四氯化碳两种途径亚急性实验染毒时某些肝酶指标的对比研究

本文用CCl_41.356g/kg和5.87g/kg分别对大鼠进行皮下和呼吸道静式染毒,为期8周亚急性中毒试验,研究临床常用血清肝酶指标的变化。结果发现:CCl_4除使大鼠体重增长减慢外,第1周起出现肝细胞脂变、浊肿,进而坏死、纤维增生和肝硬化;肝糖元及SHD酶活性减少或消失,G-6-P酶活性先升高后降低的病理形态和组织化学的改变。与此同时或稍后出现SGPT和SGOT活性升高,持续至第8周。停药两周,肝病理改变趋于恢复,SGPT和SGOT活性也恢复至接近正常,两肝酶与病理改变相平行。AKP酶活性第4周后才升高;ChE酶似有先升高后降低趋势,但无明显差异性;γ-GT酶变化不规则。提示CCl_4亚急性中毒时,SGPT和SGOT酶活性升高与肝损关系较密切,可作临床早期诊断指标。血清AKP和ChE酶亦一定程度反映肝损的发展情况,可供作临床观察病情发展的辅助指标。     

强噪声对大鼠血液粘度血糖及几种酶的影响

本文检测强噪声刺激12小时大鼠血液流变学九项指标,胆碱酯酶和谷丙转氨酶活力及血糖浓度,与对照组比较,其结果显示:(1)低切粘度,红细胞电泳时间和全血还原粘度明显增高(P<0.05;P<0.05和P<0.01);(2)真性和假性胆碱酯酶活力明显增高(二者均P<0.01);(3)血清谷丙转氨酶活力和血清葡萄糖浓度显著增高(P<0.01和P<0.05)。揭示强噪声作用后机体听觉外系统发生明显变化,长期暴露后必将严重损伤全身性调节功能而引起脏器损害与疾病。     

Morphologic evaluation of the liver in hereditary angioedema patients on long-term treatment with androgen derivatives

17 alpha-Alkylated androgens are highly effective in preventing attacks in HAE patients. These drugs, however, seem to be implicated in the development of cholestatic jaundice, peliosis hepatis, and liver tumors. In order to assess the risk-benefit balance of the long-term therapy with androgen derivatives, a follow-up investigation was performed in 13 HAE patients. The results of this study indicate that long-term treatment (15 to 47 mo) with low doses of danazol or stanozolol does not induce significant hepatic damage detectable by laboratory tests or liver biopsy. However, the limited number of patients, although in a rather long period of observation, still suggests a careful control and the use of minimal effective doses.     

妊娠肝内胆汁瘀积症380例分析

目的:探讨肝功能指标与妊娠肝内胆汁瘀积症(ICP)围产儿预后的关系.方法:选择 2002年 1月～ 2003年 12月期 间 380例 ICP患者进行分析.结果:胆酸水平, SGPT值及胆红素高低与胎儿窘迫相关,统计学分析有显著差异.结 论: ICP患者孕期应加强监护,适时终止妊娠,必要时适当放宽剖宫产指征,能有效降低围产儿死亡率.     

荞麦多糖对小鼠实验性肝损伤的保护作用

目的:研究荞麦多糖对小鼠实验性肝损伤的保护作用.方法:采用四氯化碳(CCl4)、硫代乙酰胺(TAA)、扑热息痛(AAP)致小鼠急性肝损伤模型,测定小鼠血清SGPT活性.结果:荞麦多糖溶液对四氯化碳、扑热息痛所致小鼠实验性肝损伤有明显保护作用,但对硫代乙酰胺所致小鼠实验性肝损伤无明显的保护作用.结论:荞麦多糖有保肝作用.     

三种肝炎模型的生化指标与病理形态学的对比研究

采用α-萘异硫氰酸酯(ANIT)、四氯化碳(CCl_4)和半乳糖胺(Glan)复制肝炎模型,进行血清生化指标和肝组织学的对比研究。结果证明,ANIT 复制肝炎模型能明显升高血清胆红素和谷丙转氨酶,肝细胞和胆管亦见明显损害。可用于筛选退黄和降酶药物的研究。CCl_4复制肝炎模型则以升高SGPT 为主,组织学仅见明显的肝细胞损害,可用于筛选降酶药物的研究。Glan 复制肝炎模型,生化指标和肝组织学改变均不明显,认为该模型不甚理想。     

Antidiabetic and antihyperlipidaemic activity of ethanol extract of Melastoma malabathricum Linn. leaf in alloxan induced diabetic rats

