桃仁提取物对小鼠急性肝损伤的保护作用

目的:研究桃仁乙醇提取物对四氯化碳(CCl4)和乙醇所致小鼠急性肝损伤的保护作用。方法:采用CCl4和乙醇制备小鼠急性肝损伤模型,观察桃仁乙醇提取物对小鼠血清和肝匀浆谷丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)活性;肝匀浆超氧化物歧化酶(SOD)活性、丙二醛(MDA)和谷胱甘肽(GSH)含量的影响。结果:桃仁乙醇提取物能降低急性肝损伤小鼠血清中ALT、AST活性;降低肝匀浆AST活性和MDA含量;提高SOD活性和GSH含量。结论:桃仁乙醇提取物对急性肝损伤有一定的保护作用,其机制可能与抗脂质过氧化作用有关。     

黄芩素对急性肝损伤模型小鼠的保护作用及其机制

目的探讨黄芩素对四氯化碳（CCl4）诱导小鼠急性肝损伤的保护作用及其机制。方法建立CCl4诱导小鼠急性肝损伤模型,在预防性给药与治疗性给药两种给药方式中,检测小鼠血清丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）活性、肝匀浆丙二醛（MDA）含量及超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH Px）、过氧化氢酶（CAT）活性。结果黄芩素能降低模型小鼠肝脏指数,血清ALT、AST活性,肝匀浆MDA含量,并提高小鼠肝匀浆SOD、GSH PX、CAT活性。结论黄芩素对CCl4诱导肝损伤的保护作用,可能与其抗氧化作用机制有关。     

南沙参多糖对小鼠CCl4急性肝损伤的保护作用

目的探讨南沙参多糖(RAPS)对肝损伤的保护作用.方法采用四氯化碳(CCl4)诱导小鼠急性肝损伤模型,测定血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)活性、肝匀浆中超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量,观察肝组织病理学改变.结果RAPS各剂量组(2000,1000,500 mg·kg-1)不仅能显著降低肝损伤小鼠血清AST、ALT活性,而且能够降低肝损伤小鼠肝组织MDA含量,并能提高SOD活性;病理形态学观察显示,RAPS能够明显减轻肝细胞肿胀、减少中性粒细胞浸润,其对急性肝损伤具有治疗作用.结论RAPS对CCl4诱导的急性肝损伤具有显著的保护作用,该保护作用可能与其抗氧化作用有关.     

连翘苷元对四氯化碳大鼠急性肝损伤的保护作用

目的探讨连翘苷元对四氯化碳(CCl4)所致急性肝损伤的保护作用。方法用CCl4诱导化学性急性肝损伤模型,测定血清中丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、总胆红素(TBIL)水平;肝脏组织切片,苏木精-伊红(HE)染色,光镜观察病理学改变;用试剂盒测定肝组织中SOD、GSH-Px和GSH的活性及脂质过氧化产物MDA含量。ELISA法检测血清中TNF-α、IL-8含量。结果在CCl4诱导的大鼠急性肝损伤模型中,连翘苷元(0.05、0.15、0.5mg·kg-1,sc)明显降低血清ALT、AST和TBIL水平;明显改善肝脏病理组织状况;连翘苷元(0.05、0.15、0.5 mg·kg-1,sc)明显降低CCl4诱导的急性肝损伤大鼠的肝组织匀浆中MDA的含量,明显增加SOD、GSH-Px和GSH的活性。连翘苷元(0.15、0.5 mg·kg-1,sc)明显降低TNF-α、IL-8含量。结论连翘苷元对CCl4诱导大鼠急性肝损伤具有保护作用,该作用与其增加肝组织中抗氧化酶的活性、降低脂质过氧化水平、降低TNF-α、IL-8等促炎因子水平有关。     

