基于方剂配伍含药血清“谱-效关系”的茵陈蒿汤保肝作用药效物质研究

目的：初步阐明茵陈蒿汤保肝作用的药效物质。方法：SD大鼠灌胃制备茵陈蒿汤及其各单味药、各缺味方含药血清,一方面采用已建立的方法测定不同方剂配伍含药血清HPLC指纹图谱;另一方面建立H₂O₂诱导的HL-7702肝细胞损伤模型,并对不同方剂配伍含药血清进行保肝作用药效评价,最后分别采用双变量相关性分析和多元回归分析,指认含药血清指纹图谱中与药效相关的色谱峰。结果：茵陈蒿汤含药血清指纹图谱中6号峰与肝细胞保护作用明显相关,1~6,8,9,11,20号峰与肝细胞保护作用有一定关系。结论：茵陈蒿汤保肝作用的药效物质主要包括来源于大黄的蒽醌类成分及体内代谢产物、来源于栀子的环烯醚萜类成分及体内代谢产物和西红花酸类成分体内代谢产物,其中1个蒽醌类成分体内代谢产物活性较强。     

小柴胡汤和柴胡—黄芩含药血清对CCl_4损伤肝细胞的影响

目的　建立CCl4肝细胞损伤模型 ,考察小柴胡汤及柴胡—黄芩配方含药血清对CCl4损伤肝细胞的保护作用。方法　制备小柴胡汤及柴胡—黄芩配方的大鼠含药血清 ,体外10mol·L-1CCl4诱导肝细胞损伤模型 ,观察体积分数为 0 1的含药血清对损伤肝细胞增殖率、GPT、细胞形态学以及凋亡率的影响。结果　与正常组比较 ,模型组肝细胞增殖率降低 (P <0 0 1) ,细胞培养上清液中GPT含量升高 (P <0 0 1) ;与模型组比较 ,小柴胡汤及柴胡—黄芩配方组的肝细胞增殖率提高 (P <0 0 1) ,细胞培养上清液中GPT含量降低 (P <0 0 1)。倒置显微镜和Giemsa染色观察到模型组肝细胞存在着明显的坏死和凋亡 ,小柴胡汤及柴胡—黄芩配方的凋亡细胞明显减少。与正常组比较 ,CCL4模型组细胞凋亡增高 (P <0 0 1) ;与模型组比较 ,柴芩组和小柴胡汤全方组的细胞凋亡率降低 (P <0 0 1)。结论　小柴胡汤及柴胡—黄芩配方含药血清对体外CCl4诱导的肝细胞损伤有保护作用。CCl4引起的肝损伤同时存在着明显的凋亡和坏死 ,小柴胡汤及柴胡 -黄芩配方可能具有抗CCl4诱导的肝细胞凋亡的作用。     

茵陈蒿汤对实验性肝纤维化大鼠肝细胞的保护作用及超微结构观察

目的 :观察茵陈蒿汤对实验性肝纤维化大鼠肝细胞损伤的保护作用及超微结构变化。方法 :Wistar大鼠被随机分为 4组 :正常对照组、CCl4 模型组、秋水仙碱组、茵陈蒿汤组。采用 4 0 % CCl4 皮下注射制备大鼠实验性肝纤维化模型 ,观察茵陈蒿汤对肝功能、肝脏组织病理变化和超微结构变化的影响。结果 :茵陈蒿汤能明显改善实验性肝纤维化大鼠的肝功能、肝脏组织病理变化和超微结构变化 ,与 CCl4 组比较差异有显著性意义 (P <0 .0 5 )。结论 :茵陈蒿汤对 CCl4 损伤性肝细胞有保护作用 ,可改善肝功能 ,对线粒体等细胞器的损伤具有保护作用     

