首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 78 毫秒
1.
我国天然解酒制品的研究进展   总被引:1,自引:0,他引:1  
酗酒和酒精中毒已经成为我国的公共卫生问题,开发有效的解酒药物具有重要的意义和广阔的市场前景。当前天然解酒药物的作用机制是通过抑制乙醇胃肠吸收和加速代谢以降低机体血醇浓度,解除醉酒状态。文章论述了开口箭、蛇菰、人参、葛花等多种天然解酒药物的解酒作用及药理研究的最新进展,探讨其活性成分的药效作用,并对此类天然药物在今后的研制方向上提出了浅见。  相似文献   

2.
天然植物药解酒的研究概况   总被引:1,自引:0,他引:1  
大量饮酒能引起人体生理功能紊乱以至死亡,从天然植物药中开发研究低毒、高效解酒药物有着重要意义。目前天然解酒药物的作用机制是通过抑制乙醇胃肠吸收和加速代谢并降低体内血中醇浓度,解除醉酒状态。此文综述了人参、葛根、三七等多种天然植物药解酒药物的单方和复方解酒作用药理研究最新概况,并对天然植物解酒研究提出了粗浅见解。  相似文献   

3.
蒋杨  邹丽宜 《现代医药卫生》2008,24(10):1435-1437
目的:探讨解酒合剂的作用。方法:观察和比较解酒合剂对小鼠的攀爬活动、翻正反射和睡眠的影响。结果:解酒合剂能明显缓解小鼠因醉酒引起的平衡失调现象,延长小鼠睡眠耐受时间,缩短睡眠维持时间,降低急性酒精中毒的死亡率。结论:解酒合剂具有良好的解酒作用。  相似文献   

4.
解酒肝康颗粒主要由人参、五味子、白芍、丹参等药物组成,具有疏肝理脾,解酒祛湿,祛瘀行滞的功效,临床用于治疗酒精性脂肪肝。现对解酒肝康中的人参、丹参、五味子、白芍的化学成分进行综述。  相似文献   

5.
解酒药物的研究进展   总被引:2,自引:0,他引:2  
随着人们对酒需求的增加,酒精对人体健康的影响开始引起广泛的重视,过度饮酒会造成急性肝损伤甚至死亡。因此,急需开发具有醒酒功能的药物。本文查阅近5年相关文献,对植物类解酒药物如葛根、葛花、红景天、枳椇子、五味子以及动物类解酒药物如牡蛎、熊胆粉和解酒处方如醒酒颗粒、葛花醒酒养胃颗粒、永生宜康的醒酒功效进行有效成分及药理研究的归纳总结,为进一步的研发提供参考。  相似文献   

6.
葛根总黄酮及葛根素解酒的药理研究进展   总被引:13,自引:0,他引:13  
目的:归纳葛根总黄酮及葛根素用于解酒的实验进展。方法:通过查阅国内外相关文献,介绍葛根在古代的解酒作用及其主要化学成分,概述葛根总黄酮和葛根素用于解酒的研究。结果:葛根总黄酮是葛根提取物中的主要有效成分,葛根素则是总黄酮中的一种活性单体成分,均具有防醉酒、治醉酒和对抗酒精性肝损伤等作用。结论:虽然对葛根总黄酮和葛根素解酒的研究取得了一定进展,但对其作用的分子生物学机制方面应做进一步的研究,使其机制更加明确。  相似文献   

7.
随着抗菌药物使用的增加,肠杆菌科细菌耐药的情况越发严重,可供选择的抗菌药物将越来越少。天然药物因其作用范围广、毒副作用较小在抗感染研究中备受关注,而天然药物单体即是其发挥药理学作用的物质基础。就近年来天然药物单体对肠杆菌科细菌的作用及其机制进行综述,为抗菌药物的筛选和开发提供参考。  相似文献   

8.
随着抗菌药物使用的增加,肠杆菌科细菌耐药的情况越发严重,可供选择的抗菌药物将越来越少。天然药物因其作用范围广、毒副作用较小在抗感染研究中备受关注,而天然药物单体即是其发挥药理学作用的物质基础。就近年来天然药物单体对肠杆菌科细菌的作用及其机制进行综述,为抗菌药物的筛选和开发提供参考。  相似文献   

9.
解酒饮的药理学研究   总被引:3,自引:0,他引:3  
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.  相似文献   

