汉防己甲素对大鼠肝保护和抗氧化作用的实验研究

目的：研究汉防己甲素对大鼠肝保护与抗氧化作用。方法：选取40只大鼠作为实验对象,随机分为模拟组、溶剂对照组及治疗3组（20 mg/mL,60 mg/mL,100 mg/mL）,每组8只大鼠;模型组每隔3 d给予四氧化碳溶液,溶液浓度为30%,持续给予10 d,给药方法为灌胃;溶剂对照组每日行同等剂量溶剂实验;治疗3组每日给予汉防己甲素并给予四氧化碳溶液;比较汉防己甲素对大鼠肝保护与抗氧化效果。结果：治疗3组大鼠肝损伤程度指标显著优于其他2组,经比较其差异有统计学意义（P〈0.05）;对CAT、GPx、SOD、GST、GSH等抗氧化指标显著优于其他2组,经比较其差异有统计学意义（P〈0.05）;汉防己甲素可有效清除超氧化物离子形成的自由基,且清除能力与药物浓度呈正相关（P〈0.05）。结论：汉防己甲素对大鼠肝保护与抗氧化具有显著作用。     

D-氨基半乳精诱导肝损伤的过氧化机理和锌的保护作用(英文)

本实验从脂质过氧化的角度对D-氨基半乳糖(Galn)诱导肝损伤的机理进行了观察和探讨,并通过体内和体外实验研究了锌对该种肝损伤的保护作用及其机理,实验结果显示,有关自由基代谢和脂质过氧化的几项指标在Galn处理的大鼠体内均发生明显变化,其变化规律基本与四氯化碳处理大鼠体内变化一致,这就提示,自由基诱导的脂质过氧化可能是Galn诱导肝损伤的主要原因之一。 对Galn诱导肝损伤大鼠进行预补锌实验表明,醋酸锌im 50mg Zn·kg~1,d~1×5 d,可以维持大鼠体内锌的水平,降低大鼠中毒死亡率,减轻肝脏组织病理变化,抑制脂质过氧化,促进蛋白质合成并改善肝脏功能,体外实验表明,补锌可以减少Galn染毒游离肝细胞的中毒死亡数,降低培养液中丙二醛浓度并维持还原型谷胱甘肽水平,由此证明,锌对肝损伤具有明显的保护作用,该作用是通过抗氧化和促进蛋白质合成来进行的。     

肝复康胶囊对四氯化碳所致小鼠肝损伤的保护作用

目的 研究肝复康胶囊对四氯化碳(CCl4)所致小鼠肝损伤的保护作用.方法 将肝复康胶囊灌胃给予小鼠,腹腔注射四氯化碳所致肝损伤小鼠,用半自动生化分析仪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,以比色分析法测定肝匀浆丙二醛(MDA)含量及超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性.结果 肝复康胶囊(0.9、1.8、3.6 g·kg-1·d-1)均可显著降低四氯化碳致肝损伤小鼠血清ALT和AST活性,也能明显降低肝脏MDA含量和提高肝匀浆SOD和GSH-Px活性.结论 肝复康胶囊对小鼠急性肝损伤有一定保护作用,其保护作用机制可能与清除自由基,抗脂质过氧化作用有关.     

红细胞、血浆蛋白及溶酶体对汉防己甲素和汉防己乙素系统暴露的影响

目的:汉防己为防己科植物粉防己(Stephania tetrandra S. Moore)的干燥根。汉防己甲素和汉防己乙素是其两个主要成分,具有抗肿瘤等多方面药效活性。为了帮助进一步考察汉防己甲素和汉防己乙素的药效作用,我们对两个双苄基异喹啉类生物碱开展了大鼠和体外药代研究。方法:大鼠口服或静脉给药汉防己提取物、汉防己甲素或汉防己乙素单体化合物以阐明汉防己甲素和汉防己乙素的药代动力学特征;在体外检测汉防己甲素和汉防己乙素的血浆蛋白结合、全血-血浆分配、溶酶体捕获。以上实验产生的生物样品均采用液质联用技术进行分析。结果:研究发现汉防己甲素和汉防己乙素有两个药代特征,其一是这两个化合物的全血系统暴露水平均高于其各自血浆系统暴露水平,其二是在相同的给药剂量、动物实验条件及分析检测条件下,两个化合物在灌胃汉防己水提物后的系统暴露水平均高于其各自在灌胃单个化合物后的暴露水平。汉防己甲素和汉防己乙素的大鼠血浆游离药物分数约为2%～5%,其在大鼠红细胞浓度比在大鼠血浆浓度高5倍左右。溶酶体抑制剂阻碍溶酶体捕获这两个化合物并显著减少其在HEK-293细胞中浓度。结论:血浆蛋白结合、红细胞结合及组织细胞...     

