茵陈紫金汤对小鼠四氯化碳急性肝损伤的保护作用

[目的]观察茵陈紫金汤对四氯化碳(CCl4)诱导的小鼠急性肝损伤保护作用.[方法]以0.12?l4花生油溶液经腹腔注射,制备小鼠急性化学性肝损伤模型,测定给药后模型小鼠血清丙氨酸氨基转移酶(ALT)、天冬氨酸转氨酶(AST),肝组织匀浆超氧化物歧化酶(SOD)活性以及丙二醛(MDA)水平,计算肝脏指数,光镜下观察肝组织病理学变化.[结果]茵陈紫金汤高、中剂量组均能显著降低CCl4所致小鼠急性肝损伤血清ALT、AST活性,提高肝组织匀浆SOD活性,降低MDA及肝脏指数,明显改善肝组织损伤的程度,与模型组比较差异有统计学意义(P＜0.05).[结论]茵陈紫金汤对CCl4诱导的小鼠急性肝损伤有保护作用,其作用机制可能与抗脂质过氧化有关.     

石榴多酚对小鼠急性肝损伤的保护作用

目的观察石榴多酚对小鼠肝损伤的防护作用。方法用四氯化碳(CCl4)致小鼠急性肝损伤模型,观察石榴多酚(200、400、600mg/kg)对小鼠血清丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)活性和肝脏组织超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量的影响。结果石榴多酚能明显降低急性肝损伤小鼠血清ALT、AST水平;并可使肝脏中MDA含量降低,SOD活性升高。各实验组小鼠的肝体比值均低于肝损伤模型组。结论石榴多酚对肝损伤具有保护作用,其作用可能与抗氧化有关。     

白术莪术提取物对小鼠急性肝损伤的保护作用

目的 研究白术莪术提取物对四氯化碳(CCl4)诱导的小鼠急性肝损伤的影响.方法 给予小鼠白术莪术提取物灌胃,连续7d,腹腔注射CCl4-花生油溶液造模急性肝损伤,16 h后测定血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)含量、肝组织中超氧化物歧化酶(SOD)活性及其肝脏、脾脏指数.结果 白术莪术提取物能显著降低急性肝损伤小鼠血清中ALT、AST含量及提高肝组织中SOD活性,减小肝脏指数(P＜0.01).结论 白术莪术提取物对CCl4诱导的小鼠急性肝损伤具有很好的保护作用.     

软坚护肝片对四氯化碳所致小鼠急性肝损伤的保护作用

目的观察软坚护肝片(RJHGT)对四氯化碳(CCl4)所致小鼠急性肝损伤的保护作用,并探讨其作用机制。方法腹腔注射CCl4制备小鼠急性肝损伤模型,检测血清谷丙转氨酶(AST)、谷草转氨酶(ALT)、碱性磷酸酶(AKP)活性及总抗氧化能力(T-AOC);检测肝组织丙二醛(MDA)含量、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-PX)活性。结果 RJHGT各组能够减轻肝细胞损伤程度,与模型组比较,RJHGT能降低血清ALT、AST、AKP的活性及肝组织中MDA、GSH的含量(P0.01或0.05);提高T-AOC能力及SOD、GSH-PX的活力(P0.01或0.05)。结论 RJHGT对CCl4所致小鼠急性肝损伤具有明显的保护作用,其机制可能与其抗脂质过氧化作用有关。     

柴胡疏肝散对四氯化碳所致大鼠急性肝损伤的防治作用

观察柴胡疏肝散对四氯化碳(CCl4)所致大鼠急性肝损伤的防治作用.方法:用CCl4造成大鼠急性实验性肝损伤模型,检测大鼠血清中丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、超氧化物歧化酶(SOD)、脂质过氧化物丙二醛(MDA)和谷胱甘肽(GSH)含量,同时检测肝组织中MDA和GSH的含量.结果:该方能显著降低CCl4所致急性肝损伤大鼠血清中ALT、AST含量,升高其SOD水平,并可显著降低该模型大鼠血清及肝组织中MDA的含量,而升高GSH水平.结论:柴胡疏肝散对此模型大鼠的肝损伤具有显著的防治作用,其机制可能与降低、抑制脂质过氧化反应以及抗自由基损伤有关.     