基于含药血清经时谱效关系的茵陈蒿汤保肝作用药效物质研究

目的：阐明茵陈蒿汤的保肝作用药效物质。方法：以SD大鼠为供体制备茵陈蒿汤灌胃给药后10个时间点含药血清,高效液相色谱法（HPLC）测定含药血清指纹图谱,采用HL-7702肝细胞损伤模型对含药血清进行保肝作用药效评价,分别采用药时曲线和时效曲线比较及双变量相关性分析的谱-效关系分析方法指认含药血清指纹图谱中与药效相关的色谱峰。结果：药时曲线和时效曲线比较发现,含药血清指纹图谱中4~7、20号峰对损伤肝细胞具有明显保护作用,8、11~19号峰对损伤肝细胞具有保护作用,但可能也具有一定肝细胞毒性有关,1~3及9号峰具有肝细胞毒性;双变量相关性分析发现,含药血清指纹图谱中1~9、15~17、20号峰对损伤肝细胞具有一定保护作用,其中4、5、20号峰活性较强,6号峰活性最强。结论：茵陈蒿汤保肝作用的药效物质主要包括来源于大黄的蒽醌类成分、来源于栀子的环烯醚萜类成分和西红花酸类成分及以上三类成分的体内代谢产物,其中1个蒽醌类成分、1个蒽醌类成分代谢产物和1个西红花酸类成分代谢产物活性较强,另1个蒽醌类成分代谢产物活性最强。但以上三类成分剂量较高时也具有一定肝细胞毒性,即具有肝细胞保护和毒性双重作用。     

海风藤挥发油含药血清影响小鼠脾细胞增殖的实验性研究

目的 研究不同条件下制备的海风藤挥发油含药血清对BLAB/c小鼠脾淋巴细胞增殖作用的影响.方法 大鼠口服海风藤挥发油溶液3天,末次给药后1h--3h取血,采用MTT法观察制备的含药血清对刀豆蛋白(ConA)、脂多糖(LPS)诱导的T、B淋巴细胞的异常增殖的影响.结论实验结果显示海风藤挥发油含药血清能显著抑制ConA、L...     

加味茵陈汤含药血清制备及其对体外肝细胞损伤模型的作用

目的：探索加味茵陈汤含药血清的制备方法及其对体外培养大鼠肝细胞损伤模型的作用。方法：制备加味茵陈汤（茵陈、栀子、大黄、三七、丹参、赤芍、生地、丹皮、白芍、柴胡）汤剂（2 g生药/ml）;大鼠中药灌胃（30 g/kg,2次/d,连续3 d）制备药物血清;改进Seglen胶原酶原位灌注分离大鼠肝细胞,培养体系中加入D-氨基半乳糖（25μg/ml）诱导肝细胞损伤模型,以不同浓度（5%、10%1、5%）加入药物血清培养24 h,于培养1、36、1、2和24 h取上清液测定ALT、AST和LDH,同步测定肝细胞的MTT反应,并于倒置相差显微镜下观察肝细胞形态变化。结果：从各时间点观察,随含中药血清浓度的增加,肝细胞培养上清液ALT、AST、LDH水平逐渐下降,10%药物血清与15%药物血清剂量组之间在各时间点比较无统计学差异（P〉0.05）,其余各组比较统计学差异均有显著性（P〈0.05）,培养肝细胞增殖活性则呈升高趋势。结论：大鼠的含中药血清可以降低肝细胞损伤模型AST、ALT及LDH等指标,增加细胞活性指标,随浓度增加而作用增强。     

异甘草素对大鼠急性化学性肝损伤的保护作用

目的研究异甘草素(ISL)对CCl4所致大鼠急性化学性肝损伤的保护作用及其机制.方法①在体实验选用♂Wistar大鼠48只,随机分6组,每组8只.ISL三剂量给药组分别灌服ISL 10,20,40 mg·kg-1·d-1;甘草酸二铵胶囊(DG)组灌服DG 500 mg·kg-1·d-1;正常对照组和模型组每日灌服等容量的溶媒.连续给药7 d,qd.以CCl4诱导大鼠急性肝损伤模型,酶学测定各组大鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)和超氧化物歧化酶(SOD)活性,以及肝组织丙二醛(MDA)、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)含量.②体外实验采用大鼠离体肝细胞原代培养,并建立CCl4诱导肝细胞损伤模型,检测ISL对其作用的影响.结果①lSL剂量依赖性降低大鼠血清中升高的ALT和AST活性,升高肝组织中降低的GSH含量、SOD和GSH-Px活性,同时降低过氧化物终产物含量.②ISL浓度(5.0～20.0 μmol·L-1)依赖性抑制CCl4引起的ALT和AST升高,ISL 20.0 μmol·L-1可阻断CCl4产生的肝细胞ALT和AST漏出.结论ISL对大鼠化学性肝损伤具有显著的保护作用.其机制与清除肝组织中的自由基和抗脂质过氧化等作用有关.     