10.
目的探讨天然药物抗肿瘤的有效成分及其作用机理,为进一步开发天然抗肿瘤药物提供理论基础。方法通过收集和查找近年来有关天然药物在抗肿瘤方面的报道和研究,整理和总结出天然药物在抗肿瘤方面的有效成分和作用机制。结果天然药物抗肿瘤成分主要有生物碱类,中药多糖类,萜类,醌类,蛋白质类等;对抗肿瘤主要作用机制有对肿瘤细胞的直接杀灭作用;干扰细胞周期;诱导肿瘤细胞的分化;逆转多药耐药性肿瘤细胞的抗凋亡作用;诱导肿瘤细胞凋亡;提高机体免疫力来抗肿瘤等方面进行。结论天然抗肿瘤药物的有效成分类别有多样性,但主要为生物碱类,多糖类等为主;作用机制为直接对肿瘤细胞杀灭作用,干扰细胞生长的各个周期及提高机体免疫力等方面。  相似文献   

11.
Drug interactions with alcohol.   总被引:2,自引:0,他引:2  
Ethanol and drugs can affect each other's absorption, distribution, metabolism, and excretion. When ingested together, ethanol can increase drug absorption by enhancing the gastric solubility of drugs and by increasing gastrointestinal blood flow. However, high concentrations of ethanol induce gastric irritation causing a pyloric spasm which in turn may delay drug absorption and/or reduce bioavailability. The 'quality' of the alcoholic beverage, independent of its ethanol content, can contribute to altered absorption of a drug. Ethanol is not bound to plasma proteins extensively enough to modify drug distribution. However, serum albumin levels in chronic alcoholics may be abnormally low so that some drugs, e.g. diazepam, have an increased volume of distribution. In addition to the amount ingested, the duration of regular intake determines the effect of ethanol on drug metabolism. Acute intake of ethanol inhibits the metabolism of many drugs but long term intake of ethanol at a high level (greater than 200g of pure ethanol per day) can induce liver enzymes to metabolise drugs more efficiently. At the present time there are no accurate means, with the possible exception of liver biopsy, to clinically predict the capacity of an alcoholic to metabolise drugs. Several drugs can inhibit the metabolism of ethanol at the level of alcohol dehydrogenase. Individual predisposition determines the severity of this drug-ethanol interaction. During its absorption phase, ethanol inhibits the secretion of antidiuretic hormone and is also able to induce increased excretion of a drug through the kidneys. However, chronic alcoholics with water retention may show reduced excretion of drugs via this route. At the pharmacodynamic level, ethanol can enhance the deleterious effects of sedatives, certain anxiolytics, sedative antidepressants and antipsychotics and anticholinergic agents, on performance. Mechanisms of lethal interactions between moderate overdoses of ethanol and anxiolytics/opiates/sedatives are poorly understood. On the other hand, certain peptides, 'nonspecific' stimulants, dopaminergic agents and opiate antagonists can antagonise alcohol-induced inebriation to a significant degree.  相似文献   

12.
1. Ethanol and nicotine are commonly coabused drugs. Cytochrome P450 2E1 (CYP2E1) metabolizes ethanol and bioactivates tobacco-derived procarcinogens. Ethanol and nicotine can induce hepatic CYP2E1 and we hypothesized that both centrally active drugs could also induce CYP2E1 within the brain. 2. Male rats were treated with saline, ethanol (3.0 g kg(-1) by gavage) or nicotine (1.0 mg kg(-1) s.c.) for 7 days. Ethanol treatment significantly increased CYP2E1 in olfactory bulbs (1.7-fold), frontal cortex (2.0-fold), hippocampus (1.9-fold) and cerebellum (1.8-fold), while nicotine induced CYP2E1 in olfactory bulbs (2.3-fold), frontal cortex (3.0-fold), olfactory tubercle (3.1-fold), cerebellum (2.5-fold) and brainstem (2.0-fold). Immunocytochemical analysis revealed that the induction was cell-type specific. 3. Consistent with the increased CYP2E1 found in rat brain following drug treatments, brains from alcoholics and alcoholic smokers showed greater staining of granular cells of the dentate gyrus and the pyramidal cells of CA2 and CA3 hippocampal regions as well as of cerebellar Purkinje cells compared to nonalcoholic nonsmokers. Moreover, greater CYP2E1 immunoreactivity was observed in the frontal cortices in the alcoholic smokers in comparison to nonalcoholic nonsmokers and alcoholic nonsmokers. 4 To investigate if nicotine could contribute to the increased CYP2E1 observed in alcoholic smokers, we treated human neuroblastoma IMR-32 cells in culture and found significantly higher CYP2E1 immunostaining in nicotine-treated cells (0.1-10 nM). 5. CYP2E1 induction in the brain, by ethanol or nicotine, may influence the central effects of ethanol and the development of nervous tissue pathologies observed in alcoholics and smokers.  相似文献   

