抗脂肪肝中剂对大鼠高脂血症防治的实验研究

目的：探讨抗脂肪肝冲剂对高脂血症大鼠脂质代谢的影响,寻求防治高脂血症的有效药物。方法：采用高脂饮食喂养大鼠,形成高脂血症模型,饲以抗脂肪肝冲剂,观察大鼠血清总胆固醇（TC）及甘油三酯（TG）的含量,结果：抗脂肪肝冲剂能显著降低高脂血症大鼠血清中TC含量（与模型对照组比较P＜0．01）及TG含量（大、中、小剂量组与模型对照组比较P＜0．01,P＜0．05,P＜0．05）。结论：抗脂肪肝冲剂能够降低高脂血症大鼠TC、TG的含量,具有防治高脂血症的作用。     

清肝冲剂对小鼠急性肝损伤治疗作用的观察

目的：研究清肝冲剂对小鼠急性肝损伤的治疗作用。方法：分别采用四氯化碳（CCl4)和D－氨基半乳糖腹腔内注射造成小鼠急性肝损伤,清肝冲剂治疗组小鼠于造模2h后用清肝冲剂灌胃给药连续3d,然后检测肝功能,观察肝脏病理变化。结果：CCl4及D－氨基半乳糖造模后,造成小鼠急性肝脏损伤,出现明显肝功能异常。用清肝冲剂治疗3d后,CCl4模型治疗组小鼠丙氨酸转氨酶（ALT）和天冬氨酸转氨酸（AST）较CCl4模型组均有所降低,但差异无显著性意义（P＞0．05）。D－氨基半乳糖模型给药组的小鼠AST、AST／ALT、白蛋白、球蛋白（A、G）等肝功能指标与D－氨基半乳糖模型组比较都有明显的改善（P＜0．01）。病理观察清肝冲剂治疗组小鼠肝细胞变性、肿胀程度较模型组减轻。结论：清肝冲剂对CCl4和D－氨基半乳糖造成小鼠急性肝损伤模型具有改善肝功能、减轻肝脏病理损害的作用。     

胃康冲剂防治大鼠胃溃疡的作用

目的：探讨胃康冲剂促进溃疡愈合的作用和机制。方法：用乙酸浸渍的滤纸片腐蚀胃壁复制大鼠胃溃疡模型,测定胃粘膜表面粘液厚度,胃液中的表皮生长因子（EGF）,胃组织的一氧化氮（NO）与血浆6－酮－前列腺素F1α（6－K－PGF1α）水平。结果：造模后各组与正常对照组比较,胃粘膜表面粘液厚度显著降低（P＜0．01）,胃液中EGF、胃组织中NO与血浆6－K－PGF1α－水平平均显著降低（均P＜0．01）,胃饲不同剂量胃康冲剂使胃粘膜表面粘液厚度显著增加（P＜0．01）,胃液中EGF、胃组织NO水平,血浆6－K－PGF1α均显著升高（P＜0．05）。结论：胃康冲剂对胃粘膜具有明显的保护作用,其机制是增加胃粘膜表面粘液厚度与提高EGF、NO6－K－PGF1α细胞保护因子的水平。     

夏丹冲剂对脂肪肝患者肝纤维化指标的影响

从1999年1月至2002年12月我们应用自拟夏丹冲剂对脂肪肝患者肝纤维化指标进行观察,以探讨夏丹冲剂治疗脂肪肝及抗肝纤维化的作用,现报告如下。 1 资料与方法 1.1 病例选择 110例均为我院门诊、住院的脂肪肝患者,其诊断符合文献标准,亦符合中医痰湿证、血瘀证分型标准。随机分组,治疗组80例,其中男58例,女22例,年龄     

益肝康冲剂抗大鼠D—半乳糖胺急性肝损伤的实验研究

实验设益肝康冲剂大、中、小剂量组、正常组、病理组、齐墩果酸（阳性对照）组。结果表明，益肝素冲剂３个剂量组均能显著降低Ｄ－半乳糖胺急性肝损伤大鼠的丙氨酸转氨酶、天门冬氨酸转氨酶活性、疗铲与齐墩果酸片无差异（Ｐ〉０．０５）；肝组织病检表明中、小剂量组几乎与阳性组一致，说明益肝康冲剂具有良好地保护Ｄ－半乳糖胺致大鼠肝损伤的作用。     

