慈菇对小鼠四氯化碳肝损伤保护作用的探讨

对给予新鲜慈菇汁连续４周灌胃的小鼠，用ＣＣｌ４急性染毒建立自由基过氧化损伤模型进行观察，同时设立对照组．结果表明：与损伤对照组比较，灌饲慈菇汁的小鼠红细胞ＳＯＤ明显为高，肝匀浆ＬＰＯ和血清ＳＧＰＴ明显为低，肝组织病理改变明显减轻．提示慈菇具有清除氧自由基和抗脂质过氧化作用，对小鼠的ＣＣｌ４肝损伤有保护作用．     

氧化苦参碱对四氯化碳损伤大鼠肝细胞的保护作用

目的 :研究氧化苦参碱对肝细胞的保护作用。方法 :采用原代肝细胞培养的方法 ,选用CCl430mmol/L制备肝损伤模型 ,同时加以不同浓度的氧化苦参碱以保护肝细胞 ,培养 12h后以MTT法测细胞存活率 ,并测定培养基中AST、ALT、LDH。结果 :氧化苦参碱对肝细胞的保护呈剂量依赖性 ,氧化苦参碱组细胞存活率明显高于CCl4损伤组 (98.3% /3.2 % ,P <0 .0 5 ) ;其AST、ALT、LDH较CCl4损伤组明显降低 (依次为 6 .13± 0 .4 4 /896 .87±13.2 3、2 1.5± 0 .76 /15 0 2 .13± 35 .80、19.5± 0 .6 8/2 87.38± 5 .79,均P <0 .0 5 )。结论 :氧化苦参碱对CCl4损伤的肝细胞具较好的保护作用 ,存在最佳剂量性关系。     

牛磺酸对四氯化碳致肝细胞凋亡影响的研究

本文观察了四氯化碳亚慢性染毒后血清ＡＬＴ、肝脏ＧＳＨ、ＭＤＡ及肝脏的形态学变化，同时研究了牛磺酸对ＣＣｌ４肝毒性的干预作用。结果表明：ＣＣｌ４引起了肝脏明显的脂质过氧化及肝损伤，但ＡＬＴ与ＭＤＡ之间并不完全并行，说明ＬＰＯ并非肝损伤的一唯一原因。ＣＣｌ４组肝组织中凋亡小体明显增加，可能是机体对损伤的一种反应，ｔａｕ干预组肝ＬＰＯ减轻，凋亡小体明显减少，表明ｔａｕ对ＣＣｌ４肝毒性有一定干预作用，其机     

三七总甙对四氯化碳所致肝损伤的保护作用

用CCl4诱发大鼠急性肝损伤模型，观察三七总甙对损伤肝的影响。结果表明，三七总皂甙可抑制SGPT，SGOT升高（P＜0．01），提高肝组织及血清SOD含量（P＜0．05），减少MDA生成量及肝糖原消耗，改善肝微循环，减轻线粒体，内质网等细胞器损伤。提示三七总甙对CCl4所致肝损伤具有保护作用。     

新鲜蔬菜对实验性肝损伤小鼠的抗氧化作用探讨

对连续给予新鲜芥蓝菜、胡萝眩、灯笼椒３种菜汁２５天的小鼠用ＣＣＬ４急性染毒建立自由基过氧化损伤模型进行观察。结果表明，与蒸馏水组比较，各蔬菜组损伤后血ＳＯＤ降低明显减轻，肝匀浆ＬＰＯ和血清ＳＧＰＴ增高显著低于对照，肝组织病理改变明显减轻，胡萝卜和灯笼椒组更为明显，提示蔬菜提供的营养成分增强体内清除自由基和抗脂过氧化是其保健作用的主要机制。     

小型猪肝硬化模型建立过程中肝脏功能及组织病理学的改变

为观察小型猪肝硬化模型建立过程中肝功能及病理学改变，采用CCl4，苯巴比妥和无水酒精喂养小型猪共12头，辅以高脂，低蛋白和低胆碱饮食，动态检测猪的肝功能并取组织行病理学检查，4个月后，12头小猪成功诱导出肝硬化，病理学检查按Madden分级，7头达到Ⅲ级，5头达到Ⅳ级，结果提示，CCl4，苯巴比妥和无水酒精喂养辅以高脂低蛋白低胆碱饮食的多因素诱导小型猪肝硬化，成功率高，死亡率低，死亡率低，病理学改变分期界限明显。     

秋水仙碱对四氯化碳所致大白鼠慢性肝损害治疗作用的实验形态学观察

本文报告秋水仙碱治疗四氯化碳所致大白鼠慢性肝损害的胶原纤维和肝细胞酶活性、糖原和核糖核酸量的变化。所试动物以组织化学和组织学方法进行观察。结果提示秋水仙碱有抑制慢性肝损害胶原纤维形成的作用,但对肝细胞功能的恢复作用不明显。     

