溪黄草水煎剂对大鼠急性肝损伤的保护作用

目的:观察溪黄草水煎剂对大鼠实验性肝损伤的保护作用及其机制。方法:建立CCl4致大鼠急性肝损伤模型,用比色分析法测定大鼠血清天冬氨酸转氨酶(ALT)、丙氨酸转氨酶(AST)的活性;测定大鼠血清超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性及丙二醛(MDA)的含量。结果:溪黄草水煎剂显著降低CCl4所致急性肝损伤大鼠血清ALT、AST的活性;升高急性肝损伤大鼠血清SOD、GSH-Px的活性及降低MDA的含量。结论:溪黄草水煎剂对CCl4所致大鼠急性肝损伤有保护作用。     

虎杖方剂对四氯化碳致大鼠肝损伤的保护作用研究

目的 观察虎杖方剂对四氯化碳(CCl4)致大鼠肝损伤的保护作用.方法 参照文献.方法 制备CCl4致大鼠肝损伤模型,实验分正常对照组、药物对照组、CCl4肝损伤组、药物预防组、药物不同剂量治疗组.测定肝组织超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量,血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、碱性磷酸酶(AKP)活性及血清一氧化氮(NO)与肿瘤坏死因子(TNF-α)水平,并进行肝组织学检查.结果 CCl4致大鼠肝损伤组肝组织SOD活性明显降低,MDA含量显著升高(P<0.01);血清ALT、AST、AKP活性及NO与TNF-α水平显著升高(P<0.01).虎杖方剂本身对正常肝脏无损伤作用,而且虎杖方剂预防组与治疗组均能明显提高肝组织SOD活性,降低肝组织MDA含量;显著降低血清ALT,AST,AKP活性及NO与TNF-α水平(P<0.01).肝组织学检查发现虎杖方剂能明显减轻CCl4引起的肝组织及肝细胞损伤.结论 虎杖方剂本身对肝组织无明显损伤作用,通过抑制脂质过氧化、抑制TNF-α的表达和保护内皮细胞功能减轻CCl4引起的肝损伤.     

古日古木对小鼠CCl4急性肝损伤模型的影响

目的:探讨古日古木对小鼠四氯化碳(CCl4)肝损伤模型的保护作用。方法:连续9d给予小鼠腹腔注射CCl4制作肝脏损伤模型,通过测定小鼠血清中ALT、AST、总蛋白、白蛋白、白球蛋白比和肝脏组织中SOD、MDA、NO等指标,以及肝脏的组织病理学检查,研究红花对小鼠CCl4肝损伤模型的保护作用。结果:古日古木高、中、低剂量组不同程度抑制CCl4损伤后血浆中ALT和AST的异常增高,提高血清和肝脏中SOD活性,减少MDA形成,降低小鼠肝脏MDA含量,并降低肝组织的NO,升高血浆中总蛋白、白蛋白水平,减轻肝脏疏松化及脂肪变性。结论:古日古木对CCl4所致急性肝损伤有一定的保护作用。     

左旋虾青素对四氯化碳致小鼠急性肝损伤保护作用的研究

目的:探讨左旋虾青素对四氯化碳致小鼠急性肝损伤的保护作用。方法:通过皮下注射四氯化碳(CCl4)诱导小鼠急性肝损伤,检测小鼠血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)的含量、肝脏中超氧化物歧化酶(SOD)的活性以及丙二醛(MDA)的含量,考察左旋虾青素的保肝作用。结果:左旋虾青素能显著降低小鼠血清中ALT、AST的活性与肝脏中MDA含量,提高小鼠肝脏的SOD活性。结论:左旋虾青素对CCl4所致肝脏毒性具有一定保护作用。     

左旋虾青素对四氯化碳致大鼠慢性肝损伤保护作用的研究

目的 探讨左旋虾青素对四氯化碳(CCl4)致大鼠慢性肝损伤的保护作用.方法 通过皮下注射CCl4诱导大鼠慢性肝损伤,检测大鼠血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)的含量、肝脏中超氧化物歧化酶(SOD)的活性、丙二醛(MDA)的含量及肝组织损伤情况,考察左旋虾青素的保肝作用.结果 左旋虾青素能有效降低大鼠血清氨基转氨酶的含量,明显提高大鼠肝脏的SOD活性(P＜0.05,P＜0.01),大鼠肝脏MDA含量得到明显降低(P ＜0.05,P＜0.01),有效减轻肝细胞的坏死程度减轻肝细胞的坏死程度.结论 左旋虾青素对四氯化碳( CCl4)致大鼠慢性肝损伤有保护作用.     