番茄红素对急性肝损伤模型大鼠的保护作用

目的:探讨番茄红素对四氯化碳(CCl4)所致大鼠急性肝损伤的保护作用。方法:将Wistar大鼠分为正常组(蒸馏水)、模型组(蒸馏水)及番茄红素低、高剂量组(10、20mg.kg-1),各组预防性给药(或蒸馏水)7d后除正常组外以CCl4制备急性肝损伤大鼠模型,24h后测定大鼠血清中天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)活性及肝脏指数,以及血清及肝组织匀浆中超氧化物歧化酶(SOD)和丙二醛(MDA)活性,并且取肝组织进行病理学检测评分。结果:番茄红素能明显降低模型大鼠血清中AST、ALT活性及肝脏指数(P<0.05),降低血清和肝组织匀浆中MDA活性(P<0.05),升高SOD活性(P<0.05),减轻肝组织变性、坏死程度,缓解肝组织的病理改变。结论:番茄红素对CCl4所致的大鼠急性肝损伤具有保护作用。     

蛇黄肝炎汤对小鼠急性肝损伤的保护作用研究

目的:研究蛇黄肝炎汤对小鼠急性肝损伤的保护作用。方法:采用四氯化碳(CCl4)复制小鼠急性肝损伤模型,观察蛇黄肝炎汤对小鼠血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)活性和肝脏组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量的影响。电镜下观察小鼠肝脏形态学。结果:蛇黄肝炎汤60、40g·kg-1剂量下可显著降低急性肝损伤模型小鼠血清中ALT、AST活性和肝组织匀浆中MDA含量,升高肝组织匀浆中SOD活性。同时,HE染色结果显示蛇黄肝炎汤能明显减轻肝脏的病理损伤。结论:蛇黄肝炎汤对CCl4所致小鼠急性肝损伤模型具有保护作用。     

绞股蓝多糖对小鼠四氯化碳肝损伤的保护作用

目的从绞股蓝中分离纯化绞股蓝多糖,并研究绞股蓝多糖对小鼠CCl4肝损伤的保护作用。方法经去蛋白、除果胶、脱色、超滤之后得绞股蓝多糖,以绞股蓝多糖对小鼠连续灌胃7 d之后,腹腔注射0.5%的CCl4花生油溶液,建立肝损伤模型,继续给药2次,检测血清丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)活性;测定肝组织中丙二醛(MDA)含量和谷胱甘肽(GSH)活性;采用光学显微镜观察肝组织病理组织学变化。结果绞股蓝多糖各剂量组能明显抑制肝损伤小鼠ALT、AST活性的升高;抑制肝组织中MDA含量的升高,提高肝组织中GSH活性;减轻CCl4对肝脏细胞的病理损伤。结论绞股蓝多糖对CCl4造成的小鼠急性肝损伤具有明显保护作用。     

壳寡糖对四氯化碳致急性肝损伤小鼠的保护作用

目的研究壳寡糖对四氯化碳(CCl4)诱导的化学性肝损伤小鼠的保护作用。方法小鼠随机分组,连续7d灌胃给予50,167,500mg.kg-1.d-1壳寡糖,于第7天腹腔注射四氯化碳制备小鼠急性肝损伤模型,检测血清丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)活性;测定肝组织中丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性;采用光学显微镜观察肝脏组织形态学变化。结果中、高剂量的壳寡糖能明显抑制肝损伤小鼠血清ALT和AST活性的升高(P<0.05),抑制肝组织中MDA含量的升高(P<0.01),提高肝组织中SOD的活力(P<0.05),减轻CCl4对肝脏细胞的病理损伤。结论壳寡糖对四氯化碳造成的小鼠急性肝损伤具有一定的保护作用。     

红丝线多糖对大鼠急性肝损伤的保护作用

目的 研究红丝线多糖对大鼠急性肝损伤的保护作用.方法 采用CCl4诱导大鼠急性肝损伤模型,观察红丝线多糖对大鼠血清中丙氨酸氨基转换酶(ALT)、天门冬氨酸氨基转换酶(AST)、丙二醛(MDA)、超氧化物歧化酶(SOD)水平的影响.结果 红丝线多糖各剂量组可抑制急性肝损伤大鼠血清中ALT、AST的活性,降低MDA的水平,升高SOD的活性.结论 红丝线多糖对CCl4致大鼠急性肝损伤具有较好的保护作用.     

