The Protective Effect of Arabinose + Mannose on Mice with Acute Liver Injury Induced by CCl_4 and Its Mechanism

[Objectives] Taking mice with acute liver injury induced by CCl_4 as the model,the effect of arabinose + mannose( w/w = 1∶ 1) on mice with acute liver injury induced by CCl_4 was studied. [Methods]60 experimental mice were selected and then randomly divided into normal control,model group and positive group( bifendate 120 mg/kg),high-dose arabinose + mannose group( 800 mg/kg),middle-dose arabinose + mannose group( 400 mg/kg) and low-dose arabinose + mannose group( 200 mg/kg),each group had 10 mice,which were fed adaptively for 1 week. Except normal control group and model group,each treatment group was given medicine by gavage once a day and lasted for7 days according to the dosage of 20 ml/kg. After the last drug,except normal control group,the mice of other groups were injected 10 ml/kg0. 12% CC14 peanut oil through enterocoelia,thereby establishing acute liver injury model. The mice were fasted but not water for 24 h,after that,blood was sampled from mice eyes,then dissected rapidly. The activities of ALT and AST in the serum were determined,the expression levels of TNF-α,IL-1β and IL-6 from the hepatic tissues were detected by enzyme-linked immunosorbent assay( ELISA); then after HE dye,the changes of liver histopathology were observed. [Results]Compared with CCl_4 model,the activities of ALT and AST from the serum of mice from high-dose and middle dose groups decreased significantly( P < 0. 01); the contents of TNF-α,IL-1β and IL-6 from the hepatic tissues of mice decreased significantly( P < 0. 01); the pathological section showed that the liver injury of mice from the combined drug groups showed alleviating trend to varying degrees,in which the liver injury of mice from the high-dose group was the best. [Conclusions] Arabinose + mannose has an obvious protective effect on mice with acute liver injury induced by CCl_4,and its mechanism may relate to anti-inflammatory.

Protective effects of NYG-1 on CCl4-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.

Portulaca oleracea alleviates CCl4-induced acute liver injury by regulating hepatic S100A8 and S100A9

Objective: Acute liver injury(ALF) is a potential factor of many serious hepatopathies. Carbon tetrachloride(CCl4) is a possible environmental toxicant that can induce ALF. Portulaca oleracea(PO) is one of the most popular edible herbs and has several biological activities such as antioxidant, antimicrobial, antiinflammatory effects. We explored the significance of PO in regulating inflammatory function in animal models and cultured hepatocytes during liver damage caused by CCl4.Methods: The effect of PO on ALF was evaluated by CCl4-induced mice models in vivo. Hepatic levels of transaminase activities and inflammatory factors were examined. The gene and protein expression of S100A8 and S100A9 were measured by RT-PCR and Western blot analysis. Meanwhile, the efficacy of PO was certified by HepG2 cells in vitro. The transaminase activities, inflammatory factors, and the protein expression of S100A8 and S100A9 were also detected.Results: Animal tests showed that pretreatment with PO reduced the liver pathological tissue damage and the serum levels of ALT, AST, ALT and LDH, as well as reducing the pro-inflammatory cytokines(IL-1β, IL-6, TNF-a) secretion in CCl4-induced liver injury mice. Simultaneously, Hep G2 cells pretreated with PO exhibited a significant decrease in the activities of ALT and AST. Moreover, PO resulted in a significant downregulation of the pro-inflammatory markers S100A8, S100A9 gene and protein expression on CCl4induced acute liver injury was demonstrated entirely in vivo and vitro experiments.Conclusion: PO may down-regulate S100A8 and S100A9 and inhibit pro-inflammatory cytokines’ release,indicating a potential clinical effect for controlling the disease.