秦艽对四氯化碳致小鼠急性肝损伤的保护作用

目的:研究秦艽对四氯化碳(CCl4)所致小鼠急性肝损伤的保护作用。方法:腹腔注射10%CCl4花生油溶液引起小鼠急性肝损伤,以联苯双酯为阳性对照,灌胃给药7天,测定血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)和肝组织中超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量及脏器重量,并做病理切片,观察肝组织病理改变。结果:同模型组相比较,秦艽水提取物高、中、低剂量(8,4,2 g/kg)组均能降低CCl4所致急性肝损伤小鼠血清ALT、AST活性(P<0.01,P<0.05),降低肝脏MDA的含量,增强SOD活性(P<0.01,P<0.05);病理学切片显示,秦艽提取物能明显减轻模型动物肝脏病变程度。结论:秦艽水提物对CCl4所致小鼠急性肝损伤具有保护作用。     

美味猕猴桃根提取物对小鼠急性肝损伤的保护作用

目的研究美味猕猴桃根提取物对小鼠急性肝损伤的保护作用。方法分别采用CCl4和D-半乳糖胺作为化学毒物制成急性肝损伤模型,采用赖氏法测定各组动物血清丙氨酸氨基转移酶(ALT)和血清天门冬氨酸氨基转移酶(AST)的活性,并测定肝匀浆MDA含量。结果CCl4肝损伤模型组和D-半乳糖胺肝损伤模型组小鼠的血清ALT和AST均明显高于正常对照组(P<0.01),MDA含量高于正常对照组(P<0.01),表明CCl4和D-半乳糖胺均造模成功。CCl4造模实验中美味猕猴桃根提取物高剂量组较模型组血清ALT和AST活性明显降低(P<0.01),肝脏MDA含量明显降低(P<0.01),而在D-乳糖胺造模实验中美味猕猴桃根提取物中剂量组较模型组血清AST明显降低(P<0.01),肝脏MDA含量降低(P<0.05),低剂量组较模型组ALT?AST活性和MDA含量均明显降低(P<0.01)。结论美味猕猴桃根提取物对小鼠急性肝损伤有一定的保护作用。关键词:     

龙胆草水提物对大鼠肝损伤的保护作用

目的:研究龙胆草水提物的保肝作用.方法:给动物灌胃给药,用CCl4、D-半乳糖制作大鼠急性肝损伤模型,用比色分析法测定大鼠血清天冬氨酸转氨酶(aspartate transaminase,ALT)、丙氨酸转氨酶(alanine transaminase,AST)的活性;测定大鼠血清超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione perioxidase,GSH-Px)的活性及丙二醛(malondialdehyde,MDA)的含量.结果:龙胆草水提物显著降低因CCl4、D-半乳糖所致急性肝损伤大鼠血清ALT、AST的升高;对急性肝损伤大鼠血清SOD、GSH-PX的活性有明显的升高作用及降低MDA的含量.结论:龙胆草水提物对CCl4、D-半乳糖所致大鼠急性肝损伤有保护作用.     

血塞通对CCl_4高脂低蛋白诱导大鼠肝脂肪变性脂质过氧化的影响

目的:观察血塞通胶囊对四氧化碳(CCl4)诱导大鼠肝脂肪变性脂质过氧化的影响.方 法:复制CCl4高脂低蛋白大鼠肝脂肪变性模型,给予血塞通灌胃,进行预防性治疗3周,并以东宝甘泰为对照,观察各组大鼠血清ALT、AST;肝组织超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量.结果:与正常组比较,模型组大鼠血清ALT、AST明显升高,SOD活性明显下降,MDA含量显著升高,表现为显著的脂质过氧化损伤和肝损伤.经药物治疗后,血塞通组血清ALT、AST明显下降,SOD活性升高,MDA含量降低,显示有抗肝损伤和抗肝脂质过氧化作用.结 论:血塞通具有一定的抗肝损伤作用,其机制可能与抗脂质过氧化有关.     