瘦素对四氯化碳所致小鼠急性肝损伤的影响

探讨瘦素对四氯化碳(CCl4)所致的小鼠急性肝损伤是否有加重作用.方法:分别在小鼠腹腔注射CCl4和/或重组小鼠瘦素,测其血清转氨酶(AST和ALT),并取肝组织作病理学观察,用RT-PCR法检测肝组织TGF-β1和α1(Ⅰ)前胶原mRNA表达.结果:与对照组相比,CCl4处理组和CCl4加瘦素处理组小鼠血清转氨酶增高(P均＜0.01);肝脏的炎症和坏死程度明显加重;肝组织TGF-β1和α1(Ⅰ)前胶原的mRNA表达都升高(P＜0.05和P＜0.01).瘦素处理组则无明显变化.但CCl4加瘦素处理组和CCl4处理组相比,各项指标进一步升高(P均＜0.01).结论:瘦素可以明显增加小鼠肝脏急性损伤后的炎症反应和早期纤维的形成,可能是肝纤维化的促进因子.     

余甘子抗慢性肝损伤性肝纤维化的实验研究

目的：观察余甘子（Phyllanthus emblica L.)抗慢性肝损伤性肝纤维化的作用，并揭示其作用机理。方法：采用四氯化碳（CCl4)建立小鼠肝纤维化, 余甘子水提醇沉物高，中，小剂量组并与秋水仙碱组作对照。观察小鼠血清丙氨酸转氨酶（ALT，天门冬氨酸转氨酶（AST），总蛋白（TP），白蛋白（Alb），肝组织羟脯氨酸（Hyp)及肝脏系数，肝脏组织病理改变。结果：各剂量余甘子可显著降低小鼠肝脏Hyp含量及血清ALT，AST的活性，抑制Alb和A／G比值的降低，减轻肝组织病理损害程度，其作用呈剂量依赖性。结论：余甘子对实验性慢性肝损伤具有保护肝细胞，减少肝损伤，抗肝纤维化作用。     

叶黄素对化学诱导急性肝损伤小鼠的预防研究

目的 研究叶黄素对四氯化碳(CCl4)所致急性化学性肝损伤小鼠的保护作用.方法 雄性昆明种小鼠60只,随机分为正常对照组、急性化学性肝损伤模型组(模型组)、联苯双酯阳性对照组(阳性对照组)(联苯双酯15 mg/kg)以及叶黄素低、中、高剂量组(10、15、20 mg/kg)共6组,每组10只.测定并比较各组小鼠肝脏系数,血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性与丙二醛(MDA)含量;测定肝组织中SOD、GSH-Px活性、MDA含量以及组织病理系数.结果 叶黄素各剂量组均能升高急性化学性肝损伤小鼠血清与肝组织SOD、GSH-Px活性(P＜0.01),降低血清ALT、AST活性(P＜0.01)和血清与肝组织MDA含量(P＜0.01),并能不同程度地改善肝脏病理组织损伤.结论 叶黄素对CCl4所致急性化学性肝损伤具有预防性保护作用.     

CCl4诱导的急性肝损伤小鼠肝组织HSP27表达的变化

目的 研究热休克蛋白(HSP)27在CCl4诱导的急性肝损伤小鼠肝组织中的动态变化.方法 将100只健康雄性小鼠随机分为模型组90只和对照组10只.应用CCl4腹腔注射诱导小鼠急性肝损伤,在3h、6h、12h、24h、30h、36h、42h、48h和54h及正常对照小鼠分别眼球取血或取肝脏制备10％肝匀浆,采用Western blotting法检测肝组织HSP27表达的变化.结果 小鼠注射CCl4后,血清AST和ALT活性逐渐升高,24h达到高峰,54h逐渐恢复到正常水平;肝组织HSP27在注射CCl4后3h表达量略有增高,在24h表达量达到高峰,此后逐渐恢复到正常水平.结论 在CCl4诱导的急性肝损伤小鼠肝组织HSP27表达出现显著变化,可能在肝损伤的修复和再生过程中起到重要的作用.     

