。结论:二至丸乙酸乙酯部位对抗大鼠酒精性肝损伤作用最显著,其作用机制可能与内毒素-CD14/TLR4的抑制作用有关。
Objective: To investigate the effect of different parts of Erzhi Pills on alcoholic liver injury in rats and its mechanism. Methods: The extracts from Erzhi Wan were sequentially extracted with different solvents. After drying, extracts of petroleum ether, ethyl acetate, n-butanol and raffinate were obtained in 4 parts and dissolved in water to prepare the solution. Seventy male Wistar rats were randomly divided into 7 groups. The blank control group, model group, positive control group (60 mg · kg -1), Erzhiwan aqueous extract of petroleum ether, ethyl acetate , N-butanol extract and raffinate 4 fractions (15.12 g · kg-1), while modeling ig administration for 28 d. Alcoholic liver injury model was established by intragastric administration of ethanol for 28 days. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) , Alcohol dehydrogenase (ADH), triglyceride (TG), serum endotoxin, tumor necrosis factor α (TNF-α), interferon γ (IFN- γ) and interleukin 18 (IL-18) And liver homogenate superoxide dismutase (SOD), malondialdehyde (MDA) were observed liver pathological changes. Results: Compared with the blank control group, the activities of ALT, AST, ADH, TG, serum endotoxin, TNF-α, IFN-γ and IL-18 in the model group were significantly increased (P <0.01) The results showed that the model was successfully prepared. The increase of ALT, AST, ADH and TG in each administration group was significantly inhibited compared with the model group (P <0.01 or P <0.05). Compared with the blank control group, the content of MDA in the liver homogenate of the model group was significantly increased and the activity of SOD was decreased (P <0.01). Compared with the model group, (P <0.01 or P <0.05). Compared with the model group, the decrease of SOD in the tiopronin, ethyl acetate group, n-butanol group and raffinate group was significantly inhibited (P <0.01 or P <0.05). Pathological sections were observed, each treatment group to a certain extent, can significantly improve the pathological changes of liver tissue. CONCLUSION: Erythritol acetate is most effective against alcoholic liver injury in rats. The mechanism may be related to the inhibitory effect of endotoxin-CD14 / TLR4.