益肝康冲剂抗大鼠D-半乳糖胺急性肝损伤的实验研究

实验设益肝康冲剂大、中、小剂量组、正常组、病理组、齐墩果酸（阳性对照）组。结果表明，益肝康冲剂。3个剂量组均能显著降低卜半乳糖胺急性肝损伤大鼠的丙氨酸转氨酶、天门冬氨酸转氨酶活性，疗效与齐墩果酸片无差异（P＞0．05）；肝组织病检表明中、小剂量组几乎与阳性组一致，说明益肝康冲剂具有良好地保护D-半乳糖胺致大鼠急性肝损伤的作用。     

中药解毒养肝冲剂对豚鼠抗—HBs的调节和对小鼠实验性肝损伤的抑制作用

实验结果表明,解毒养肝冲剂能增强豚鼠对 HBV 的免疫性,促使机体产生抗—HBs。在用不同浓度 CCl_4所致的小鼠肝损伤模型上,不同剂量的解毒养肝冲剂均可降低小鼠血清中 ALT 活力,与对照组比较,有统计学意义。此外,本冲剂对于降低小鼠的肝脏系数也有作用。     

清肝活血饮抗大鼠脂肪肝的实验研究

目的 :探讨清肝活血饮治疗脂肪肝的疗效和机制。方法 :采用复合方式建立大鼠脂肪肝模型 ,通过肉眼、血液生化、病理学检查 ,观察该方对脂肪肝大鼠的一般情况、血脂、肝酶、肝体比、病理改变等的影响。结果 :清肝活血饮能明显降低脂肪肝大鼠血脂和减轻肝脂变、肝细胞坏死程度 ,调整血脂蛋白比例和肝体比 ,与对照组比较差异有显著性意义 (P <0 .0 5 ,<0 .0 1)。结论 :清肝活血饮对大鼠脂肪肝有肯定治疗作用且优于东宝肝泰 ,推测其降低血脂和肝脂 ,减少肝脏脂质沉积 ,保护肝细胞 ,改善肝脏微循环等是其主要作用机制。     

褪黑素防治高脂饮食大鼠脂肪肝的实验研究

目的观察褪黑素对高脂饮食大鼠脂肪肝的影响。方法将50只雄性Wistar大鼠随机分成5组:正常对照组、模型组和低、中、高3个剂量褪黑素组。采用喂饲高脂饲料复制大鼠脂肪肝模型。褪黑素组分别在造模同时以褪黑素2.5mg/(kg·d)、5.0mg/(kg·d)和10.0mg/(kg·d)剂量腹腔注射进行干预。12周后观察血清ALT、AST、血清及肝匀浆中总胆固醇(Tch)、甘油三酯(TG)以及肝脏指数和肝脏病理形态学的变化。结果与模型组相比,高剂量褪黑素组血清AST水平明显下降(P<0.01),中、高剂量褪黑素组肝指数、肝内Tch和TG明显降低(P<0.05,P<0.01)。中、高剂量褪黑素组大鼠肝脏病理变化明显减轻(P<0.001),以高剂量组更明显。结论褪黑素可明显减轻高脂饮食诱导的大鼠脂肪肝,且与剂量有一定关系。     

抗脂益肝汤治疗脂肪肝31例

1 资料与方法 1.1 病例选择 B超诊断的31例脂肪肝患者,其中2例合并有胆结石,2例合并有慢性胆囊炎,4例合并有高血压病,2例合并有糖尿病,1例合并有慢性结肠炎,3例合并有酒精性肝中毒,6例合并有病毒性肝炎。男17例,女14例,平均年龄44岁。 1.2 治疗方法 我院研制的纯中药制剂口服抗脂益肝汤(田     

克肝胶囊对小鼠实验性急性肝损伤的影响

目的：观察克肝胶囊对实验性急性肝损伤的影响,方法：分别用ＣＣｌ４、Ｄ－ＧＬａＮ、ＡＮＩＴ制成肝损伤模型,运用克肝胶囊治疗,观察ＡＬＴ、ＡＳＴ、ＴＢｉｌ、肝脏指数及肝脏组织病理改变,以乙肝解毒胶囊作对照。结果：与乙肝解毒胶囊一样,克肝胶囊各剂量组都能显著降低ＡＬＴ、ＡＳＴ、ＴＢｉｌ,肝脏指数及改善肝脏病理（Ｐ〈０．０５－０．０１）,对某些指标的影响甚至优于乙肝解毒胶囊,结论克肝胶囊有抗急性４肝损伤的     