The new antioxidant 1-benzoyl-6-hydroxy-2,2,4-trimethyl-1,2- dihydroquinoline has a protective effect against carbon tetrachloride-induced hepatic injury in rats

Liver diseases with the central pathogenetic mechanism of oxidative stress are one of the main causes of mortality worldwide.Therefore,dihydroquinoline derivatives,which are precursors of hepatoprotectors and have antioxidant activity,are of interest.We have previously found that some compounds in this class have the ability to normalize redox homeostasis under experimental conditions.Here,we initially analyzed the hepatoprotective potential of the dihydroquinoline derivative 1-benzoyl-6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline(BHDQ)for carbon tetrachloride(CCl4)-induced liver injury in rats.Results suggested that BHDQ normalized the alanine aminotransferase,aspartate aminotransferase,and gamma-glutamyl transpeptidase in serum.We also observed an improvement in liver tissue morphology related to BHDQ.Animals with CCl4-induced liver injuries treated with BHDQ had less oxidative stress compared to animals with CCl4-induced liver injury.BHDQ promoted activation changes in superoxide dismutase,catalase,glutathione peroxidase,glutathione reductase,and glutathione transferase on control values in animals with CCl4-induced liver injury.BHDQ also activated gene transcription in Sod1 and Gpx1 via nuclear factor erythroid 2-related factor 2 and forkhead box protein O1 factors.Therefore,the compound of concern has a hepatoprotective effect by inhibiting the development of necrotic processes in the liver tissue,through antioxidation.

小分子多肽LK-5对CCl4致急性肝损伤小鼠的保护作用研究

【目的】研究小分子多肽LK-5(氨基酸序列为LHMFK)对CCl4致急性肝损伤模型小鼠的保护作用,探讨其作用机制。【方法】72只小鼠随机分为正常组、模型组、联苯双酯组(150 mg/kg)及LK-5低、中、高剂量组(30、60、120 mg/kg),每组12只。连续给药10 d, 1次/d,每次10 mL/kg。末次给药2 h后,各组(除正常组外)腹腔注射0.1%CCl4花生油溶液,建立CCl4致小鼠急性肝损伤模型,16 h后,按照试剂盒方法,检测小鼠血清天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、总胆汁酸(TBA)和碱性磷酸酶(AKP)水平,检测肝脏超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、肿瘤坏死因子(TNF-α)、白细胞介素-6(IL-6)、IL-10、血管紧张素1-7(Ang 1-7)和血管紧张素Ⅱ(AngⅡ)水平。制作肝脏病理组织切片,苏木精-伊红染色(HE)后观察肝脏组织病理学变化。【结果】与正常组比较,模型组小鼠肝细胞有明显的脂肪变性,炎细胞分散分布于肝小叶血管周围和肝实质内,血清ALT、AST、AKP活性和TBA水平均显著上升,肝组织SOD、GSH-Px活性显著下降,MDA水平显著上升(P<0.05),说明成功建立急性肝损伤模型,TNF-α、IL-6、AngⅡ水平显著升高(P<0.05)。与模型组比较,LK-5中、高剂量组能够显著降低血清ALT、AST活性(P<0.05),各剂量组均可降低血清TBA水平和AKP活性(P<0.05),LK-5高剂量组能够显著提高小鼠肝组织SOD、GSH-Px活性(P<0.05),LK-5中、高剂量组能够显著降低肝组织MDA水平(P<0.05),LK-5高剂量组TNF-α水平显著降低(P<0.05),各剂量组能够显著降低肝组织IL-6、AngⅡ水平(P<0.05)。病理切片结果显示,LK-5各剂量组炎细胞均有不同程度减少,LK-5高剂量组肝小叶血管周围和肝实质内无炎细胞浸润。【结论】LK-5各剂量组对CCl4致急性肝损伤小鼠具有保护作用,其中60、120 mg/kg LK-5效果更为明显,其作用机制可能与抗氧化、抗炎及对肾素-血管紧张素系统(RAS)的调控有关。