金银花对四氯化碳所致小鼠急性肝损伤的影响

目的 研究金银花对四氯化碳所致小鼠急性肝损伤的保护作用.方法 采用四氯化碳腹腔注射诱导小鼠急性肝损伤模型,观察金银花对小鼠血清谷丙转氨酶(AST)、谷草转氨酶(AST)的活性及肝组织匀浆超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px),肿瘤坏死因子(TNF-α)水平的影响.结果 金银花提取物能显著降低血清中ALT、AST水平(P<0.05或P<0.01),提高肝组织匀浆SOD、GSH-Px水平(P<0.05或P<0.01),减少TNF-α、MDA含量(P<0.05或P<0.01).结论 金银花提取物具有显著的保肝作用.     

Protective effect of recombinant human IL-1Ra on CCl4-induced acute liver injury in mice

AIM: To evaluate the effects of positive regulation of recombinant human interleukin 1 receptor antagonist (rhIL-1Ra) on hepatic tissue recovery in acute liver injury in mice induced by carbon tetrachloride (CCl 4 ). METHODS: Acute liver damage was induced by injecting 8-wk-old mice with CCl 4 1 mL/kg (1:3 dilution in corn oil) intraperitoneally (ip). Survival after liver failure was assessed by injecting 8-wk-old mice with a lethal dose of CCl 4 2.6 mL/kg (1:1 dilution in corn oil) ip. Mice were subcutaneo...     

蓝莓下调Toll样受体4表达减轻肝损伤的作用机制

目的研究蓝莓对Toll样受体4(TLR4)表达的调节,进一步探讨其在急性肝损伤中的作用。方法 48只SD大鼠随机分为空白对照组(对照组)、CCl4急性肝损伤组(模型组)、蓝莓低剂量组、蓝莓高剂量组和胸腺肽组。蓝莓低剂量组、蓝莓高剂量组造模开始前先分别给予蓝莓果汁(0.5 ml/100 g、1.0 ml/100 g)灌胃7 d。实验结束时测定肝脏指数、血清ALT、AST含量,WesternBlot检测肝组织TLR4蛋白表达量。结果模型组大鼠的肝脏指数、血清ALT、AST含量(0.047 30±0.002 85、4536.00±535.39,7959.33±108.89)高于对照组(0.031 90±0.002 87,48.00±5.57,137.00±12.53)(P<0.05);蓝莓低、高剂量组上述指标(0.040 80±0.003 77,0.040 80±0.003 81;2138.00±980.32,4049.67±466.01;1247.00±609.00,2063.33±1357.32)均低于模型组,模型组肝组织TLR4蛋白表达量(1.392±0.204)显著高于对照组(0.781±0.132)(P<0.05)。蓝莓低剂量组、高剂量组和胸腺肽组大鼠肝组织TLR4蛋白表达量(1.273±0.203,1.110±0.168,0.943±0.161)低于模型组(1.392±0.204)(P<0.05)。结论蓝莓可能通过下调肝组织中TLR4的表达,起到减轻急性肝损伤的作用。     

Protective effects of BML-111, a lipoxin A4 receptor agonist, on carbon tetrachloride-induced liver injury in mice

Background: Lipoxins (LX) are trihydroxytetraene-containing eicosanoids that display unique anti-inflammatory and pro-resolving actions during various inflammatory conditions, but the pathophysiological significance of LX in liver disorders remains unknown. Methods: In the present study, we used a murine model of carbon tetrachloride (CCl(4))-induced acute liver injury to investigate the effects of LX on the progression of acute liver injury. Results: The results indicated that the lipoxin A(4) receptor (ALX) was upregulated after giving CCl(4). BML-111, a commercially available ALX agonist, effectively protected the liver from CCl(4)-induced injury as evidenced by decreased serum aminotransferase (ALT, AST) levels and improved histological damage. The dampened liver injury was accompanied byreduced malondialdehyde (MDA) content in liver homogenates and decreased concentration of tumor necrosis factor-alpha (TNF-alpha) in the serum. Most interestingly, BML-111 markedly upregulated hepatic heme oxygenase-1 (HO-1) expression in CCl(4)-treated mice, which might provide antioxidative activities in the liver. Conclusion: These data indicate that ALX agonist BML-111 plays a critical protective role in CCl(4)-induced acute liver injury through limiting the inflammatory response and promoting antioxidative protein expression.     