海珠益肝胶囊对小鼠免疫性肝损伤的影响

目的:进一步证实海珠益肝胶囊对肝损伤小鼠的保肝降酶作用。方法:来用卡介苗 脂多糖(BCG LPS)造成免疫性肝损伤模型小鼠,观察本品对血清中ALT、AST活力单位、肝脾脏器系数和肝脏病理组织学损伤程度的影响。结果:药物能降低血清中ALT、AST活力单位(P<0.01);减小肝脾肿大及脏器系数(P<0.01);减轻肝组织病理损伤程度。结论:海珠益肝胶囊对BCG LPS所致肝损伤小鼠有明显保肝降酶作用。     

Effect of Ethanol Intake on Pancreatic Exocrine Secretion in Mice

Swiss mice were fed conventional lab chow and 10% ethanol or water as drinking fluid for 2 weeks. Pancreatic juice was obtained by cannulation of the bile pancreatic common duct of mice anesthetized with urethane. Isolated pancreatic lobules were also obtained. The flow rate and the amylase output were determined in pure pancreatic juice. The release of amylase was measured in pancreatic lobule preparations. The basal pancreatic juice flow rate and the amylase output were significantly increased by ethanol consumption. The magnitude of the pancreatic juice flow rate and the amylase output responses to increasing doses of bethanechol, a cholinergic agent, was significantly decreased in ethanol-fed mice. The amount of spontaneously released amylase was higher in pancreatic lobule preparations from ethanol-fed animals than that from control mice, and the difference was abolished by addition of atropine to the incubation media. The amylase release rate in response to increasing doses of bethanechol was significantly reduced in lobule preparations from the ethanol-fed group. These data indicate that ethanol intake in mice has a stimulating effect on the spontaneous pancreatic secretion and lends support to the hypothesis that ethanol consumption increases the intrapancreatic cholinergic tone.     

肝舒康冲剂防治二甲基亚硝胺致大鼠肝纤维化的实验研究

目的：研究肝舒康冲剂对肝纤维化的防治作用。方法：采用二甲基亚硝胺）ＤＭＮ）所致大鼠肝纤维化模型,研究肝舒康冲剂对大鼠血清透明质酸（ＨＡ）和Ⅲ型胶原（ＰＣⅢ）及病理组织形态学的影响。结果：肝舒康冲剂能降低肝纤维化血清学指标ＨＡ、ＰＣⅢ数值,改善肝组织病理损害,明显优于对照组（Ｐ〈０．０５－０．０１）。结论：肝舒康冲剂具有良好的预防和治疗肝纤维化效果。     

抗纤软肝冲剂预防大鼠肝纤维化的实验研究

目的:观察抗纤软肝冲剂对肝纤维化的预防作用并探讨其机理。方法:采用四氯化碳、高脂、高胆固醇、低蛋白等复合因素制造肝纤维化模型,同时用抗纤软肝冲剂治疗,观察其对肝纤维化指标的影响,以秋水仙碱作为对照,结果:抗纤软肝冲剂对肝纤维化大鼠有升高白蛋白(Alb),降低谷丙转氨酶(ALT)和球蛋白(G)的作用;可调整机体免疫功能,降低血清免疫复合物(IC);具有显著降低血清透明质酸(HA)、层粘蛋白(LN)、Ⅲ型前胶原(PCⅢ)、Ⅳ型胶原(Ⅳ-C)、肝脏羟脯氨酸(Hyp)的作用;可以改善肝脏病理,抑制纤维化形成。结论:抗纤软肝冲剂具有确切的预防肝纤维化的作用。     

抗纤软肝颗粒对肝星状细胞凋亡的影响

探讨抗纤软肝颗粒对肝星状细胞(HSC)凋亡的影响.方法:传代培养的大鼠肝星状细胞系HSC-T6与中药复方抗纤软肝颗粒(终浓度为5mg/ml、2.5mg/ml、1.25mg/ml)及药物血清(5%、10%、20%)共同培养48小时后,应用TUNEL法及流式细胞仪测定细胞凋亡、免疫组化检测Bcl-2/Bax.结果:TUNEL法及流式细胞仪测定结果显示抗纤软肝颗粒药物及含药血清均可诱导HSC凋亡(P＜0.05);并能下调凋亡抑制分子Bcl-2,上调促凋亡分子Bax(P＜0.01).结论:抗纤软肝颗粒可下调Bcl-2/Bax比率,以增加细胞对凋亡的敏感性,从而促进HSC凋亡.     