黄芩苷镁盐对CCl4诱导的SD大鼠急性肝损伤的影响

目的探讨黄芩苷镁盐对四氯化碳(CCl4)诱导的SD大鼠急性肝损伤的影响及有效的治疗浓度。方法80只SD大鼠,随机分为正常对照组、模型组、阳性对照组〔异甘草酸镁,18mg/(kg·d)〕及黄芩苷镁盐Ⅰ〔12.5mg/(kg·d)〕、Ⅱ〔25.0mg/(kg·d)〕、Ⅲ〔50.0mg/(kg·d)〕、Ⅳ〔100.0mg/(kg·d)〕、Ⅴ〔200.0mg(kg·d)〕组。连续尾静脉注射1w。末次给药2h,除正常对照组外,其余组腹腔注射1ml/kg50%CCl4橄榄油溶液造模。采用苏木素-伊红(HE)染色观察肝组织病理改变,全自动生化检测各组血清中天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)的变化情况,丙二醛(MDA)测定试剂盒检测各组MDA的水平变化。结果模型组肝细胞结构破坏明显,各组黄芩苷镁盐肝细胞结构较模型组有所改善,尤以黄芩苷镁盐Ⅲ、Ⅳ、Ⅴ组肝细胞改善明显。模型组ALT、AST水平显著高于正常对照组(P<0.01)。黄芩苷镁盐Ⅲ、Ⅳ、Ⅴ组ALT、AST水平均显著低于模型组(P<0.05)。与阳性对照组相比,黄芩苷镁盐Ⅲ、Ⅳ、Ⅴ组ALT水平均显著性降低(P<0.05),但AST两者无显著区别(P>0.05)。模型组MDA水平显著高于正常对照组(P<0.01)。黄芩苷镁盐Ⅲ、Ⅳ、Ⅴ组均可显著降低肝组织MDA水平(P<0.05)。与阳性对照组相比,黄芩苷镁盐Ⅳ、Ⅴ组MDA降低水平无显著区别(P>0.05)。结论黄芩苷镁盐可减轻CCl4对SD大鼠造成的急性肝损伤,100.0mg/(kg·d)的给药剂量效果较好。

山荷降脂方对CCl_4诱导的小鼠急性肝损伤的保护作用

目的 :探讨山荷降脂方对CCl4 诱导的小鼠急性肝损伤的保护作用。方法 :用腹腔注射CCl4 法制作小鼠肝损伤模型。实验动物随机分为①正常对照组 ;②假肝损伤组 ;③肝损伤组 ;④生理盐水 +肝损伤组 ;⑤山荷降脂方 (低剂量 ) +肝损伤组 ;⑥山荷降脂方 (中剂量 ) +肝损伤组 ;⑦山荷降脂方 (高剂量 ) +肝损伤组。末次给药后 0 .5～ 1h ,腹腔注射质量分数为 0 .12 %的CCl4 花生油溶液(剂量为 0 .0 1mL/g) ,禁食 16h后处死。取肝脏 ,进行HE染色 ;球后取血 ,离心血清 ,测谷丙转氨酶、谷草转氨酶活性。结果 :(1)谷丙转氨酶、谷草转氨酶活性 :⑤、⑥、⑦组与③组比较有显著性差异 (P=0 .0 0 0 1) ,⑤、⑥、⑦组两两之间也有显著性差异 (P =0 .0 0 0 1)。 (2 )HE染色 ,光镜下观察肝脏组织病理学变化 ,⑥、⑦组肝损伤程度与③组比较 ,有显著性差异 (P <0 .0 1;P <0 .0 0 1) ,⑤、⑥组与⑦组也有显著性差异 (P <0 .0 0 1,P <0 .0 5 )。结论 :山荷降脂方对急性肝损伤具有呈量效关系的保护作用。

