泰脂安胶囊治疗酒精性脂肪肝的实验研究

目的 研究泰脂安胶囊对酒精性脂肪肝的药理作用,并探讨酒精性脂肪肝的发病机制。方法 建立酒精性脂肪肝大鼠模型并分为治疗组(80 mg/kg)和模型对照组。4周后处死,分别测定血清甘油三酯(TG)、胆固醇(TC)、高密度脂酯(HDL),血清及肝组织丙二醛(MDA)、肝脂酯(HL)、脂蛋白脂酶(LPL)及观察肝脏病理变化。结果 与模型对照组比较,泰脂安胶囊组可以显著降低血清TG、血清和肝组织MDA含量、减少肝内脂质,同时明显升高血清以及肝组织内HL、LPL的活性,血清中HDL的水平也明显增高;但血清ALP、ALT以及AST的变化无显著性差别(P>0.05)。肝脏形态学镜检显示,肝内脂肪滴完全消失,炎症细胞浸润减轻。结论 泰脂安胶囊治疗酒精性脂肪肝可以明显减少肝内脂质的含量,改善肝脏病理变化。

酗酒致酒精性心肌病67例相关因素分析

目的:探讨酒精中毒导致酒精性心肌病(ACM)的相关因素。方法:以67例ACM患者作为研究组;并采用分层随机的方法,对同期3011例酒精中毒患者按年龄、性别、饮酒量、年限相匹配抽取了89例作为对照组。对酒精浓度、饮酒频数、饮酒方式、体重指数、酒后心率、血压、意识、心电图、超声心动图、肝功等监测进行分析。结果酒精浓度、酗酒频数、体重指数、酒后血压增高或休克、心肌损害、肝功检测两组间有显著差异。而饮酒方式、意识障碍的程度在两组间无显著差异。ACM患者的肝功异常及血压异常波动与心肌损害的程度有密切相关性。结论摄入大量高浓度乙醇,较大量低度乙醇更易造成血压异常,并直接损害肝脏、心肌。长期酒精中毒,肝脏解毒能力下降,血压异常波动对心肌损害起到叠加效应,导致ACM。

锦州地区酒精性肝病相关因素分析

我院体检中心对2008-2010年的锦州铁路职工7 420人进行健康体检,发现酒精性肝病368例,现将有关资料进行分析,探讨其发病的相关因素,以便为锦州地区酒精性肝病的预防和干预提供科学依据。

Impact of asialoglycoprotein receptor deficiency on the development of liver injury

The asialoglycoprotein （ASGP） receptor is a wellcharacterized hepatic receptor that is recycled via the common cellular process of receptor-mediated endocytosis （RME）. The RME process plays an integral part in the proper trafficking and routing of receptors and ligands in the healthy cell. Thus, the missorting or altered transport of proteins during RME is thought to play a role in several diseases associated with hepatocyte and liver dysfunction. Previously, we examined in detail alterations that occur in hepatocellular RME and associated receptor functions as a result of one particular liver injury, alcoholic liver disease （ALD）. The studies revealed profound ethanol- mediated impairments to the ASGP receptor and the RME process, indicating the importance of this receptor and the maintenance of proper endocytic events in normal tissue. To further clarify these observations, studies were performed utilizing knockout mice （lacking a functional ASGP receptor） to which were administered several liver toxicants. In addition to alcohol, we examined the effects following administration of anti- Fas （CD95） antibody, carbon tetrachloride （CCh） and lipopolysaccharide （LPS）/galactosamine. The results of these studies demonstrated that the knockout mice sustained enhanced liver injury in response to all of the treatments, as shown by increased indices of liver damage, such as enhancement of serum enzyme levels, histopathological scores, as well as hepatocellular death. Overall, the work completed to date suggests a possible link between hepatic receptors and liver injury. In particular, adequate function and content of the ASGP receptor may provide protection against various toxinmediated liver diseases.