Effect of Chronic Ethanol Feeding on Hepatic and Extrahepatic Distribution of Vitamin E in Rats

The effect of chronic ethanol feeding on the status of alpha- and gamma-tocopherol in plasma, liver, lung, and testes of Sprague-Dawley rats was characterized. Rats were pair-fed liquid diets containing 36% of total calories either as ethanol or isocaloric carbohydrates. After 3 weeks, ethanol ingestion resulted in a significant (p less than or equal to 0.05) increase in liver weight and induced fatty liver without affecting total body weight. Ethanol feeding did not affect the plasma concentration of alpha-tocopherol but doubled that of gamma-tocopherol. When expressed per milligram of tissue, liver alpha-tocopherol did not vary with ethanol ingestion, whereas gamma-tocopherol concentration increased 2.5 times that of control animals. However, the concentration of alpha-tocopherol expressed per milligram of total lipids was significantly (p less than or equal to 0.01) decreased in the liver with ethanol feeding. In contrast to the liver, ethanol feeding significantly increased alpha- and gamma-tocopherol levels per milligram of total lipids in the testes. The concentration of gamma-tocopherol (but not alpha-tocopherol) per milligram of lung tissue and per total lung was significantly (p less than or equal to 0.05) increased with ethanol feeding. These data indicate that chronic ethanol ingestion significantly alters the distribution of alpha-tocopherol and gamma-tocopherol in hepatic and extrahepatic tissues of the rat.     

Effect of Dietary Fat on Ito Cell Activation by Chronic Ethanol Intake: A Long-Term Serial Morphometric Study on Alcohol-Fed and Control Rats

We studied the effects of long-term ethanol ingestion and dietary fat on Ito cell activation morphometrically in rats. Sixteen pairs of Wistar male rats were divided into two groups, one fed tallow and the other fed corn oil as the source of dietary fat. Each group of rats were pair-fed a nutritional adequate liquid diet containing either corn oil (CF) or tallow (TF) as fat as well as protein and carbohydrate. Half of each group received ethanol, the rest were pair-fed isocaloric amounts of dextrose via an implanted gastric tube for up to 5 months. Morphometric analysis of the change in fat and rough endoplasmic reticulum (RER) of Ito cells was performed on electron micrographs obtained from monthly biopsies including baseline. Ito cell activation was assessed by a decrease in the ratio of fat/RER in Ito cells. The ratio of fat/RER in Ito cells of alcoholic rats fed the CF diet (CFA) gradually decreased. The ratio was found to be lower than in the pair-fed control rats (CFC) at 5 months of feeding. CFA: 1.74 +/- 0.57, vs. 7.46 +/- 2.05, respectively, p less than 0.05, mean +/- SE). Ito cell fat also significantly decreased at 5 months of feeding (p less than 0.05). The fat/RER ratio in CFA significantly decreased only subsequent to the development of fatty change, necrosis, and inflammation followed by fibrosis of the liver. In contrast, the TFA rats did not show a significant decrease in the fat/RER ratio in the Ito cells throughout the study, while TFC rats showed an increase in the fat/RER ratio.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of Chronic Ethanol Treatment and Selective Breeding for Sensitivity to Ethanol on Calcium Release Induced by Inositol Trisphosphate for Ethanol from Brain and Liver Microsomes

Our previous work showed that ethanol increases the resting intracellular free calcium concentration (CAi) in synaptosomes and releases calcium from an inositol trisphosphate (IP3)-insensitive calcium store of brain microsomes. In this report, we investigated the effects of chronic ethanol treatment and selective breeding for hypnotic sensitivity to ethanol on IP3 and ethanol-stimulated calcium release from brain and liver microsomes. Chronic ethanol treatment did not alter IP3-stimulated calcium release from brain microsomes or ethanol-stimulated calcium release from brain or liver microsomes. Chronic ethanol treatment increased the spontaneous release of calcium from brain but not liver microsomes. In microsomes isolated from cerebellum or cerebral cortex of long-sleep (LS) and short-sleep (SS) mice, ethanol and IP3 released calcium in a concentration dependent manner. The amount of calcium released by ethanol and IP3 was larger in microsomes isolated from cerebellum than microsomes from cerebral cortex. However, the amount of calcium released by ethanol and IP3 did not differ between the two lines in either brain area. These results do not support the idea that the hypnotic effects of ethanol are due to ethanol-induced calcium release from a nonmitochondrial intracellular calcium store in brain tissue. The development of ethanol tolerance and dependence also does not appear to be associated with altered ability of ethanol to release calcium from non-mitochondrial intracellular stores; however, effects of chronic ethanol exposure on spontaneous release of intracellular calcium could alter neuronal function in ethanol dependence.