黄芪提取物对小鼠急性化学性肝损伤的保护作用

目的探讨黄芪提取物（AE）对CCl4致小鼠急性化学性肝损伤模型的保护作用。方法采用CCl4诱导小鼠急性肝损伤模型,检测血清中丙氨酸氨基转移酶（ALT）、天门冬氨酸氨基转移酶（AST）和肝匀浆中丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）含量,HE染色法对肝脏作病理检查。结果AE能显著降低小鼠血清ALT、AST、肝匀浆MDA水平,升高SOD和GSH-Px酶活性,减轻肝细胞损伤。结论AE对CCl4致小鼠急性化学性肝损伤模型具有保护作用。     

鲨鱼肝再生因子对大鼠慢性肝损伤的治疗作用

目的:探讨鲨鱼肝再生因子(sHRF)对大鼠慢性肝损伤的治疗作用。方法:CCl4致大鼠慢性肝损伤模型,给药后取血清及肝组织测定各项肝指标。结果:当用药8周时,对CCl4引起的肝损伤大鼠血清中AST、ALT活性的升高和羟脯氨酸含量的升高均有抑制作用,且0.8、1.6mg/kg剂量组的作用差异均有统计学意义。此外,sHRF能在一定程度上增加白蛋白含量,并使白蛋白/球蛋白比值有一定程度的升高。肝组织病理切片亦显示sHRF能减轻CCl4所致大鼠肝细胞脂肪变性及纤维组织增生。结论:sHRF对CCl4所致大鼠慢性肝损伤有一定的治疗作用。     

Prophylactic effect of tritoqualine (TRQ) on the CCl4-induced chronic liver injury model in rats

Tritoqualine (TRQ) administered at doses of 100 or 200 mg/kg, perorally, had a preventive effect on the liver injury in rats induced by the treatment with CCl4 for 12 weeks consecutively. Rats subjected to this chronic treatment with CCl4 showed a decrease in body weight gain and changes in several serum parameters that are indicators of hepatic function were observed: the increase of transaminases, as a parameter of hepatocyte breakdown; the increase of alkaline phosphatase, as a parameter of biliary system abnormalities, the reduction of prothrombin time, as a marker of protein biosynthesis in the liver; and the change of lipids concentrations, reflecting liver injury. After the administration of TRQ perorally, there was a notable suppression of the increment in leaked enzymes in the serum and a marked improvement of the parameters concerning protein biosynthesis and lipid metabolism in comparison with CCl4 control rats. Marked fibrosis in the liver was observed after CCl4 treatment for 12 weeks, and the collagen content in the liver was 5 times higher than that of control rats. TRQ suppressed the increment in collagen formation and also showed improvement of the decrease of the liver function with regards to protein biosynthesis in CCl4-treated rats. Judging from these results, it was concluded that TRQ had a remarkable protecting action on the liver injury chronically induced by CCl4 treatment and was a effective compound for restoring liver function.     

Protective effect of malotilate (diisopropyl 1,3-dithiol-2-ylidenemalonate) on carbon tetrachloride-induced liver injury in mice and rats

The protective effect of malotilate was studied on the liver injury induced by carbon tetrachloride (CCl4) in mice and rats. Plasma GOT and GPT activities were used as indices for the liver injury, and the liver was histopathologically examined. A remarkable suppressing effect on the liver injury was observed when malotilate was orally given 6 hr prior to oral administration of CCl4 in mice and 3, 6 or 12 hr in rats. Malotilate was also effective in preventing the liver injury caused by intraperitoneal injection of CCl4, indicating that the protective effect is not derived from the decreased CCl4 absorption. The liver injury was suppressed even when malotilate was given 12 or 24 hr prior to oral administration of CCl4 in mice and 24, 48 or 72 hr in rats. It may be the characteristic of malotilate that the protective effect lasts for a long period. It is supposed that the effect is due not only to the inhibition of the metabolic activation of CCl4 but also the other action(s) of malotilate.     

