摘要
目的探讨贵州茅台酒(下称茅台酒)与肝病的关系。方法①饮茅台酒组99例与非饮酒组33例按3:1配对,进行流行病学调查,并对饮茅台酒职工组的23名自愿者行肝穿刺活检.②60只Wistar大鼠随机分为3组,分别给予茅台酒和普通白酒、生理盐水灌胃连续8wk、12wk,分批处死动物,测血清ALT、AST、总胆红素(TBil)、AKP,剖腹取肝脏测肝系数、GSH、MDA及肝病理组织学检查.80只小鼠随机分为4组,分别给予茅台酒、乙醇、生理盐水灌胃,连续4wk后处死动物取血测ALT,剖腹取肝脏测肝系数、MDA.结果 99例饮茅台酒组和33例非饮酒组有肝病症状、脾大、ALT增高、A/G倒置、门静脉增宽的检出率分别为1.0％(1/99)、1.0％(1/99)、1.0％(1/99)、1.0％(1/99)、0(0/99)和0(0/99)、0(0/99)、0(0/99)、0(0/99)、0(0/99),茅台酒组与非饮酒组无明显差异(P>0.05);23例饮茅台酒组职工作肝穿刺活检均有轻重不同肝细胞脂肪变性,但均无明显的肝纤维化、肝硬化的表现.茅台酒组与普通白酒组相比,大鼠、小鼠肝脏MDA(A值)分别为0.33±0.10、0.49±0.23和0.61±0.22、0.66±0.32,茅台酒组明显降低(P<0.05);大鼠肝脏GSH分别为0.12mg.g^(-1)±0.06mg.g^(-1)和0.08mg.g^(-1)±0.02mg.g^(-1),茅台酒组明显增高(P<0.05).普通白酒组20只大鼠灌胃8wk后均可见肝细胞索排列紊乱,肝细胞脂肪变性和肝纤维结缔组织增生形成宽窄不等的纤维间隔,12wk后纤维结缔组织进一步增生,并有早期肝硬化表现;而用茅台酒灌胃大鼠8wk和12wk均有肝细胞脂肪变性,全部均无明显肝细胞坏死、肝纤维化、肝硬化。结论茅台酒可致脂肪肝但不引起明显的肝纤维化及肝硬化,有增加肝脏的脂质抗氧化作用。
AIM To explore the relationship between Maotai liquor and liver diseases. METHODS ①Epidemiological study was conducted 99 alcoholics of Maotai and 33 non-alcoholics. Liver biopsy was performed on 23 volunteers from Guizhou Maotai Distillery with a long history of consuming Maotai constantly. ②Sixty male Wistar rats were divided into 3 groups randomly and ingested with Maotai, ordinary liquor, physiological saline, respectively for 8-12 weeks. The rats were sacrificed in batches, and serum ALT, AST, TBil, and AKP were measured. The livers were harvested, and liver indexes, GSH and MDA measured. Pathohistological examination was also made. Eighty mice were randomly divided into 4 groups and ingested with Maotai, ethanol, and physiological saline. The animals were sacrificed after 4 consecutive weeks and serum ALT determined. The livers were harvested and liver indexes and MDA measured. RESULTS The incidence rate of liver inflammatory symptoms, splenomegaly, liver function impairment, reverse of albumin/globulin and widening of portal veins in the Maotai and non-alcoholics were 1.0% (1/99), 1.0% (1/99), 1.0%(1/99), 1.0%(1/99), 0(0/99) and 0(0/99), 0(0/99), 0(0/99), 0(0/99), and 0(0/99). There was no significant difference (p>0.05) between the two groups. Various degrees of fatty degeneration of hepatocytes were detected in the 23 volunteers receiving liver biopsy, but no obvious hepatic fibrosis or cirrhosis occurred. A comparison was made between the Maotao group and ordinary liquor group. Hepatic MDA of rats and mice were 0.33±0 and 10, 0.49±0.23 respectively in Maotai group and 0.61±0.22 and 0.66±0.32 in the ordinary group (p< 0.05). Hepatic GSH was 0.12mg.g^(-1)±0.06mg.g^(-1) in rats and 0.08mg.g^(-1)±0.02mg.g^(-1)(p<0.05 ) in Maotai group. After the 20 rats were ingested with ordinary liquor for 8 weeks consecutively, disordered hepatocyte cords, fatty degeneration of hepatocytes, and fibrous septa of various width due to hepatic fibrous connective tissues proliferation were observed. After 12 weeks, the fibrous connective tissue proliferation continued and early signs of hepatic cirrhosis appeared. In the Maotai group, however, though fatty degeneration was observed in week 8 and 12, no obvious hepatocyte necrosis, hepatic fibrosis or cirrhosis were found (p<0.05) in comparison between Maotai and ordinary liquor groups. CONCLUSIONS Maotai may lead to fatty liver but not obvious hepatic fibrosis and cirrhosis, and strengthen lipid peroxidation in liver.
出处
《世界华人消化杂志》
CAS
2001年第12期1376-1378,共3页
World Chinese Journal of Digestology
基金
贵州省科学技术重点项目
黔科合计字 No.19992015
关键词
茅台酒
肝病
病组织学
流行病学
alcoholic beverages
liver diseases/epidemiology
liver/pathology
lipid peroxidation