杨桃果提取物对CCl_4所致小鼠急性肝损伤的保护作用

目的:研究杨桃果提取物(YTGE)对小鼠急性肝损伤的保护作用。方法:将60只昆明种小鼠随机分为正常对照组,模型对照组,YTGE高剂量(YTGEH)、YTGE中剂量(YTGEM)、YTGE低剂量(YTGEL)组,阳性药联苯双酯组(阳性对照组),每组10只。小鼠经YTGE预处理7d后,采用腹腔注射四氯化碳(CCl4)建立小鼠急性肝损伤模型,用比色分析法测定小鼠血清丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)的活性;测定小鼠肝匀浆超氧化物歧化酶(SOD)的活性及丙二醛(MDA)的含量;HE染色观察各组小鼠肝细胞损伤程度。结果:与模型对照组比较,YTGE能降低CCl4所致急性肝损伤小鼠血清ALT和AST(P<0.01或P<0.05);升高小鼠肝匀浆SOD的活性,降低MDA的含量(P<0.01或P<0.05);能够减轻肝细胞损伤程度。结论:YTGE对CCl4所致小鼠急性肝损伤有保护作用,其机制可能与其抗氧自由基和抑制脂质过氧化作用有关。

空心莲子草醇提物抗CCl_4肝损伤的实验研究

目的 :观察空心莲子草醇提物对CCl4 肝损伤的保护作用。方法 :给小鼠腹腔注射CCl4 制成肝损伤模型 ,分为 3组 ,每组 10只。分别经口给予生理盐水、空心莲子草醇提物 (0 0 2g g)和联苯双酯 (0 2mg g)。连续用药6天后 ,第 7天将小鼠断头处死 ,取血和肝脏 ,分别测定空白对照组、空心莲子草组和联苯双酯组小白鼠的血清ALT和血清AST、肝指数及肝细胞镜检 ,并进行比较。结果 :空心莲子草组能明显对抗CCl4 引起的血清ALT和血清AST增高 ,减轻CCl4 对肝细胞的损伤。空白对照组与联苯双酯组和空心莲子草组比较均有显著性差异 (P <0 0 1)。结论 :空心莲子草醇提物对CCl4

脂糖舒对CCl_4所致大鼠肝损伤的保护作用

目的探讨脂糖舒对实验性损伤的保护作用。方法建立大鼠CCL4 肝损伤模型 ,将大鼠随机分为正常组、模型组、治疗组。治疗组于建模后灌胃施药。检测丙氨酸转氨酶 (ALT) ,观察肝脏病理学变化。结果脂糖舒可以抑制CCl4 导致的大鼠血清ALT升高 ,使肝细胞变性、坏死得到明显的改善和恢复。

在急性肝损伤状态下蒙药地格达-4味汤、栀子加肋柱花药对及栀子单味药中栀子苷血清含量的动态观察

目的:通过血清药物化学方法,追踪观察单味药、药对及全方中入血指标性化学成分栀子苷在急性肝损伤大鼠体内的动态变化,揭示栀子单味药在地格达-4味汤中的作用和地位,并初步探讨地格达-4味汤保肝效应的有效成分。方法:色谱条件:Dimaonsil C18柱(250 mm×4.6 mm,5μm);流动相:甲醇-0.1%磷酸水溶液(22:78);流速:1 m L·min-1;柱温:30℃;波长:238nm;选择急性肝损伤大鼠为研究对象,地格达-4味汤、栀子加肋柱花药对及栀子单味药为示例药物观察给药后不同时间点的血清中栀子苷含量变化。结果:栀子与肋柱花药对相应时间点血中栀子苷含量均高于单味栀子和全方;地格达-4味汤全方相应时间点血中栀子苷含量均低于单味栀子及药对。结论:经方法学考察,本试验方法简单、易行,实验结果可靠,可用于含栀子苷血清的测定;栀子与肋柱花组合产生了增强栀子苷含量的作用而栀子与肋柱花、瞿麦、胡黄连组合产生了消弱栀子苷含量的作用。