蛇床子素对小鼠实验性肝损伤的保护作用

目的:探讨蛇床子素对小鼠CCl4肝损伤的保护作用。方法:采用CCl4小鼠急性肝损伤模型,测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性、肝组织MDA含量,并观察肝组织病理变化。结果:蛇床子素能保护CCl4所致小鼠肝损伤,表现为血清ALT、AST活力和肝脏MDA含量下降,同时其肝脏病变较模型组为轻。结论:蛇床子素对CCl4所致小鼠肝损伤具有保护作用。     

Ameliorative effects of pycnogenol on carbon tetrachloride-induced hepatic oxidative damage in rats

This study evaluated the putative antioxidant activity of Pycnogenol (PYC) against CCl4-induced hepatic oxidative damage in Sprague-Dawley rats. A single oral dose of CCl4 (1.25 mL/kg) produced significantly increased levels of serum aminotransferase (AST) and alanine aminotransferase (ALT) activities. In addition, increased malondialdehyde (MDA) concentration, reduced glutathione (GSH) content, and decreased catalase, superoxide dismutase (SOD) and glutathione-S-transferase (GST) activities were observed in the hepatic tissues. However, concomitant administration with PYC (10 or 20 mg/kg) significantly improved CCl4-induced hepatic injury, as evidenced by the decline of serum AST and ALT activities in a dose dependent manner. Moreover, PYC reduced MDA concentration and increased GSH levels and catalase, SOD and GST activities in hepatic tissues, indicating that concomitant administration with PYC efficiently prevent the CCl4-induced oxidative damage in rats. The free radical scavenging assay showed that PYC has a dose-dependent scavenging activity against 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radicals. These results indicate that PYC has an antioxidant effect against CCl4-induced hepatic oxidative damage and is useful as a hepatoprotective agent against various liver diseases induced by oxidative stress.     

齐墩果酸对四氯化碳诱导大鼠肝硬化门静脉高压的影响

目的:研究齐墩果酸(Oleanolic acid,OA)对四氯化碳(CCl4)诱导的大鼠肝硬化门静脉高压的影响及其可能的作用机制。方法:大鼠采用CCl4灌胃给药诱发肝硬化门静脉高压,给予OA低(30 mg/kg)、高(60 mg/kg)剂量治疗,正常对照组与模型组给予等容积溶剂。1个月后分别测定血清中丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)等血清生化指标及肝组织中丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、NOx、内皮型一氧化氮合酶(eNOS)、环磷酸鸟苷(cGMP)、I型胶原蛋白的含量;采用血液动力学的方法测定大鼠主动脉的血压(MAP)、门静脉压(PP)、心率(HR)等指标;采用Western blotting技术测定肝硬化大鼠eNOS的表达;采用Masson染色对大鼠肝纤维化的进展进行研究。结果:与模型组比较,给予OA治疗1个月后显著降低血清ALT、AST、ALP、γ-GT、MDA的水平和提高肝组织中GSH-Px的含量(P0.05);显著降低模型大鼠肝脏的胶原沉积及肝纤维化的进展,进而降低了门静脉压(P0.05),而主动脉压(MAP)和心率(HR)无显著变化;并能显著提高肝内eNOS蛋白表达水平,进而提高了肝硬化大鼠肝内的cGMP和NOx的含量(P0.05)。结论:OA对四氯化碳诱导大鼠肝硬化门静脉高压具有良好的治疗作用,其作用机理可能是通过促进肝内的eNOS蛋白表达从而提高肝内NOx的含量。     

黄芩苷元对小鼠四氯化碳肝损伤的保护作用

目的探讨黄芩苷元对小鼠CCl4肝损伤的保护作用。方法采用CCl4小鼠急性肝损伤模型,测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性、肝组织MDA含量,并观察肝组织病理变化。结果黄芩苷元能保护CCl4所致小鼠肝损伤,表现为血清ALT,AST活力和肝脏MDA含量下降,同时其肝脏病变较模型组为轻。结论黄芩苷元对CCl4所致小鼠肝损伤具有保护作用。     

京尼平苷对CCl4诱导的大鼠慢性肝损伤保护作用研究

目的:研究京尼平苷对CCl4诱导的大鼠慢性肝损伤的保护作用。方法:每周给大鼠腹腔注射2次一定体积比的CCl4豆油混悬液,连续9周,致大鼠肝纤维化。然后对肝损伤大鼠每天灌服一定剂量的京尼平苷进行治疗,连续4周,末次灌服13小时后,取血以及肝脏,对血清中的AST、ALT、AKP、NO以及肝匀浆中CuZn-SOD、GSH-Px、MDA、HYP和CAT等各项生化指标进行测定,并对肝组织进行光镜分析。结果:当京尼平苷的灌服剂量为100mg/kg时,能显著改善肝损伤大鼠血清中AST、ALT水平,提高肝组织中SOD、CAT和GSH的活力,降低肝组织中MDA的含量,并减轻组织炎症及纤维化。结论:京尼平苷对大鼠慢性肝损伤有较好的保护作用。     