In vitro and in vivo protective effects of proteoglycan isolated from mycelia of Ganoderma lucidum on carbon tetrachloride-induced liver injury

AIM: To investigate the possible mechanism of the protective effects of a bioactive fraction,Ganoderma lucidum proteoglycan (GLPG) isolated from Ganoderma lucidum mycelia, against carbon tetrachloride-induced liver injury. METHODS: A liver injury model was induced by carbon tetrachloride. Cytotoxicity was measured by MTT assay.The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined with an automatic multifunction-biochemical analyzer and the levels of superoxide dismutase (SOD)and TNF-alpha were determined following the instructions of SOD kit and TNF radioimmunoassay kit. Liver sections were stained with hematoxylin and eosin (H and E) for histological evaluation and examined under light microscope. RESULTS: We found that GLPG can alleviate the L-02 liver cells injury induced by carbon tetrachloride (CCl4) through the measurements of ALT and AST activities and the administration of GLPG to L-02 cells did not display any toxicity. Furthermore, histological analysis of mice liver injury induced by CCl4 with or without GLPG pretreatment indicated that GLPG can significantly suppress the toxicity induced by CCl4 in mice liver. We also found that GLPG reduced TNF-alpha level induced by CCl4 in the plasma of mice, whereas increased SOD activity in the rat serum. CONCLUSION: GLPG has hepatic protective activity against CCl4-induced injury both in vitro and in vivo. The possible anti-hepatotoxic mechanisms may be related to the suppression of TNF-alpha level and the free radical scavenging activity.     

慢性肝损伤致肝纤维化过程中微小RNA200家族的表达

目的观察肝组织中微小RNA200(miR-200)家族成员在慢性肝损伤致肝纤维化过程中表达变化并探讨其机制。方法雄性Wistar大鼠皮下注射四氯化碳(CCl4)制备肝纤维化模型,分别在2、4、6、8周处死大鼠测定肝脏指数、血清ALT、AST含量,观察肝组织病理改变,Real-time PCR检测肝组织miR-200a、b、c、141、429mRNA表达变化。结果模型各组大鼠肝脏指数、血清ALT、AST含量显著高于正常对照组(P<0.01),8周模型组肝纤维化明显,8周模型组肝组织中miR-200a、b、c、141、429mRNA表达较正常组显著增加(P<0.05)。结论 miR-200s在慢性肝损伤致肝纤维化过程中的表达变化,提示其参与慢性肝损伤及肝纤维化的发生发展。     

Protective effects of 5,4''-dihydroxy-3'',5''- dimethoxy-7-O-β-D -glucopyranosyloxy-flavone on experimental hepatic injury

AIM: To investigate the pharmacological effects of rice flavone (5,4'-dihydroxy-3',5'-dimethoxy-7-O-β-D-glucopyranosyloxy-flavone, RF) separated from panicledifferentiating to flowing rice on rat experimental hepatic injury.METHODS: Models of rat acute hepatic injury induced by carbon tetrachloride (CCl4) administration, rat hepatic fibrosis induced by thioacetamide, injury of primary cultured rat hepatocytes induced by CCl4, respectively,were established. After treated with RF, content of serum alanine transaminase (ALT), aspartate aminotransferase (AST) and albumin (Alb), hyaluronic acid (HA), the activity of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and hydroxyproline (Hyp) were measured and liver tissue was observed pathologically by hematoxylin-eosin (HE) staining. Effects of RF on pathological changes,function index, enzyme of scavenging free radicals and blood rheology were evaluated.RESULTS: In model of rat acute hepatic injury induced by CCl4, RF can significantly decrease the contents of serum ALT, AST, increase the content of Alb, improve the dropsy and fat denaturalization of hepatocytes. In model of rat hepatic fibrosis induced by thioacetamide,RF can inhibit the increase of HA, Hyp and whole blood viscosity, and improve the activities of GSH-Px and SOD,and inauricular microcirculation.CONCLUSION: RF has apparent protective effects on hepatic injury by increasing activity of GSH-Px and SOD,scavenging free radicals produced by CCl4, reducing blood viscosity, and improving microcirculation and blood supply.     

