Prevention and Cure of Acute Alcohol Intoxication in Mice by Administration of Compound of Japanese Raisintree Fruit, Lobed Kudzuvine Flower Bud and Lightyellow Sophora Root

[Objective] We aimed to investigate the preventive and therapeutical effect of compound of traditional Chinese drugs （Japanese raisintree fruit, lobed kudzuvine flower bud and lightyel ow sophora root） on acute alcohol intoxication in mice. [Method] Acute alcohol intoxication was induced by administering alcohol to mice. Three different doses （low, middle and high） of compound of traditional Chinese drugs were administered to mice before and after administering alcohol respectively to investigate the preventive and therapeutical effect of drugs on acute alcohol intox-ication through doing statistical analysis about drunk mice and their sleeping time. The concentration of malondialdehyde （MDA）, reduced glutathione （GSH） and triglyc-erides （TG） in liver was also determined to investigate the protective effect of drugs on liver. [Result] The efficacy of compound of traditional Chinese drugs on acute al-cohol intoxication was dose-dependent. High-dose administration decreased the number of drunk mice significantly compared with control group; middle- and high-dose administration reduced the sleeping time of drunk mice and the concentration of MDA and TG in liver tissue; three doses al increased the concentration of GSH. [Conclusion] The compound of Japanese raisintree fruit, lobed kudzuvine flower bud and lightyel ow sophora root had preventive and therapeutical effect on hangover, and it also had certain preventive and therapeutical effect on liver damage caused by alcohol.

Oxidative stress and nitric oxide in rats with alcohol-induced acute pancreatitis

AIM: Oxygen free radical mediated tissue damage is well established in pathogenesis of acute pancreatitis (AP).Whether nitric oxide (NO) plays a deleterious or a protective role is unknown. In alcohol-induced AP, we studied NO, lipooxidative damage and glutathione in pancreas, lung and circulation.METHODS: AP was induced in rats (n = 25) by injection of ethyl alcohol into the common biliary duct. A sham laparatomy was performed in controls (n = 15). After 24 h the animals were killed, blood and tissue sampling were done.RESULTS: Histopathologic evidence confirmed the development of AP. Marked changes were observed in the pulmonary tissue. Compared with controls, the AP group displayed higher values for NO metabolites in pancreas and lungs, and thiobarbituric acid reactive substances in circulation. Glutathione was lower in pancreas and in circulation. Glutathione and NO were positively correlated in pancreas and lungs of controls but negatively correlated in circulation of experimental group. In the experimental group, plasma thiobarbituric acid reactive substances were negatively correlated with pancreas thiobarbituric acid reactive substances but positively correlated with pancreas NO.CONCLUSION: NO increases in both pancreas and lungs in AP and NO contributes to the pathogenesis of AP under oxidative stress.

In vitro and in vivo models of acute alcohol exposure

Alcohol abuse is a global problem due to the financial burden on society and the healthcare system. While the harmful health effects of chronic alcohol abuse are well established, more recent data suggest that acute alcohol consumption also affects human wellbeing. Thus, there is a need for research models in order to fully understand the effect of acute alcohol abuse on different body systems and organs. The present manuscript summarizes the interdisciplinary advantages and disadvantages of currently available human and non-human models of acute alcohol abuse, and identifi es their suitability for biomedical research.

The Protective Effect of Jiujiuguiyi, a Medicine and Food Homologous Formula, on Acute Alcohol Poisoning Mice

Background: Nowadays, acute alcoholic intoxication has become the third public problem in China, and the anti-inebriation products mainly aimed at increasing the activity of enzyme involved in the alcohol metabolism, which is a single mechanism that can accelerate alcohol metabolism. Thus, a new formula, Jiujiuguiyi (JJGY) which could protect liver, relieve the abnormal excitability of the center and improve muscle retardation at the same time is designed by us. Methods: The model of acute alcoholic intoxication was established by intragastric administration with 0.12 ml/10g 50% alcohol in mice. JJGY was orally administrated (gavage) once a day for 20 consecutive days before the establishment of acute alcoholic model. Mice were randomly divided into 8 groups with 8 each: blank control group (CON), model group (M), Haiwangjinzun positive control group (HWJZ), experimental groups (AL, AH, BL, BH, AB). Giant, crawling time on the rota-rod, the activities of aspartate amino trans- ferase (AST), alanine amino transferase (ALT) and superoxide dismutase (SOD) in both liver and serum, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), glutathione peroxidase (GSH-PX) in liver as well as the HE staining of liver slices, the formation of malondialdehyde (MDA) in serum were determined after acute alcoholic intoxication. Results: Compared with model group, JJGY significantly decreased the AST and ALT activity in liver and serum and MDA activity in serum. Meanwhile, it enhanced the ADH and ALDH level in liver as well as the hepatic and serous SOD activity, indicating more efficient metabolism of alcohol and less hepatic injury. HE staining results also proved that JJGY could reduce alcoholic liver cell injury, and the effect was more obvious in the group medicated before alcohol administration. Moreover, JJGY significantly prolonged the crawling time on the rota-rod and improved the gait of mice and the effect was proved to be better than the widely used health product Haiwangjinzun. Conclusions: This study suggests that JJGY is able to protect liver, relieve the abnormal excitability of the center and improve muscle retardation after acute alcoholic intoxication. Its liver protection effect is likely related to its modulation on the alcohol metabolizing and antioxidant enzymes.