解酒保肝口服液对小鼠酒精中毒的影响

目的：观察解酒保肝口服液对小鼠醉酒实验,血清乙醇浓度和肝、胃组织乙醇脱氢酶活性的影响。方法：将生理盐水和将葛根,甘草等中药用水煎煮制成解酒保肝口服液灌服于小鼠后30min,灌服白酒,记录小鼠翻正反射消失（醉酒）至恢复（醒酒）所需时间（min),及24h内小鼠的死亡只数,另以相同操作连续6d后眼眶取血并处死动物,立即取出肝脏和胃,分别用生化比色法测定血肖乙醇浓度和肝、胃组织乙醇脱氢酶活性。结果：在醉酒实验中,。与对照组相比服用解酒保肝口服液组小鼠从饮酒到翻正反射消失（醉酒）的时间明显延长（P＜0．01）,醒酒时间明显缩短,且小鼠的死亡率明显降低（P＜0．05）,血清乙醇含量明显降低,肝脏ADH高于对照组, 结论：解酒保肝口服液具有解酒作用。     

乙酰半胱氨酸对小鼠酒精中毒的影响

目的 :观察5 %N—乙酰—L—半胱氨酸 (NAC)口服液对小鼠醉酒后血清乙醇浓度和肝、胃组织乙醇脱氢酶活性的影响。方法 :用生理盐水或5 %NAC口服液灌服小鼠30min后 ,再灌服白酒 ,记录小鼠翻正反射消失 (醉酒 )至恢复 (醒酒 )所需时间及24h内小鼠的死亡只数 ;另对小鼠以相同灌服方法连续6d灌服后眼眶取血并处死小鼠 ,立即取出其肝脏和胃 ,分别用生化比色法测定血清乙醇浓度和肝、胃组织乙醇脱氢酶活性。结果 :在醉酒实验中 ,与对照组比较 ,服用5 %NAC口服液组小鼠从饮酒到醉酒的时间明显延长 (P<0 01) ,醒酒时间明显缩短 ,且小鼠的死亡率明显降低 (P<0 05) ;服用5 %NAC口服液组小鼠血清乙醇浓度明显低于单纯服用白酒的小鼠 (P<0 01)。结论 :5 %NAC口服液具有解酒作用。     

解酒保肝剂对小鼠酒精中毒的影响

目的 观察解酒保肝剂对小鼠醉酒实验、血清乙醇浓度和肝组织丙二醛含量的影响。方法 50只小鼠随机分为给药组和对照组,每组25只。给药组小鼠给予解酒保肝剂灌胃,对照组给予双蒸馏水灌胃。记录小鼠翻正反射消失及恢复时间,取肝匀浆,检测肝脏丙二醛(MDA)含量,用顶空气相色谱法检测血酒精浓度。结果 与对照组比较,给药组翻正反射消失时间明显延长(P<0.01),翻正反射时间明显缩短(P<0.05),肝MDA含量显著降低(P<0.05),血酒精含量显著降低(P<0.01)。结论 解酒保肝剂具有良好的解酒作用。     

大籽獐牙菜醇提物解酒保肝作用的实验研究

目的：对大籽獐牙菜乙醇提取物在解酒保肝方面的作用进行初步研究探讨。方法采用纠正运动失调作用实验、解酒实验和预防醉酒实验,同时测定急性酒精性肝损伤小鼠的血清丙氨酸转换酶（ALT）和肝糖原的含量。结果大籽獐牙菜醇提取物可显著延长小鼠酒后在网停留时间;使给药组的翻正反射恢复时间较对照组显著缩短;给药后醉酒小鼠数较未给药组显著减少;可对抗乙醇对小鼠肝脏造成的损伤,使谷丙转氨酶活力显著下降,促进肝糖原的分解,对抗乙醇造成的低血糖。结论大籽獐牙菜提取物具有纠正运动失调、解酒以及预防酒醉作用,其对乙醇所致的肝损伤有防治作用。     