岗松挥发油对实验性肝损害的防治作用

本研究表明,岗松油对四氯化碳、硫代乙酰胺、醋酸强的松龙引起的小鼠SGPT升高有明显的降低作用,使BSP潴留量减少,相应肝组织病变减轻。此外,岗松油对四氯化碳损害小鼠和正常小鼠戊巴比妥钠的睡眠时间均能明显缩短。对巴豆油引起小鼠耳部炎症有明显的抗炎作用。岗松油的毒性很低,口服半数致死量(LD_(50)为3,758±539mg/kg,给兔灌胃687～1030mg/kg每天一次,连续30天,一般表现、血象、肝肾功能及病理检查均未见明显的改变。     

四氯化碳诱导犬早期肝损害所致门静脉高压的形态学观察

目的　探讨实验性犬肝脏早期损害所致的门静脉高压形成的形态学基础。方法　以小剂量四氯化碳 (CCl4)腹腔内注射诱导犬早期肝损害 ,制备门静脉高压犬模型。通过光镜、电镜观察肝脏形态学的改变。结果　腹腔内注射CCl47周后 ,共有 15头犬形成门静脉高压 (门静脉压力 2 2 7cmH2 O± 1 5cmH2 O ,1cmH2 O =0 0 98kPa,与给药前相比 ,P <0 0 5 )。HE染色示肝脏损害轻微。Masson染色、电镜 ,示肝窦毛细血管化。α 平滑肌肌动蛋白 (α SMA)免疫组化染色示肝星形细胞(HSC)大量活化。结论　肝脏受损早期 ,门静脉高压形成的可能原因是肝窦毛细血管化和HSC活化所致的肝窦血流阻力增加。     

Effects of estradiol on liver estrogen receptor-alpha and its mRNA expression in hepatic fibrosis in rats

AIM:Estradiol treatment regulates estrogen receptor (ER) level in normal rat liver.However,little information is available concerning the role of estrogen in regulating liver ER in hepatic fibrosis in rats.The present study was conducted to determine whether estradiol treatment in CCl4-induced liver fibrosis of female and ovariectomized rats altered liver ERα and its mRNA expression,and to investigate the possible mechanisms.METHODS:Seventy female rats were divided into seven groups with ten rats in each. The ovariectomy groups were initiated with ovariectomies and the sham operation groups were initiated with just sham operations.The CCl4 toxic fibrosis groups received 400mL/L CCI4 subcutaneously at a dose of 2 mL/kg twice weekly.Estrogen groups were treated subcutaneously with estradiol 1mg/kg, the normal control group and an ovariectomy group received injection of peanut oil vehicle twice weekly.At the end of 8 weeks,all the rats were killed to detect their serum and hepatic indicators,their hepatic collagen content, and liver ER and ER mRNA expression.RESULTS: Estradiol treatment in both ovariectomy and sham ovariectomy groups reduced liver levels of ALT (from 658&#177;220nkat/L to 311&#177;146nkat/L and 540&#177;252nkat/L to 314&#177;163nkat/L,P&lt;0.05) and AST (from 697&#177;240nkat/L to 321&#177;121nkat/L and 631&#177;268nkat/L to 302&#177;153nkat/L,P&lt;0.05),increased serum nitric oxide (NO) level (from 53.7&#177;17.1μmol/L to 93.3&#177;4.2μmol/L and 55.3&#177;3.1μmol/Lto 87.5&#177;23.6μmol/L, P&lt;0.05) and hepatic nitric oxide synthase (NOS) activity (from 1.73&#177;0.71KU/g to 2.49&#177;1.20KU/g and 1.65&#177;0.46KU/g to 2.68&#177;1.17KU/g, P&lt;0.05),diminished the accumulation of hepatic collagen,decreased centrolobular necrotic areas as well as the inflammatory reaction in rats subjected to CCl4. The positive signal of ER and ER mRNA distributed in parenchymal and non-parenchymal hepatic cells,especially near the hepatic centrolobular and periportal areas.Ovariectomy decreased ER level (from 10.2&#177;3.2 to 4.3&#177;1.3) and ER mRNA expression (from 12.8&#177;2.1 to 10.9&#177;1.3) significantly (P&lt;0.05). Hepatic ER and ER mRNA concentrations were elevated after treatment with estradiol in both ovariectomy (15.8&#177;2.4, 20.8&#177;3.1) and sham ovariectomy(18.7&#177;3.8, 23.1&#177;3.7) fibrotic groups (P&lt;O.05).CONCLUSION: The increase in hepatic ER and mRNA expression may be part of the molecular mechanisms underlying the suppressive effect of estradiol on liver fibrosis induced by CCI4 administration.