大蒜油对对乙酰氨基酚所致小鼠急性肝损伤的保护作用

目的 观察大蒜油对对乙酰氨基酚(AP)所致小鼠急性肝损伤是否有保护作用.方法 将75只小鼠随机分为阴性对照组、模型组以及大蒜油低、中、高三个剂量组(分别为25、50、100 mg/kg),给药后2 h除阴性对照组其他各组小鼠均灌胃AP 240 mg/kg;24 h后小鼠摘眼球取血,离心,测定血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)的活性,同时比较各组小鼠的肝脏系数和肝脏病理组织学变化.结果 与模型组相比,大蒜油低、中、高剂量组的肝脏系数明显减小,血清ALT、AST活性显著降低(P＜0.01),同时肝脏组织病理学检查发现模型组肝细胞发生气球样变,甚至坏死,炎细胞浸润,而大蒜油组无明显病理学改变.结论 大蒜油对AP所致小鼠急性肝损伤有明显的保护作用.     

四氯化碳诱导小鼠急性肝损伤模型的建立和优化

目的通过单次腹腔注射不同剂量的四氯化碳(CCl4)致小鼠急性肝损伤,检测小鼠血浆转氨酶水平的变化,建立适合本研究的小鼠模型。方法采用6~8周龄雄性C57BL/6小鼠单次腹腔注射CCl4诱导急性肝损伤。比较不同剂量的CCl4诱导急性肝损伤小鼠的血浆转氨酶水平。将182只小鼠随机分出32只。32只小鼠随机分为3组CCl4实验组(每组8只)和正常对照组(8只),分别腹腔注射0.1%、0.2%、0.3%的CCl4橄榄油溶液(10 ml/kg)或等体积橄榄油。注射12小时后取血,检测血浆丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)的水平。比较0.1%和0.2%剂量组小鼠不同时间点血浆转氨酶水平的变化。将剩余150只小鼠随机分为正常对照组(10只)、实验Ⅰ组(0.1%剂量,70只)、实验Ⅱ组(0.2%剂量,70只),实验组小鼠在造模6、12、16、20、24、48、72小时后取血,检测血浆ALT、AST的水平。结果与正常对照组相比,分别用0.1%、0.2%、0.3%CCl4处理后12小时小鼠血浆ALT、AST均明显升高(P0.05),并呈剂量依赖性。与正常对照组相比,0.1%和0.2%剂量组小鼠血浆ALT、AST的水平在早期均呈上升趋势,并分别在16小时和20小时达到高峰,随后逐渐下降,在72小时接近至正常水平。结论单次腹腔注射CCl4诱导小鼠急性肝损伤呈剂量依赖性。0.1%剂量的CCl4以及该剂量处理后16小时是建立C57BL/6小鼠急性轻度肝损伤的合适剂量与检测转氨酶水平的合适时间点。     

Mechanism of protective action of bicyclol against CCl-induced liver injury in mice.

Bicyclol is a novel synthetic drug for the treatment of chronic viral hepatitis in China. This paper reports the protective action of bicyclol against experimental liver injury in mice and its mechanism of action. Oral administration of bicyclol markedly reduced the elevated serum transaminases (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)) and the hepatic morphologic changes induced by CCl(4) in mice. Mechanistic studies demonstrated that bicyclol significantly inhibited CCl(4)-induced lipid peroxidation of liver microsomes and (14)CCl(4) covalent binding to microsomal lipids and proteins in vitro, and decreased the level of the trichloromethyl free radical (*CCl(3)) generated from CCl(4) metabolism by NADPH-reduced liver microsomes. On the other hand, bicyclol neither directly inhibited the activity of ALT or AST in vitro nor affected hepatic ALT protein content in mice. These results suggest that bicyclol has remarkable hepatoprotective effects and its mechanism of action may be related to a decrease in free radical-induced damage to hepatocytes.     

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。