乙酰半胱氨酸对四氯化碳诱导的原代培养大鼠肝细胞损伤的保护作用

目的观察乙酰半胱氨酸（NAC）对四氯化碳（CCl4）诱导的原代培养大鼠肝细胞损伤的作用。方法在24孔细胞培养板上,用CCl4诱导原代培养肝细胞损伤,分别加入不同浓度的NAC,培养20 h后,测定上清液谷草转移酶（AST）活性,并MTT法检测细胞活力。结果 NAC在100μmol.L-1内,对正常培养的大鼠肝细胞没有影响;在4～100μmol.L-1内,NAC能剂量依赖性地抑制CCl4诱导的肝细胞活性的降低,EC50约为20μmol.L-1;当浓度为100μmol.L-1时,可以逆转CCl4诱导的肝损伤,使肝细胞释放AST降到接近正常水平,并明显改善肝细胞形态学变化。结论 NAC对CCl4诱导的肝损伤具有保护作用。     

制首乌含药血清对L02肝细胞增殖和凋亡的影响

目的: 研究制首乌含药血清对L02肝细胞增殖和凋亡的影响。方法: 采用皮下注射氢化可的松,建立大鼠肾阴虚模型,分为空白对照组、制首乌低、中、高剂量组(10.8,21.6,43.2 g·kg^-1)。连续给药7 d后处死大鼠,制备含药血清。分别采用MTT法测定L02肝细胞线粒体功能、流式细胞术检测肝细胞凋亡率及显微镜观察肝细胞形态结构。结果: 15%的肾阴虚高剂量组含药血清作用48 h后对L02肝细胞增殖具有明显抑制作用,抑制率为16.83%(P<0.05)。肾阴虚中、高剂量组的细胞凋亡率显著性升高,分别为19.6%(P<0.05)和27.8%(P<0.01)。结论: 制首乌对证治疗肾阴虚证侯,当给药剂量超过21.6 g·kg^-1时,对肝细胞的毒性明显增强。     

氧化苦参碱对卵巢癌HO8910细胞凋亡影响的血清药理学研究

目的探讨氧化苦参碱体内生物转化及含氧化苦参碱血清对人卵巢癌细胞HO8910的诱导凋亡作用机制。方法采用中药血清药理学实验方法,获得大鼠含氧化苦参碱血清,通过HPLC测定含药血清中氧化苦参碱的生物转化情况,通过MTT法、荧光显微镜、DNA琼脂糖凝胶电泳测定含药血清对人卵巢癌HO8910细胞的诱导凋亡作用,流式细胞术检测含药血清作用后细胞周期时相分布。结果给药大鼠血清中出现保留时间为10.8m in的氧化苦参碱峰图,且血清提取液中氧化苦参碱的浓度为40μg/mL,含氧化苦参碱血清能抑制HO8910细胞生长,经含药血清处理的细胞48h出现典型的细胞凋亡形态学变化和DNA片段的梯形条带,HO8910细胞被阻滞在G0-G1期。结论氧化苦参碱经肌注体内生物转化后,血清中的主要代谢成分仍保持不变,含氧化苦参碱血清也具有诱导HO8910细胞凋亡的作用。     

不同剂型的垂盆草对急性肝损伤大鼠的防治作用

目的 探讨不同剂型的垂盆草对大鼠四氯化碳（CCl₄）急性肝损伤模型的保护作用。方法 Wistar大鼠80只,随机分成正常组、模型组、鲜垂盆草榨汁高、低剂量组及鲜垂盆草煎煮组、干垂盆草煎煮组、垂盆草颗粒组、垂盆草配方颗粒组。ig给药,1 次/d,连续7 d。第7天,除正常组外,给予大鼠ip 50% CCl₄橄榄油造模。观察大鼠的一般情况,检测肝功能指标总胆红素（Tbil）、丙氨酸氨基转移酶（ALT）、门冬氨酸氨基转移酶（AST）及肝组织丙二醛（MDA）、超氧化物歧化酶（SOD）、一氧化氮（NO）的含量和肝脏组织学变化情况。结果 干垂盆草煎煮组可显著降低大鼠肝质量。干垂盆草煎煮组、垂盆草颗粒组、垂盆草配方颗粒组均能降低大鼠血清ALT水平,干垂盆草煎煮组能降低大鼠血清AST水平。干垂盆草煎煮组、垂盆草颗粒组和垂盆草配方颗粒组均可降低大鼠肝组织MDA、NO的含量,提高大鼠肝组织SOD活力。干垂盆草煎煮组、垂盆草颗粒组、垂盆草配方颗粒组显著改善肝小叶细胞的变性和炎症坏死,减轻汇管区的炎细胞浸润。结论 干垂盆草煎煮液、垂盆草颗粒、垂盆草配方颗粒可保护CCl₄导致的大鼠急性肝损伤,且起到抗脂质过氧化的作用。     