13.
Oxidation of ethanol via alcohol dehydrogenase (ADH) explains various metabolic effects of ethanol but does not account for the tolerance. This fact, as well as the discovery of the proliferation of the smooth endoplasmic reticulum (SER) after chronic alcohol consumption, suggested the existence of an additional pathway which was then described by Lieber and DeCarli, namely the microsomal ethanol oxidizing system (MEOS), involving cytochrome P450. The existence of this system was initially challenged but the effect of ethanol on liver microsomes was confirmed by Remmer and his group. After chronic ethanol consumption, the activity of the MEOS increases, with an associated rise in cytochrome P450, especially CYP2E1, most conclusively shown in alcohol dehydrogenase negative deer mice. There is also cross-induction of the metabolism of other drugs, resulting in drug tolerance. Furthermore, the conversion of hepatotoxic agents to toxic metabolites increases, which explains the enhanced susceptibility of alcoholics to the adverse effects of various xenobiotics, including industrial solvents. CYP2E1 also activates some commonly used drugs (such as acetaminophen) to their toxic metabolites, and promotes carcinogenesis. In addition, catabolism of retinol is accelerated resulting in its depletion. Contrasting with the stimulating effects of chronic consumption, acute ethanol intake inhibits the metabolism of other drugs. Moreover, metabolism by CYP2E1 results in a significant release of free radicals which, in turn, diminishes reduced glutathione (GSH) and other defense systems against oxidative stress which plays a major pathogenic role in alcoholic liver disease. CYP1A2 and CYP3A4, two other perivenular P450s, also sustain the metabolism of ethanol, thereby contributing to MEOS activity and possibly liver injury. CYP2E1 has also a physiologic role which comprises gluconeogenesis from ketones, oxidation of fatty acids, and detoxification of xenobiotics other than ethanol. Excess of these physiological substrates (such as seen in obesity and diabetes) also leads to CYP2E1 induction and nonalcoholic fatty liver disease (NAFLD), which includes nonalcoholic fatty liver and nonalcoholic steatohepatitis (NASH), with pathological lesions similar to those observed in alcoholic steatohepatitis. Increases of CYP2E1 and its mRNA prevail in the perivenular zone, the area of maximal liver damage. CYP2E1 up-regulation was also demonstrated in obese patients as well as in rat models of obesity and NASH. Furthermore, NASH is increasingly recognized as a precursor to more severe liver disease, sometimes evolving into "cryptogenic" cirrhosis. The prevalence of NAFLD averages 20% and that of NASH 2% to 3% in the general population, making these conditions the most common liver diseases in the United States. Considering the pathogenic role that up-regulation of CYP2E1 also plays in alcoholic liver disease (vide supra), it is apparent that a major therapeutic challenge is now to find a way to control this toxic process. CYP2E1 inhibitors oppose alcohol-induced liver damage, but heretofore available compounds are too toxic for clinical use. Recently, however, polyenylphosphatidylcholine (PPC), an innocuous mixture of polyunsaturated phosphatidylcholines extracted from soybeans (and its active component dilinoleoylphosphatidylcholine), were discovered to decrease CYP2E1 activity. PPC also opposes hepatic oxidative stress and fibrosis. It is now being tested clinically.  相似文献   

14.
Decreased plasma binding of phenytoin and diazepam has previously been described in patients with alcoholic liver diseases. It has been attributed to hypoalbuminemia, endogenous displacers and/or qualitative changes in albumin such as formation of adducts with acetaldehyde, a highly reactive metabolite of ethanol. In the present report this hypothesis was tested. After treating the sera with activated charcoal to remove the endogenous displacers and adjusting albumin concentration to a constant level, the binding parameters of both drugs, phenytoin and diazepam, were determined in 14 healthy men and 16 alcoholic patients by equilibrium dialysis. In these conditions, no significant difference in the number of binding sites nor in the affinity constant was observed, which suggests that acetaldehyde adducts with proteins do not contribute, to a major extent, to the defect of drug binding observed in alcoholic patients.  相似文献   

15.
In rats, a complex longitudinal analysis of alcohol intake behaviour and electrophysiological sleep pattern was performed during different periods of stable voluntary alcohol consumption. By the sleep pattern, the existence of alcohol abuse and dependence development could be confirmed. Acute ethanol withdrawal was shown to be the obligatory and necessary element in alcohol abuse and dependence evaluation. The proposed behavioural and sleep pattern models might be used in the search for anti-alcoholic drugs in combination with the study of alcoholic aging processes.  相似文献   