醒酒浓缩液的药效学研究

目的观测醒酒浓缩液对醉酒小鼠防醉和解酒作用。方法采用醉酒模型并测试小鼠翻正反射消失时间及恢复时间（min），气相色谱检测血中乙醇含量。结果(1)30mL/kg、40mL/kg醒酒浓缩液对醉酒小鼠具有明显防醉和解酒作用（P<0.05～0.01）；（2）醉酒前给小鼠ig醒酒浓缩液，中、高剂量组能明显降低酒后40～120min内血液中乙醇含量（P<0.05～0.01）。结论本品具有较好预防醉酒和解酒作用，其作用机理可能与其降低血中乙醇含量有关。     

葛根、葛花、枳椇子混合物对小鼠急性酒精中毒醒酒作用的研究

目的 探讨中药葛根、葛花、枳椇子混合物对小鼠急性酒精中毒的醒酒效果。方法 采用酒精灌胃法建立小鼠急性酒精中毒模型,观察混合物不同配比对小鼠的醒酒效果,选择最佳配比;按最佳配比将小鼠分为低剂量组和高剂量组,通过测定小鼠的耐受时间、醉酒时间、血液中的乙醇浓度和肝中乙醇脱氢酶的活性观察葛根、葛花、枳椇子混合物的醒酒效果。结果 葛根、葛花、枳椇子混合物能够增加小鼠对酒精的耐受时间,同时缩短小鼠的醉酒时间,降低血液中的乙醇浓度,提高肝中乙醇脱氢酶的活性。结论 葛根、葛花、枳椇子混合物对小鼠急性酒精中毒具有醒酒作用。     

醒酒浓缩液的药效学研究

目的观测醒酒浓缩液对醉酒小鼠防醉和解酒作用.方法采用醉酒模型并测试小鼠翻正反射消失时间及恢复时间(min),气相色谱检测血中乙醇含量.结果 (1)30mL/kg、40mL/kg醒酒浓缩液对醉酒小鼠具有明显防醉和解酒作用(P<0.05～0.01);(2)醉酒前给小鼠ig醒酒浓缩液,中、高剂量组能明显降低酒后40～120min内血液中乙醇含量(P<0.05～0.01).结论本品具有较好预防醉酒和解酒作用,其作用机理可能与其降低血中乙醇含量有关.     

解酒饮的药理学研究

目的:研究解酒饮的解酒作用.方法:40只小鼠随机分成空白对照组,胆维他对照组(25mg·g-1)和高低剂量解酒饮组(25,12.5g·kg-1).用自制30%白酒按14mL·kg-1灌胃造成小白鼠醉酒模型,分别在造模前后单次给药,观察小白鼠翻正反射消失的时间和小鼠酒醉持续时间.结果:与空白对照组比较,解酒饮25g·kg-1组小鼠翻正反射消失时间显著延长,酒醉持续时间显著缩短.而解酒饮12.5g·kg-1组无显著性差异.结论:按生药25g·kg-1给予解酒饮,对于小白鼠具有预防醉酒和醒酒的作用.     

赶黄草对预防醉酒及解酒效能研究

目的研究赶黄草的预防醉酒和解酒作用。方法通过五粮春造成小白鼠醉酒的模型,再分别按试验组给予一定剂量的赶黄草、郁金、生理盐水,观察其醒酒时间,翻正反射。结果赶黄草组与生理盐水组比较,小鼠翻正反射消失时间和酒醒时间有显著性差异。而郁金组与生理盐水组比较,小鼠翻正反射消失时间和酒醒时间无显著性差异。     

加味醒酒汤解酒作用的研究

目的 研究加味醒酒汤对醉酒小鼠的解酒作用。方法 根据建立的小鼠醉酒模型,通过测定小鼠醉酒潜伏期与醒酒时间,确定加味醒酒汤的最佳工艺;通过测定小鼠血液乙醇浓度的含量及肝脏乙醇代谢酶的活性来观察加味醒酒汤的解酒效果。结果 加味醒酒汤能够增加小鼠对酒精的耐受时间,同时缩短小鼠的醒酒时间,降低血液中的乙醇浓度,提高肝脏中ADH、ALDH与GSH-Px的活性。结论 加味醒酒汤对醉酒小鼠具有解酒作用,其机制可能与提高乙醇代谢酶的活性有关。     