星蒌承气汤对急性脑出血大鼠肝、肠系膜淋巴结IRAK-4 mRNA表达的影响

目的:研究白细胞介素-1受体相关激酶-4(IRAK-4)活性对急性脑出血应激性肝损害的影响,以及星蒌陈气汤的靶向调控机制。方法:采用大脑注射Ⅶ型胶原酶法建立SD大鼠急性脑出血模型,随机分为正常组、脑出血组、脑出血痰热腑实证组、星蒌承气汤组,每组分24 h、48 h、72 h三个时间亚组,实时荧光定量PCR观察肝组织、肠系膜淋巴结IRAK-4 mRNA表达,并观察肝组织HE染色结果。结果:脑出血组、脑出血痰热腑实证组肝组织及肠系膜淋巴结IRAK-4 mRNA在三个不同时间点表达较正常组升高,星蒌承气汤组肝组织IRAK-4 mRNA表达较脑出血痰热腑实证组降低,星蒌承气汤组还能明显减轻肝组织病理损伤。结论:星蒌承气汤对脑出血急性期痰热腑实证肝脏具有一定的保护作用。

在急性肝损伤状态下地格达-4味汤血中三种移行成分动态观察

目的:建立地格达-4味汤血中三种移行成分的HPLC检测方法.方法:将蒙药地格达-4味汤水提物灌胃给予D-GlaN致急性肝损伤模型大鼠后,在不同时间点取血,离心分离血清,以高效液相色谱(HPLC)法测定獐牙菜苦苷、栀子苷、胡黄连苷Ⅱ含量.结果:在HPLC含量分析中,血中獐牙菜苦苷、栀子苷及胡黄连苷Ⅱ均具有良好的线性关系,在急性肝损伤状态下大鼠血清不同时间点均能检测到三种化学成分,而且在30min-1h内含量较高.结论:三种成分可作为地格达-4味汤质量控制及物质基础研究的有效指标.

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

AIM： To investigate the possible mechanism of the protective effects of a bioactive fraction, Ganoderma lucidum proteoglycan （GLPG）isolated from Ganoderma luddum mycelia, against carbon tetrachloride-induced liver injury. METHODS： A liver injury model was induced by carbon tetrachloride. Cytotoxicity was measured by MTY 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-α were determined following the instructions of SOD kit and TNF radioimmunoassay kit. Uver sections were stained with hematoxylin and eosin （H＆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 （CCh） 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 CCh with or without GLPG pretreatment indicated that GLPG can significantly suppress the toxicity induced by CCh in mice liver. We also found that GLPG reduced TNF-α level induced by CCh 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 antihepatotoxic mechanisms may be related to the suppression of TNF-α level and the free radical scavenging activity.

蝙蝠草醇提物对四氯化碳所致大鼠急性肝损伤的影响

研究蝙蝠草醇提物对四氯化碳(CCl_(4))所致大鼠急性肝损伤的保护作用及其机制。40只雄性SD大鼠随机分为5组,包括正常组、模型组、水飞蓟素组(120 mg/kg)、蝙蝠草醇提物组(260和520 mg/kg),连续灌胃给药15 d。于第14天,除正常组外,其余大鼠腹腔注射12%CCl_(4)(5 mL/kg)建立急性肝损伤模型。造模24 h后,采血剖检大鼠,并计算肝指数,检测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)水平,检测肝组织白介素-1β(IL-1β)、IL-6、肿瘤坏死因子α(TNF-α)、超氧化物歧化酶(SOD)、丙二醛(MDA)和谷胱甘肽(GSH)水平,HE染色观察肝组织病理学改变。结果显示,蝙蝠草醇提物各剂量组均可降低肝指数(P<0.05),降低血清AST、ALT和肝组织IL-1β、IL-6、TNF-α和MDA水平(P<0.05),升高肝组织SOD、GSH水平(P<0.05),明显改善肝组织病理学损伤。认为,蝙蝠草醇提物对CCl_(4)所致急性肝损伤具有良好的保护作用,可减轻肝损伤,其机制可能与增强肝功能,促进组织修复,降低促炎因子水平和增强机体抗氧化损伤能力有关。