Protective effects of total flavonoids of Bidens pilosa L. (TFB) on animal liver injury and liver fibrosis

The hepatoprotective effects of total flavonoids of Bidens pilosa L. (TFB), a traditional Chinese medicine were evaluated in carbon tetrachloride (CCl(4))-induced liver injury in mice and rats. Total flavonoids of Bidens pilosa L. (25, 50 and 100mg/kg) were administered via gavage daily for 10 days to CCl(4)-treated mice as well as TFB (30, 60 and 90mg/kg) administered for 6 weeks to CCl(4)-treated rats. Liver index (liver weight/body weight), serum levels of transaminases (alanine aminotransferase, ALT and aspartate aminotransferase, AST), hepatic malondialdehyde (MDA) content, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were evaluated following the 10 days treatment in mice. In addition histopathologic changes and nuclear factor-kappaB (NF-kappaB) expression of the liver were detected with hematoxylin-eosin (HE) and immunohistochemistry methods, respectively. The results showed that TFB (50 and 100mg/kg) effectively reduced the CCl(4)-induced elevated liver index, serum ALT, AST levels, hepatic MDA content, and restored hepatic SOD, GSH-Px activities in acute liver injury mice. TFB (60 and 90mg/kg) treatment significantly inhibited NF-kappaB activation in liver fibrosis of rats. The histopathological analysis suggested that TFB reduced the degree of liver injury in mice and severity of liver fibrosis in rats. These results suggested that TFB had a protective and therapeutic effect on animal liver injury, which might be associated with its antioxidant properties and inhibition of NF-kappaB activation.     

Protective effects of dehydrocavidine on carbon tetrachloride-induced acute hepatotoxicity in rats

AIM OF THE STUDY: To investigate the protective effects of dehydrocavidine (DC), a main active ingredient of Corydalis saxicola Bunting (Yanhuanglian), on carbon tetrachloride (CCl4)-induced hepatotoxicity and the possible mechanisms involved in male Sprague-Dawley rats. MATERIALS AND METHODS: Acute hepatotoxicity was induced by CCl4 intoxication in rats. Serum biological analysis, lipid peroxides and antioxidants estimation, histopathological studies were carried out. RESULTS: Both pre-treatment with DC prior to CCl4 administration and post-treatment with DC after CCl4 administration significantly prevented increases in serum enzymatic activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and total bilirubin (TBIL). In addition, pre- and post-treatment with DC also significantly prevented formation of hepatic malondialdehyde (MDA), depletion of glutathione peroxidase (GPx) and depression of superoxide dismutase (SOD) in the liver of CCl4-intoxicated rats. ALT, AST, LDH, ALP and TBILL levels, as well as MDA, SOD and GPx activities were unaffected in normal rats by treatment with DC alone. GST, a phase II enzyme, had no significant changes during our experiments. Histopathological changes induced by CCl4 were also significantly attenuated by DC treatment in both preventive and curative experiments. CONCLUSIONS: DC has a potent hepatoprotective effect on CCl4-induced liver injury in rats through its antioxidant activity.     

18α、18β-甘草酸及其不同配比物对CCl4肝损伤大鼠的影响

目的：研究不同配比的18α-、18β-甘草酸（GL）对四氯化碳（CCl4）肝损伤大鼠的保护作用,探讨临床应用合理比例。方法取健康雄性sD大鼠（2004-20）g70只,随机分为7组,即正常组、CCl4肝损伤组、180L—GL、18β-CL和3个不同配比组（α：13比例分别为4：6、3：7和2：8）。采用腹腔注射CCl4复制大鼠急性肝损伤模型。分别于24h和48h后摘眼球取血,测定血清谷丙转氨酶（ALT）、谷草转氨酶（AST）、乳酸脱氢酶（LDH）活性,同时测定肝脾重量,肝脏超氧化物歧化酶（SOD）,并对肝细胞的组织形态学进行观察。结果：模型组大鼠ALT、AsT、肝脏系数显著增高,脾脏系数和SOD活性显著降低,组织病理学亦有显著差异,造模成功。5个药物组中以18α-和18β-GL配比为3：7最佳,能显著抑制CCl4引起的大鼠血清ALT、AST及肝脏系数的升高以及脾脏系数和肝脏SOD活性的降低,并能显著减轻CCl4引起的肝细胞组织病理学改变。结论：18α-与18β-GL3：7配比组对CCI。致大鼠肝损伤具有较强的保护作用,     