Protective effects of NYG-1 on CCl_4-induced acute liver injury in rats

OBJECTIVE To study the protection effects and mechanisms of NYG-1 on CCl4-induced acute liver injury.METHODS Acute liver injury model of rats was established by using CCl4.48 male SPF SD rats were weighed and randomly divided into six groups with 8 in each group,normal group,model group,positive control group(silibinin),low-,medium-and high-dose NYG-1 group.Silibinin was given orally to rats in the positive control group,NYG-1(high-,medium-and low-dose)was given orally in the high-,medium-and low-dose NYG-1group,respectively.Those rats were administered appropriately according to the group once daily for seven consecutive days.On the seventh day,rats were treated with 10% CCl4(10mL·kg-1 of0.1% CCl4 solution in olive oil)intraperitoneally injecting(ip)to induce acute liver injury,except the normal group.At 16 h after CCl4 treatment,rats were weighed,then anaesthed with ether,the blood and liver were collected.Serum ALT,AST,LDH and ALP were measured.MDA content and SOD activity in liver homogenate were detected.The histopathological changes of liver were observed by H&E staining.RESULTS Acute liver injury model was established successfully in rats by intraperitoneally injecting CCl4.Pretreatment with medium and high dose NYG-1 decreased the increase of ALT,AST and MDA induced by CCl4,but it had no influence on serum LDH,ALP level and SOD activity in the liver homogenate.CONCLUSION The obtained results suggest that oral administration of NYG-1 hasve the protective effects against CCl4-induced acute hepatic injury in rats,Its mechanism may be related to antioxidant-like action.     

Antioxidative effect of chitosan on chronic carbon tetrachloride induced hepatic injury in rats

Carbon tetrachloride (CCl(4)) is a toxic material known to induce lipid peroxidation and liver damage. To determine if chitosan has antioxidative effects on CCl(4)-induced liver injury, we administered 1 ml/kg of CCl(4) resolved in a 50% corn oil solution to rats every week by intraperitoneal injection. Chitosan (200 mg/kg body weight per day, MW 380,000 Da) was administered to the CCl(4) + chitosan treated rats by oral gavage during the experimental period. Chitosan significantly decreased liver thiobarbituric acid reactive substances (TBARS) and increased antioxidant enzyme activities (catalase and superoxide dismutase (SOD)). Fatty acid composition was not remarkably changed by chitosan; only arachidonic acid (20:4n-6) levels were significantly altered by CCl(4). Chitosan administration in the present experiment did not restore the decreased delta5-desaturase activity. In addition, chitosan supplementation did not prevent the CCl(4) induced degradation of CYP2E1. In conclusion, our results suggest that chitosan has antioxidative but not detoxifying effects on chronic CCl(4) induced hepatic injury in rats.     

大黄酸抑制四氯化碳诱导的大鼠肝纤维化形成

目的:观察大黄酸对实验性肝纤维化的影响.方法:采用60％的四氯化碳(CCl_4)及5％的乙醇制备肝纤维化动物模型,分别用小剂量、大剂量大黄酸(25 mg/kg,100 mg/kg体重)干预,测定血清丙氨酸氨基转移酶(ALT)、透明质酸(HA)、Ⅲ型前胶(PC-Ⅲ)及肝组织丙二醛(MDA)含量,免疫组化方法观察转化生长因子 β1(TGF-β1)、α平滑肌肌动蛋白(α-SMA)的表达情况,并观察肝组织胶原面积及病理变化.结果:大黄酸组较模型组:(1)血清ALT、HA、PC-Ⅲ水平及肝组织中MDA含量显著降低(P<0.01);(2)肝组织中TGF-β1,α-SMA的表达显著减少(P<0.05或P<0.01);③肝组织胶原面积明显减少,纤维化程度明显改善(P<0.05或P<0.01).结论:大黄酸具有保肝作用和抑制肝纤维化作用,其作用机制可能与其抗炎、抗氧化作用及抑制HSC活化、抑制TGF-β1作用有关.     