逍遥散对急性肝损伤大鼠模型保护作用的代谢组学研究

目的:运用代谢组学方法探讨逍遥散对急性肝损伤的保护作用机理。方法:雄性大鼠连续7 d灌胃给予逍遥散水煎液,第7天给药1 h后腹腔注射0.2%CCl4花生油溶液,禁食不禁水16 h取肝组织进行病理学检查,取血清以柱前衍生-气质联用技术检测血清中代谢产物变化,运用质谱解析、主成分分析(PCA)等多元统计技术分析差异代谢产物,解析内源性代谢产物的变化。结果:与正常对照组比较,模型组大鼠肝组织明显破坏,可见明显的结节状再生细胞,血清中丙氨酸、甘氨酸、丝氨酸、苏氨酸、氨基丙二酸、苹果酸、天冬氨酸、鸟氨酸、赖氨酸、肌醇、谷氨酰胺等浓度均显著升高,逍遥散保护组各项指标均明显回调。结论:逍遥散对于急性肝损伤具有较好的治疗作用,调节脂肪酸代谢、促进氨基酸生成可能是其治疗急性肝损伤的作用机理。

肝勃宁对四氯化碳致大鼠慢性肝损害的保护作用

四氯化碳（ＣＣｌ４）致大鼠慢性肝损害，用肝勃宁（ＧＢＮ）２．３１，０．７７，０．２６ｇ／ｋｇ分别给大鼠每天１次ｉｇ，连续４５天。经病理学检查显示能减轻肝纤维化程度，肝脂肪变、嗜酸性坏死发生率明显减少；血清总蛋白量增高，ＳＧＰＴ、ＳＧＯＴ、唾液酸浓度、羟脯氨酸含量下降。结果表明ＧＢＮ对ＣＣｌ４致大鼠慢性肝损害有一定保护作用。

儿茶素类化合物对四氯化碳致大鼠慢性肝损伤的保护作用

目的 观察儿茶素类化合物保肝降酶的作用。方法 制备大鼠的四氯化碳 (CCl4)慢性肝损伤模型 ,观察儿茶素类化合物对肝损伤大鼠血清丙氨酸转氨酶 (ALT)、天冬氨酸转氨酶 (AST)、丙二醛 (MDA)等的影响 ,以及肝组织羟脯氨酸含量和肝脏组织结构的变化。结果 儿茶素类化合物给药 2个月后 ,中、高剂量给药组 (10 0 ,2 0 0mg/kg)均能降低血清ALT的活力以及脂质过氧化产物MDA和肝组织羟脯氨酸的含量 (P <0 0 1或P <0 0 5 ) ,其降低肝组织羟脯氨酸含量的作用与联苯双酯相当。肝组织的病理改善情况两药相似 ,而抗膜脂质过氧化作用优于联苯双酯。结论 儿茶素类化合物具有保护化学性肝损伤作用 ,有降低转氨酶活力。

委陵菜对四氯化碳致小鼠肝损伤保护作用

目的 :研究委陵菜对四氯化碳 (CCl4)致小鼠急性肝损伤的保护作用。方法 :用委陵菜给小鼠灌胃 7天 ,观察对四氯化碳致小鼠肝损伤所引起血清谷丙转氨酶和谷草转免酶升高、肝脂质过氧化物含量的影响。结果 :委陵菜能明显降低模型组的血清转氨酶、肝脂质过氧化物含量。结论

三叶委陵菜对四氯化碳致小鼠肝损伤保护作用

目的 :研究三叶委陵菜对四氯化碳 (CCl4)致小鼠急性肝损伤的保护作用。方法 :用三叶委陵菜给小鼠灌胃 7d,观察对四氯化碳致小鼠肝损伤所引起血清谷丙转氨酶和谷草转氨酶升高、肝线粒体脂质过氧化物含量的影响。结果 :三叶委陵菜能明显降低模型组的血清转氨酶、肝线粒体脂质过氧化物含量。结论