Proliferation of Hepatocytes and Attenuation from Carbon Tetrachloride Hepatotoxicity by Gadolinium Chloride in Rats

Abstract: Intravenous injection of gadolinium chloride (GdCl₃) at a dose of 10 mg/kg caused an increase in proliferating cell nuclear antigen labeling index and the grade of pyronin positivity (RNA level) in rat liver. In CCl₄-exposed rats, pretreatment with GdCl₃ also showed a preventive effect of the liver injury both biochemically and histologically. Moreover, the proliferative action preceded the attenuative effect of the liver injury. Results suggest that GdCl₃ induces hepatocyte proliferation, and this action of GdCl₃ may modify the development of CCl₄-induced liver injury.     

Delayed liver injury and impaired hepatocyte proliferation after carbon tetrachloride exposure in BPOZ2-deficient mice

BPOZ2 is a tumor suppressive mediator in PTEN signaling pathway and plays an important role in cell proliferation. In this study, we investigated the physiology functions of BPOZ2 in CCl₄-induced liver injury and hepatocyte proliferation afterwards. After acute CCl₄ administration, BPOZ2 null mice exhibited delayed liver injury and impaired hepatocyte proliferation, which was accompanied by altered kinetics of CYP2E1 protein expression, compromised cyclin D1 expression and shortened duration of ERK activation. These results for the first time define that BPOZ2 is an important regulator involved in the injury and repair process induced by acute CC1₄ administration in mouse liver.     

Hepatoprotective effect of methylsulfonylmethane against carbon tetrachloride-induced acute liver injury in rats

This study evaluated the effect of methylsulfonylmethane (MSM) on carbon tetrachloride (CCl₄)-induced acute liver injury in rats. A single injection of CCl₄ (2 ml/kg, i.p.) increased serum aminotransferases (ALT and AST) activities. In addition, CCl₄ treatment led to elevation of hepatic malondialdehyde (MDA) content as well as decrease in superoxide dismutase (SOD) and catalase (CAT) activities. Furthermore, cytochrome P450 2E1 (CYP2E1) content was suppressed while proinflammatory cytokines tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels increased in liver tissue after CCl₄ administration. We showed that acute CCl₄-induced damage was accompanied by a rise in Bax/Bcl₂ ratio indicating apoptosis. Pre-treatment with MSM (400 mg/kg) inhibited the increases of serum ALT and AST activities, decreased hepatic MDA, TNF-α, IL-6 and Bax/Bcl₂ ratio compared to CCl₄ treated group. On the other hand, MSM raised SOD and CAT activities as well as CYP2E1 level in liver tissues. The present study shows that MSM possesses a hepatoprotective effect against CCl₄-induced liver injury in rats. This protective effect might be through its antioxidant, anti-inflammatory and antiapoptotic properties.     

Carbon tetrachloride-induced hepatotoxicity in rat is reversed by treatment with riboflavin

