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目的研究双环醇对小鼠慢性酒精性肝损伤的影响。方法小鼠连续4周给予含5%酒精Lieber-Decarli全营养液体饮食,建立慢性酒精性肝损伤模型。动物于造模前和造模后口服双环醇每日1次,连服2~4周。末次给药后24h测定血清丙氨酸氨基转移酶(ALT)、胆固醇、低/高密度脂蛋白(HDL/LDL)和肝脏甘油三酯(TG),肝脏二甲基亚硝胺脱甲基酶(NDMA-DM),谷胱甘肽(GSH)及谷胱甘肽-巯基转移酶(GST)、谷胱甘肽还原酶(GR)、乙醛脱氢酶(ALDH)水平以及病理形态改变。结果双环醇(200/300mg.kg-1.d-1,连服2~4周)可明显抑制酒精引起的血清ALT和NDMA-DH的升高和肝脏GSH、GST、GR、ALDH的减低,使其恢复至正常水平。此外,双环醇还可使肝脏升高的TG下降28%~34%,提高血清HDL水平(68%~98%),降低LDL(33%~42%)。肝脏脂肪性变也明显减轻,双环醇预防给药组(300mg.kg-1.d-1)小鼠肝脏病理积分为1.4±1.2,双环醇治疗给药组(300mg.kg-1.d-1)小鼠肝脏病理积分为0.7±0.5,与模型组比较,差异均有统计学意义(分别P<0.05,P<0.01?。结论双环醇对小鼠慢性酒精性肝损伤具有明显的保护作用,其作用机制与减轻肝脏脂肪堆积,加速乙醇和乙醛的清除以及提高肝脏抗氧化能力相关。
Objective To study the effects of bicyclol on chronic alcoholic liver injury in mice. Methods The mice were given Lieber-Decarli whole nutrition liquid diet containing 5% alcohol continuously for 4 weeks, and a chronic alcoholic liver injury model was established. Animals in the modeling and oral administration of bicyclol once a day, and even for 2 to 4 weeks. Serum levels of alanine aminotransferase (ALT), cholesterol, low / high density lipoprotein (HDL / LDL) and hepatic triglyceride (TG), hepatic dimethylnitrosamine demethylase (NDMA-DM), glutathione (GSH) and glutathione-S-transferase (GST), glutathione reductase (GR), aldehyde dehydrogenase (ALDH) levels and pathological changes. Results Bicyclol (200 / 300mg.kg-1.d-1, even for 2 to 4 weeks) significantly inhibited the increase of serum ALT and NDMA-DH and the decrease of liver GSH, GST, GR and ALDH induced by alcohol, Make it back to normal. In addition, bicyclol also reduces hepatic elevation of TG by 28% -34%, increases serum HDL levels by 68% -98%, and decreases LDL by 33% -42%. Liver fatty degeneration was also significantly reduced. The liver pathological score of the bicyclol prophylaxis group (1.4 mg · kg -1 · d -1) was 1.4 ± 1.2 and that of the bicyclol treatment group (300 mg · kg -1 · d -1) 1), the pathological score of liver in mice was 0.7 ± 0.5, which was significantly different from the model group (P <0.05, P <0.01, respectively) .Conclusion Bicyclol has obvious protective effect on chronic alcoholic liver injury in mice , Its mechanism of action and to reduce liver fat accumulation, accelerate the removal of ethanol and acetaldehyde, as well as improve the liver antioxidant capacity.