Alcohol dehydrogenase activity of human and animal blood serum in acute and chronic alcoholic intoxication

Alcohol dehydrogenase activity (ADH; KP 1.1.1.1.) in blood serum of rats and rabbits is 1 and 2 orders of magnitude higher than in humans. In chronic alcoholics, blood ADN is activated with an increase in alcoholism standing. Twelve hours after acute alcoholic intoxication alcoholics and heavy drinkers manifest a significant reduction in blood ADH activity. Acute alcoholic intoxication does not influence blood ADH in men who do not abuse alcohol. Chronic exposure of rabbits to ethanol leads to a decrease in ADH activity in the liver and to its rise in the blood. ADH activation is observed only in those animals which demonstrate the signs of fatty and protein liver dystrophy. It is concluded that chronic exposure to ethanol does not induce ADH synthesis in the liver. The blood ADH content ascends as a results of an increase in ADH transport from hepatocytes to the bloodstream.     

枳椇子乙酸乙酯提取部位的解酒作用研究

目的:研究枳椇子乙酸乙酯提取部位的解酒作用。方法:将小鼠随机分成5组,即空白、模型(生理盐水)、阳性(灌胃海王金樽20g·kg-1)和乙酸乙酯提取物高、低剂量组(乙酸乙酯提取物相当于20、10g生药.kg-1)。研究各种提取物对急性酒精中毒小鼠血清谷丙转氨酶(SGPT)活性、肝脏丙二醛(MDA)含量、醇脱氢酶(ADH)活性、还原型谷胱甘肽(GSH)含量、超氧化物歧化酶(SOD)活性的影响。结果:枳椇子乙酸乙酯提取部位可降低急性酒精中毒小鼠血清SGPT活性和肝脏MDA含量,升高小鼠肝脏ADH、SOD活性和GSH含量。结论:枳椇子乙酸乙酯提取部位具有显著的解酒效果,值得进行深入研究。     

Dietary zinc-deficiency and its recovery responses in rat liver cytosolic alcohol dehydrogenase activities

The purpose of the present study was to elucidate the effects of dietary zinc-deficient feeding and its recovery on liver cytosolic alcohol dehydrogenase (ADH; alcohol: NAD(+) oxidoreductase, EC1.1.1.1) activities and plasma zinc levels in rats. The weaned male Sprague Dawley rats were randomly divided into the zinc-deficient diet (ZDF: 1.9 mg zinc/kg diet) group and the control diet (53.5 mg zinc/kg diet) group, and were fed for 4 weeks. In the recovery periods, the rats of two groups were fed with the control diet for 3 weeks. Liver cytosolic protein content per body weight in the zinc-deficiency and its recovery period showed no significant changes between both groups. However, zinc-deficiency decreased significantly liver cytosolic ADH specific activity, total liver cytosolic ADH activity and total liver cytosolic ADH activity/body weight by 50%, 76% and 53%, respectively, as compared with the control diet group. Zinc-deficiency also decreased significantly plasma zinc concentration by 84%, as compared with the control diet group. On the contrary, no significant changes in liver cytosolic ADH specific activity, total liver cytosolic ADH activity and total liver cytosolic ADH activity/body weight in the recovery period were observed between both groups. Plasma zinc concentration in the recovery period was almost recovered to the control level. These results suggest that rat liver cytosolic ADH activity was clearly related to dietary zinc intake levels.     

Alcohol dehydrogenase isoenzymes in rat development. Effect of maternal ethanol consumption.