Liver is a vital organ for the detoxification of toxic substances present in the body and hepatic injury is associated with excessive exposure to toxicants. The present study was designed to evaluate the possible hepatoprotective effects of riboflavin against carbon tetrachloride (CCl₄) induced hepatic injury in rats. Rats were divided into six groups. Hepatotoxicity was induced by the administration of a single intraperitoneal dose of CCl₄ in experimental rats. Riboflavin was administered at 30 and 100 mg/kg by oral gavage to test its protective effect on hepatic injury biochemically and histopathologically in the blood/liver and liver respectively. The administration of CCl₄ resulted in marked alteration in serum hepatic enzymes (like AST, ALT and ALP), oxidant parameters (like GSH and MDA) and pro-inflammatory cytokine TNF-α release from blood leukocytes indicative of hepatic injury. Changes in serum hepatic enzymes, oxidant parameters and TNF-α production induced by CCl₄ were reversed by riboflavin treatment in a dose dependent manner. Treatment with standard drug, silymarin also reversed CCl₄ induced changes in biomarkers of liver function, oxidant parameters and inflammation. The biochemical observations were paralleled by histopathological findings in rat liver both in the case of CCl₄ and treatment groups. In conclusion, riboflavin produced a protective effect against CCl₄-induced liver damage. Our study suggests that riboflavin may be used as a hepato-protective agent against toxic effects caused by CCl₄ and other chemical agents in the liver.     

Hepatoprotective effect of electrolyzed reduced water against carbon tetrachloride-induced liver damage in mice

The study investigated the protective effect of electrolyzed reduced water (ERW) against carbon tetrachloride (CCl₄)-induced liver damage. Male ICR mice were randomly divided into control, CCl₄, CCl₄ + silymarin, and CCl₄ + ERW groups. CCl₄-induced liver lesions include leukocytes infiltration, hepatocyte necrosis, ballooning degeneration, mitosis, calcification, fibrosis and an increase of serum alanine aminotransferase (ALT), and aminotransferase (AST) activity. In addition, CCl₄ also significantly decreased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). By contrast, ERW or silymarin supplement significantly ameliorated the CCl₄-induced liver lesions, lowered the serum levels of hepatic enzyme markers (ALT and AST) and increased the activities of SOD, catalase, and GSH-Px in liver. Therefore, the results of this study show that ERW can be proposed to protect the liver against CCl₄-induced oxidative damage in mice, and the hepatoprotective effect might be correlated with its antioxidant and free radical scavenging effect.     

茵陈蒿汤及其不同组方提取物对雌激素诱导胆汁淤积大鼠的治疗作用及机制研究

目的：基于肝细胞膜转运体多药耐药相关蛋白1~4（multidrug resistant associated protein 1~4,Mrp1~4）、Na⁺依赖性牛磺胆酸共转运多肽（Na⁺-taurocholate co-transporting polypeptide,Ntcp）,探讨茵陈蒿汤及其不同组方提取物对胆汁淤积大鼠的治疗作用。方法： 30只Wistar雄性大鼠随机分为6组,即正常组、对照组、茵陈组、茵陈栀子组、茵陈大黄组、茵陈蒿汤组;采用皮下连续注射苯甲酸雌二醇（estradio benzoate,EB,5 mg·kg^-1·d^-1）5 d制备胆汁淤积大鼠模型。茵陈组、茵陈栀子组、茵陈大黄组、茵陈蒿汤组分别灌胃给予茵陈（0.43 g·kg^-1·d^-1）、茵陈栀子（1.08 g·kg^-1·d^-1）、茵陈大黄（1.09 g·kg^-1·d^-1）、茵陈蒿汤（1.69 g·kg^-1·d^-1）提取物14 d。干预结束后,测定各组大鼠胆汁流速,血清生化及肝脏病理,并采用Western blot检测肝组织中Mrp1~4和Ntcp的表达。结果：茵陈蒿汤及不同配伍组干预14 d后,胆汁流速均显著升高,血清生化与肝脏病理较对照组均有明显改善;与对照组相比,茵陈组、茵陈栀子组、茵陈大黄组及茵陈蒿汤组Mrp2、Mrp3、Ntcp的表达均升高;Mrp4的表达均降低;此外,茵陈栀子组Mrp1的表达降低。结论：茵陈蒿汤及其不同组方提取物对雌激素诱导的大鼠胆汁淤积均有治疗作用;其疗效可能与调控转运体Mrp1-4和Ntcp的表达相关,且不同组方提取物对Mrp1~4和Ntcp的调控作用不同。     

Methyl helicterate protects against CCl4-induced liver injury in rats by inhibiting oxidative stress,NF-κB activation,Fas/FasL pathway and cytochrome P4502E1 level