罗汉果甜苷对大鼠慢性肝损伤保护作用的实验研究

目的:研究罗汉果甜苷(mogroside,Mog)对实验性慢性肝损伤的保护作用。方法:用CCl4建立大鼠慢性肝损伤模型,观察罗汉果甜苷对大鼠血清ALT、AST活性,肝组织SOD、GSH-Px活性及MDA含量的影响,观察罗汉果甜苷对肝组织病理变化的影响。结果:罗汉果甜苷可降低血清中ALT、AST活性;升高肝组织SOD、GSH-Px活性;降低肝组织MDA含量;明显减轻肝组织病理变化程度。与模型组相比有显著性差异(P<0.05或P<0.01)。结论:罗汉果甜苷对CCl4所致大鼠慢性肝损伤有明显的保肝作用,其机制可能与抑制脂质过氧化有关。     

Protective Effect of Chlorogenic Acid against Carbon Tetrachloride-induced Acute Liver Damage in Rats

Objective To evaluate the protective effect of chlorogenic acid(CGA)on carbon tetrachloride(CCl4)-induced liver injury of rats.Methods The anti-oxidative activity of CGA was investigated with several established in vitro systems.The hepatoprotective activity of CGA against CCl4-induced acute liver injury in rats was studied.The levels of alanine aminotranferase(ALT),aspartate aminotransferase(AST),alkaline phosphatase(ALP),and total bilirubin(TB)were measured.The histopathological examination was carried out to supplement the biochemical results.Results CGA possessed strong anti-oxidative ability in vitro.The CCl4-induced liver toxicity experiment showed that the rats pretreated with CGA(300 or 500 mg/kg)had lower levels of ALT,AST,ALP,and TB than those of the CCl4-treated group.These data were supplemented with histopathological examination of rat liver sections.CGA did not show any mortality at the dose up to 5000 mg/kg.Conclusion CGA could protect the liver against CCl4-induced oxidative damage in rats,and the possible mechanism of the activity may be due to its free radical-scavenging and anti-oxidative activity.     

玉郎伞黄酮对四氯化碳诱导的大鼠肝纤维化的影响

目的:研究玉郎伞黄酮(YLSF)对四氯化碳(carbon tetrachloride,CCl4)所致大鼠肝纤维化的治疗作用,并探讨其作用机制.方法:将SD大鼠随机分成模型组及空白对照组(NC),模型组以50％ CCl4食用油溶液为诱导剂ig造模,NC组以生理盐水ig.将病理检查确认形成肝纤维化的SD大鼠,随机分成模型对照组(MC)和药物干预组.药物干预组分别以YLSF(20,40,80 mg·kg-1)及秋水仙碱片(0.20 mg·kg-1)ig;MC组以等剂量生理盐水ig.末次给药24 h后处死大鼠,采集血清及肝组织,检测大鼠血清中天冬氨酸转氨酶( AST)、丙氨酸转氨酶(ALT)活性,测定肝组织中超氧化物岐化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)和谷胱甘肽过氧化酶(GSH-Px),并观察肝组织病理学改变.结果:YLSF(20,40,80 mg·kg -1)各剂量组大鼠血清中AST和ALT分别为(207.85±101.72),(131.55 ±35.09),(129.98±37.21)U·L-1和(90.51±44.24),(47.79 ±16.11),(44.56±16.31)U·L-1;YLSF各剂量组大鼠肝组织中SOD,MDA,GSH-Px,GSH含量分别为(143.14±42.82),(146.53±31.98),(147.41±32.82) U· mg-1,(2.57±0.54),(2.19±0.57),(2.11±0.59)nmol·mg-1,( 463.55±271.07),(659.14±162.23),(752.08±200.70) nmol·mg-1,(5.06±1.09),(6.10 ±0.97),(6.89 ±0.98) nmol·mg-1.各剂量YLSF和阳性药能显著降低大鼠血清中AST(P ＜0.01)及肝组织MDA含量(P＜0.05或P＜0.01),并显著提高肝组织中SOD含量(P ＜0.05或P＜0.01);中、高剂量YLSF和阳性药可降低大鼠血清中ALT水平(P＜0.01),显著升高大鼠肝组织GSH含量(P＜0.01);中、高剂量YLSF能显著升高大鼠肝组织GSH-Px(P ＜0.01).各剂量YLSF及阳性药均能够减轻肝细胞损伤程度(P ＜0.05或P＜0.01).结论:玉郎伞黄酮对CCl4诱导的大鼠具有一定治疗作用,其机制可能与其清除自由基、抑制脂质过氧化有关系.