ObjectiveTo evaluate the antidiabetic and antihyperlipidaemic effect of ethanol extract of Melastoma malabathricum (M. malabathricum) Linn. leaf in alloxan induced diabetic rats.MethodsDiabetes was induced in albino rats by administration of alloxan monohydrate (150 mg/kg i.p). the ethanol extracts of M. malabathricum at a dose of 150 and 300 mg/kg of body weight were administrated at a single dose per day to diabetes induced rats for a period of 14 d. The effect of ethanol extract of M. malabathricum leaf extract on blood glucose, plasma insulin, creatinine, glycosylated haemoglobin, urea serum lipid profile [total cholesterol, triglycerides, low density lipoprotein-cholesterol, very low density lipoprotein-cholesterol, high density lipoprotein-cholesterol and phospholipid, serum protein, albumin, globulin, serum enzymes (serum glutamate pyruvate transaminases), serum glutamate oxaloacetate transaminases, and alkaline phosphatase] were measured in the diabetic rats.ResultsIn the acute toxicity study, ethanol extract of M. malabathricum leaf was non-toxic at 2 000 mg/kg in rats. The increased body weight, decreased blood glucose, glycosylated haemoglobin and other biochemical parameters level were observed in diabetic rats treated with both doses of ethanol extract of M. malabathricum leaf compared to diabetic control rats. In diabetic rats, ethanol extract of M. malabathricum leaf administration, altered lipid profiles were reversed to near normal than diabetic control rats.ConclusionsEthanol extract of M. malabathricum leaf possesses significant antidiabetic and antihyperlipidaemic activity in diabetic rats.     

Effect of Rubia cordifolia extract on acetaminophen and CCl4-induced hepatotoxicity

The hepatoprotective activity of an aqueous-methanol extract of Rubia cordifolia (Rubiaceae) was investigated against acetaminophen and CCl₄-induced hepatic damage. Acetaminophen produced 100% mortality at a dose of 1 g/kg in mice while pretreatment of animals with plant extract (500 mg/kg) reduced the death rate to 30%. Acetaminophen at a dose of 640 mg/kg produced liver damage in rats as manifested by the rise in serum levels of GOT and GPT to 1447±182 and 899±201 IU/L (n = 10) respectively, compared with respective control values of 97±10 and 36±11. Pretreatment of rats with plant extract (500 mg/kg) lowered significantly (p <0.005) the respective serum GOT and GPT levels to 161±48 and 73±29. Similarly, hepatotoxic dose of CCl₄ (1.5 mL/kg; orally) raised the serum transaminases (GOT and GPT) levels to 422±102 and 354±74 IU/L (n = 10) respectively compared with respective control values of 99±15 and 29±08 IU/L. The same dose of plant extract (500 mg/kg) was able to prevent significantly (p <0.01) the CCl₄-induced rise in serum enzymes and the estimated values of GOT and GPT were 95±09 and 33±07 IU/L, respectively. Moreover, it prevented CCl₄-induced prolongation in pentobarbital sleeping time confirming the hepatoprotective effects of the extract.     

右归丸的一些药理作用

右归丸是《景岳全书》中的一复方。药理实验证明:右归能增强小鼠单核吞噬细胞系统廓清功能;抑制CCl_4所致小鼠SGPT和肝脏过氧化脂质的升高;增强小鼠的耐力;对抗东莨菪碱所致小鼠记忆的障碍和对抗ADP诱导的大鼠血小板聚集。     

Protective effect of gallic acid against lindane induced toxicity in experimental rats

Lindane is an organochlorine pesticide that persists in the environment, bioaccumulate through food chain and has a risk of causing adverse effects to human health and the environment. It induces cell damage by producing free radicals and reactive oxygen species. The aim of the present study is to investigate the protective effect of gallic acid (a plant derived polyphenol) against lindane induced hepatic and renal toxicity in rats. Liver damage was assessed by hepatic serum marker enzymes like SGOT, SGPT and ALP and histopathological observation. Renal damage was observed by histopathological examination and serum markers like creatinine and urea. Treatment with lindane increased the levels of lipid peroxidation, serum marker enzyme activity with a concomitant decrease in GSH, CAT, SOD, GPx and GST. Histological alterations were also observed in kidney and liver tissue with lindane treatment. Co-treatment of gallic acid significantly prevented the lindane induced alterations in kidney and liver tissues with a decrease in LPO, serum marker enzyme activity and a significant increase in antioxidant levels. These results suggest that gallic acid has protective effect over lindane induced oxidative damage in rat liver and kidney.