恩施富硒藤茶水提液对四氯化碳致急性肝损伤小鼠的保护作用

目的 观察恩施富硒藤茶水提液对四氯化碳（CCl4）诱导的小鼠急性肝损伤的影响。方法用腹腔注射CCl4致小鼠急性肝损伤模型,测定不同剂量的恩施富硒藤茶水提液对肝损伤血清丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）活性、肝中超氧化物歧化酶（SOD）活性、肝中丙二醛（MDA）含量的影响。结果恩施富硒藤茶水提液具有剂量依赖性地降低CCl4致小鼠肝损伤血清ALT、AST值升高,降低肝组织匀浆中MDA的含量,增强SOD的活性（P〈0．01或P〈0．05）。结论恩施富硒藤茶水提液对CCl4致小鼠急性肝损伤具有一定的保护作用。     

Effect of thiol compounds on experimental liver damage (I). Preventive effect of tiopronin (2-mercaptopropionylglycine) on liver damage induced by carbon tetrachloride (author's transl)]

Effects of oral administration of tiopronin (2-mercaptopropionylglycine) on acute liver damage induced in rats by intraperitoneal administration of carbon tetrachloride (CCl4) were investigated. Tiopronin suppressed increase in serum transaminase activity, accumulation of liver triglyceride and decrease of liver glucose-6-phosphatase activity induced by CCl4. CCl4 induced a significant decrease of nonprotein thiol (NPSH) in the liver 24 hr after administration, but this decrease did not result in an increase of nonprotein disulfide in the liver. Tiopronin suppressed the decrease in NPSH induced by CCl4, but did not influence NPSH in normal rats 24 hr after administration. In addition to these biochemical findings, it was also noted that tiopronin prevented necrosis and decrease of glycogen in liver, as determined histologically. Other compounds such as cystamine, cysteine and glutathione proved to have a preventive effect on CCl4-induced liver damage as in the case of tiopronin. It was revealed that such preventive effect correlated to some extent with NPSH content in liver as well as serum transaminase activity and histological findings.     

金丝桃苷对四氯化碳诱导肝细胞损伤的保护作用

目的研究金丝桃苷(hyperfine,HP)对四氯化碳(CCl4)诱导肝细胞损伤的保护作用及其机制。方法用CCl4体外诱导人正常肝细胞L-02损伤,检测培养上清液中天门冬酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALT)水平,测定肝细胞中丙二醛(MDA)和谷胱甘肽(GSH)的含量,四甲基偶氮唑盐微量酶反应比色(MTT)法检测肝细胞存活率。结果金丝桃苷可明显降低由CCl4升高的肝细胞培养上清液中ALT和AST水平及肝细胞MDA含量,还可提高由CCl4降低的肝细胞存活率和GSH含量。结论金丝桃苷对人肝细胞氧化性损伤有直接保护作用,这可能与金丝桃苷抑制抗氧化酶活性和抗自由基活性有关。     

绞股蓝在大鼠肝的抗脂质过氧化作用

目的：观察绞股蓝（GP）对四氯化碳（CCl4)所致肝脏脂质过氧化的干预作用。方法：将Wistar大鼠随机分为4组：A（对照组）;B（CCL4）;C（GP);D(CCL4＋CP）。结果：CCL4组的脂质过氧化物（LPO）含量明显高于对照组,谷胱甘肽过氧化物酶（GSH－Px）活性低于对照组;而同时给予GP的D组可减弱CCL4诱发的上述作用。结论：GP能减弱CCL4对肝脏的损害。