16.
Using conditioned-reflex methods for active and passive avoidance with punishment reinforcement, we found pronounced memory deficits in 12-week old rats exposed perinatally to alcohol (FAS rats). Impairment of memory was observed not only with the high dose of 9 g ethanol/kg body weight (ingested with tap water in a 6% solution) to which dams were exposed during pregnancy and lactation, but also with the ten-fold lower dose of 1 g ethanol/kg body weight (0.6% ethanol). The nootropic drugs citicholine, piracetam and meclofenoxate administered orally for five days before the training session were effective in decreasing memory deficits; particularly pronounced was the effect of piracetam and meclofenoxate. The benzodiazepine tranquilizer diazepam additionally impaired learning and memory in FAS rats. It is suggested that nootropics could be used to decrease the cognitive disturbances in some humans born to alcoholic mothers.  相似文献   

17.
A series of experiments investigated the effects of a single injection of estradiol valerate (EV) on female rats' consumption of alcoholic beverages. EV provides sustained release of estradiol. Just after an injection of EV, rats' intake of a palatable alcoholic beverage, which had been taken regularly before, is reduced dramatically. Subsequently, rats' intake of alcoholic beverage returns to baseline levels. With continued opportunity to drink, rats take more ethanol than controls. When EV was given 15 and 31 days before the first opportunity to drink an alcoholic beverage, female rats markedly enhanced their intake of ethanol. Once enhanced intakes emerged, they were observed with different kinds of alcoholic beverages and endured for months.  相似文献   

18.
Ethanol is likely among the most widely and extensively used drugs in the world. It has also been demonstrated to alter the expression or activity of some drug-metabolizing enzymes. Thus, marked ethanol-provoked drug interactions could be of notable clinical importance. To date, relatively few clinically important interactions have been reported, involving cocaine, disulfiram and tacrolimus. Limited or modest interactions with ethanol have also been reported for drugs such as abacavir, cisapride, 'ecstasy' (3,4-methylenedioxymetamfetamine), gamma-hydroxybutyrate, methylyphenidate, metronidazole and verapamil. Most of these interactions do not seem to involve CYP2E1, the enzyme initially characterized and cloned based on its ability to metabolize and be induced by ethanol. Important work has elucidated the relationship between CYP2E1-mediated formation of the hepatotoxic metabolite of acetaminophen and alcohol consumption. Lastly, drug interactions involving other components of alcoholic beverages such as flavonoid and other polyphenolic components of red wine have been reported.  相似文献   

19.
肝脏是代谢乙醇及清除内毒素的主要器官,肝实质细胞及非实质细胞对乙醇及其代谢产物的影响极为敏感。酒精性肝病的发展一般包括脂肪变性、炎症反应、肝细胞坏死、肝纤维化以及肝硬化等几个过程,发展到严重的肝炎时会导致死亡。乙醇导致的肝病可呈现多种形式,并受多种因素控制,使得酒精性肝病的病理机制较为复杂。炎症细胞因子的作用、活性氧自由基的损害、乙醛的毒性以及补体系统等均可促进乙醇导致的肝损伤。目前,对于酒精性肝病的治疗主要有抗氧化、抑制枯否细胞的激活以及抑制肠道细菌的过度增殖等手段。  相似文献   

20.
Microcapsules composed of ethanol, water and dextrin as a water-soluble polymer can be used to encapsulate poorly water-soluble drugs by spray drying technique. For the encapsulation of a high dose of poorly water-soluble drugs, large amounts of ethanol and consequently large quantities of dextrin are needed for the dissolution of drug and the encapsulation of ethanol, respectively. In order to increase the ethanol content with the decreased amount of dextrin, sodium lauryl sulfate (SLS) was employed in the preparation of microcapsules without drug by a spray drying method. Phase diagrams were prepared to determine the region of microcapsule formation with a three-component system of ethanol, dextrin and water. The homogeneous phase indicated in the phase diagram was used to prepare the alcoholic microcapsules since this phase was not separated rapidly and not too viscous to be spray-dried. Interestingly, SLS at concentrations below 2% remarkably increased both the ethanol content and the encapsulation efficiency of ethanol. The maximum ethanol content and encapsulation efficiency were observed with 0.5-1% of SLS (35.4 and 67.6%, respectively). Furthermore, the increase by SLS was more pronounced at the low dextrin/water ratios than at the high dextrin/water ratios. In particular, the ethanol content and the encapsulation efficiency with the dextrin/ethanol/water ratio of 0.4/1/1, which had relatively small amounts of dextrin, were about ten times higher in the presence of SLS than those without SLS. In conclusion, this study shows that small amounts of SLS can increase the ethanol content and the encapsulation efficiency of ethanol, and allow the reduction in the amount of dextrin required to encapsulate ethanol in the preparation of microcapsules. These findings suggest that the use of SLS may permit the effective encapsulation of high dose of water-insoluble drug into microcapsules.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号