The alcohol dehydrogenase (ADH) isoenzymes (alcohol:NAD oxidoreductase, EC 1.1.1.1) of classes I, III and IV were investigated by activity and starch gel electrophoresis analyses during rat ontogeny. Class I was studied in the liver, class III in the brain and class IV in the stomach and eyes. Classes I and IV exhibited very low activity during the fetal period, reaching 12% and 3%, respectively, of the adult value at birth. Class III was relatively more active in the fetus, with 38% of the adult activity at birth. In the three cases, activity increased after birth and adult values were found around day 20 (classes I and III), day 39 (stomach class IV) and after day 91 (eye class IV). The very low activity of the isoenzymes responsible for ethanol oxidation, i.e. liver class I and stomach class IV, in the fetus demonstrates that metabolism of ethanol during gestation is essentially performed by the maternal tissues. Development of ADH isoenzymes were also studied in the offspring of rats exposed to an alcoholic liquid diet. Activities of liver class I and stomach class IV were severely reduced: they were only 30% and 50%, respectively, of the control values. In contrast, eye class IV activity did not change and brain class III showed a 30% increase. Moreover, the concentration of liver soluble protein exhibited a 1.3-1.5-fold increase with respect to control animals. The effects on activities and liver protein were more pronounced in the adult than in the perinatal period, and they seem irreversible since normal values were not recovered after 6 weeks of feeding with a non-alcoholic diet. The low activities of the alcohol-oxidizing isoenzymes indicate tht maternal ethanol consumption results in an impaired ethanol metabolism of the offspring.     

百香果对酒精中毒小鼠的解酒作用及其护肝作用的研究

目的：探讨百香果提取物对酒精中毒小鼠的解酒作用以及对酒精性肝损伤的护肝作用。方法：将小鼠随机分为空白对照组,模型对照组,阳性（联苯双酯）对照组（150 mg·kg^-1）,百香果乙酸乙酯提取物低（15 mg·kg^-1）、中（30 mg·kg^-1）、高剂量组（60 mg·kg^-1）,按照相应的剂量灌胃,空白对照组和模型对照组给予相同体积的生理盐水。（1）1 h后,给予50%乙醇（6 g·kg^-1）,建立中毒模型。记录小鼠的醉酒时间与醒酒时间,并做统计学分析。（2）连续灌胃7 d,在末次给药后,除空白对照组给予生理盐水外,其余各组每隔8小时50%乙醇灌胃（6 g·kg^-1）1次,建立急性肝损伤模型。在末次乙醇灌胃1 h后,取血,解剖取肝脏,利用试剂盒测定血清和肝匀浆的生化指标。并将肝脏组织做组织病理学检查。结果：百香果乙酸乙酯提取物对酒精中毒的小鼠有解酒作用;与模型对照组相比,百香果乙酸乙酯提取物可以降低急性肝损伤体内谷丙转氨酶（ALT）、谷草转氨酶（AST）的活性,增高肝匀浆中过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、谷胱甘肽（GSH）的活性及其含量,降低肝匀浆中丙二醇（MDA）、甘油三酯（TG）的含量。肝脏病理结果显示,百香果乙酸乙酯提取物有一定的护肝作用。结论：百香果乙酸乙酯提取物对乙醇中毒的小鼠有一定的解酒作用,并且对酒精性肝损伤有一定的预防肝损伤的作用。     

bFGF对慢性酒精中毒大鼠血清GPT、GOT活性的影响

目的：观察碱性成纤维细胞生长因子（bFGF）对慢性酒精中毒大鼠血清GPT、GOT活性的影响,探讨bFGF对酒精中毒所致的肝损伤是否具有保护作用。方法：选择成年Wistar雄性大鼠,采用白酒灌胃建立慢性酒精中毒模型,慢性酒精中毒模型建立成功的大鼠采用随机抽签法分为酒精中毒对照组、NS对照组和bFGF治疗组。另10只不灌白酒作为正常对照组。bFGF治疗组大鼠白酒灌胃的同时,1h后按12μg/kg剂量肌内注射,共14d。各组大鼠到相对应的时间点取血测定血清谷丙转氨酶（GPT）、谷草转氨酶（GOT）活性。结果：慢性酒精中毒后大鼠血清GPT、GOT活性比正常对照组均明显升高（P〈0.01）,用bFGF治疗酒精中毒大鼠后血清GPT、GOT活性均明显下降（P〈0.01）。结论：bFGF能降低酒精中毒大鼠后血清GPT和GOT活性,对酒精中毒所致的肝损伤具有保护作用。