This study was designed to investigate the protective effects of the methyl helicterate (MH) isolated from Helicteres angustifolia L. against CCl₄-induced hepatotoxicities in rats. Liver injury was induced in rats by the administration of CCl₄ twice a week for 8 weeks. Compared with the CCl₄ group, MH significantly decreased the activities of ALT, AST and ALP in the serum and increased the activities of SOD, GSH-Px and GSH-Rd in the liver. Moreover, the content of hepatic MDA was reduced. Histological findings also confirmed the anti-hepatotoxic characterisation. In addition, MH significantly inhibited the proinflammatory mediators, such as PGE₂, iNOS, COX-2, IL-6, TNF-α and myeloperoxidase (MPO). Further investigation showed that the inhibitory effect of MH on the proinflammatory cytokines was associated with the downregulation of NF-κB. Besides, MH also markedly decreased the levels of Fas/FasL protein expression and the activities of caspase-3/8, as well as the activity of cytochrome P4502E1 (CYP2E1). In brief, the protective effect of MH against CCl₄-induced hepatic injury may rely on its ability to reduce oxidative stress, suppress inflammatory responses, protect against Fas/FasL-mediated apoptosis and block CYP2El-mediated CCl₄ bioactivation.     

Protective effects of salecan against carbon tetrachloride-induced acute liver injury in mice

Carbon tetrachloride (CCl₄) is a well‐established model for screening hepato‐protective drugs. The aim of the present study was to evaluate the potential protective effects of a novel soluble β‐glucan salecan on acute liver injury induced by CCl₄ in mice and to further explore the underlying mechanisms. Mice were given salecan (40 mg kg^?1) or phosphate‐buffered saline for 3 days prior to treatment with a single intraperitoneal dose of CCl₄ (1 ml kg^?1 body weight). Animals were sacrificed at 0, 12, 24, 48, 72 and 96 h post‐injection of CCl₄. Serum liver enzyme levels, histology, lipid peroxidation, glutathione (GSH) content, expression of antioxidant enzymes and hepatocyte proliferation were subsequently evaluated. The serum levels of hepatic enzyme markers were markedly reduced in the salecan pretreatment group compared with the control group. Histopathological examination of the livers revealed that hepatocellular degeneration and necrosis were significantly attenuated at an early stage during CCl₄ intoxication and liver recovery was markedly accelerated at a later stage in salecan pre‐administered mice. Furthermore, salecan administration remarkably alleviated lipid peroxidation and restored GSH depletion. Meanwhile, the expression of antioxidant genes was significantly elevated in the salecan‐treated group. Interestingly, the administration of salecan remarkably enhanced hepatocyte proliferation in the recovery phase after CCl₄ injection. Taken together, these results demonstrated that salecan exhibits a protective action on acute hepatic injury induced by CCl₄ through attenuating oxidative stress and accelerating hepatocyte regeneration. Copyright © 2011 John Wiley & Sons, Ltd.     

Protection of the flavonoid fraction from Rosa laevigata Michx fruit against carbon tetrachloride-induced acute liver injury in mice

Protective effect of the total flavonoids (TFs) from Rosa laevigata Michx fruit against carbon tetrachloride (CCl₄)-induced hepatotoxicity in mice was investigated. Pretreatment with TFs significantly decreased CCl₄-induced elevation of serum aspartate transaminase (AST) and alanine transaminase (ALT) activities as well as the relative liver weight. Histopathological observation also revealed that TFs reduced the incidence of liver lesions and improved hepatocyte abnormality. Moreover, oral administration of TFs significantly enhanced antioxidant enzyme activities (superoxide dismutase, catalase and glutathione peroxidase), increased the content of glutathione and decreased the content of malondialdehyde. Further research indicated that TFs prevented the DNA fragmentation and mitochondrial ultrastructural alterations caused by CCl₄ based on TUNEL and transmission electron microscopy (TEM) assays. Moreover, pretreatment with TFs down-regulated the protein expressions of CYP2E1, iNOS, NF-κB, Bak and Caspase-3. Quantitative Real-time PCR assay suggested that TFs markedly decreased the levels of TNF-α, Fas/FasL and Bax gene expressions, and increased the level of Bcl-2. This is the first time to report the significant hepatoprotective effect of TFs from R. laevigata Michx fruit against CCl₄-induced liver injury in mice and the action should be through reducing oxidative stress and suppressing inflammation and apoptosis.