马齿苋多糖的抗氧化活性研究

目的研究马齿苋多糖(POP)的抗氧化作用。方法采用体外实验研究POP对超氧阴离子、羟自由基、DPPH的清除作用以及对H2O2诱导的红细胞氧化溶血和大鼠肝匀浆脂质过氧化的保护作用。结果 POP对超氧阴离子和羟自由基具有良好的清除作用,IC50分别为4.29和1.97μg/mL,对有机自由基DPPH的作用很弱。POP对自发性脂质过氧化和H2O2诱导的脂质过氧化具有良好的保护作用,但对H2O2诱导的红细胞氧化溶血作用较弱。结论 POP具有显著的体外抗氧化活性。     

樱桃叶多糖的抗氧化活性研究

目的评价樱桃叶多糖(PPP)的体外抗氧化活性。方法以抗坏血酸(Vc)作为对照,体外实验研究PPP的总还原能力及其对羟自由基、超氧负离子自由基和有机自由基(DPPH)的清除作用以及对大鼠肝脏自发性和H2O2诱导的丙二醛抑制率。结果 PPP对羟自由基、超氧负离子自由基、有机自由基的IC50依次为100.5,991.4和135.1μg/mL;对大鼠肝脏自发性和由H2O2诱导的产生的脂质过氧化均有较好的保护作用。结论 PPP有着较强的体外抗氧化活性,和同等浓度下的Vc相比,其抗氧化能力效果稍弱,具有一定的开发价值。     

汉防己多糖对急性酒精性肝损伤小鼠氧化应激及肝细胞凋亡的影响

目的:探讨汉防己多糖对急性酒精性肝损伤小鼠的保护作用及其机制。方法:将60只小鼠随机分为空白对照组(生理盐水)、模型组(生理盐水)、联苯双酯组(阳性对照,150 mg/kg)和汉防己多糖低、中、高剂量组(100、200、400 mg/kg),每组10只,ig给药,每天1次,连续7 d。末次给药1 h后,除空白对照组外其余各组小鼠均ig 50%乙醇(0.1 m L/10 g)溶液复制急性酒精性肝损伤模型。12 h后,测定小鼠血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平以及肝组织中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)水平;苏木精-伊红染色观察小鼠肝组织病理改变;流式细胞术检测肝细胞凋亡率。结果:与空白对照组比较,模型组小鼠肝组织发生水肿、细胞排列紊乱及局部坏死等病变,血清中ALT、AST水平和肝组织中MDA水平以及肝细胞凋亡率显著升高,肝组织中SOD、GSH、GSH-Px水平显著降低,差异均有统计学意义(P<0.01)。与模型组比较,汉防己多糖中、高剂量组小鼠肝组织细胞变性和坏死程度均减轻;除汉防己多糖低剂量组小鼠肝细胞凋亡率降低不明显外,其余各给药组小鼠上述指标均显著改善(P<0.05或P<0.01)。结论:汉防己多糖对急性酒精性肝损伤小鼠具有明显的保护作用,其机制可能与抗氧化应激及减少肝细胞凋亡有关。     

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.     

汉防已甲素对四氧嘧啶糖尿病大鼠高血糖的预防作用

本研究以血糖为检测指标,观察了汉防己甲素对四氧嘧啶糖尿病大鼠高血糖的预防作用。结果表明:①预先给予不同剂量的汉防己甲素,皆可不同程度地防止四氧嘧啶升高血糖的作用,其预防效果随剂量的增加而增强。②预先给予汉防己甲素(100mg/kg)预防组和注射四氧嘧啶后24h给予汉防己甲素(100mg/kg),预防组于注射四氧嘧啶(0天)后第2、3、5、7天的血糖浓度与对照组同天血糖比较均明显降低(P<0.01)。结论:注射四氧嘧啶前后一定时间给予汉防己甲素均可预防四氧嘧啶致高血糖作用的发生。动态观察1周,预防组血糖浓度稳定,无升高趋势。     

石斛多糖抗氧化活性研究

目的研究石斛多糖的体内、体外抗氧化活性。方法①体外抗氧化实验：用化学反应法检测石斛多糖对邻苯三酚自氧化反应产生的超氧阴离子和Fenton反应产生的羟自由基的清除作用;②体内抗氧化实验：昆明种小鼠随机分为空白对照组、小剂量组、中剂量组和大剂量组,每组10只。研究石斛多糖对小鼠血清及肝组织中SOD、GSH-Px、MDA的影响。结果石斛多糖具有清除羟基自由基和超氧阴离子自由基的作用,可显著提高小鼠血清和肝组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活力,降低丙二醛（MDA）含量。结论石斛多糖具有明显的抗氧化活性,为进一步开发石斛药材提供依据。     

Antioxidant and hepatoprotective effects of Cyathea phalerata Mart. (Cyatheaceae)

The present study investigated the antioxidant properties of Cyathea phalerata Mart. (Cyatheaceae) using in vitro and in vivo assays. The in vitro antioxidant potential of the crude extract (CE), precipitate (PPT), aqueous fraction (AQF), n-butanolic fraction (BUF) and ethyl acetate fraction (EAF) from C. phalerata was evaluated through the scavenging of diphenyl-1-picryl-hydrazyl-hydrate (DPPH), superoxide anion (O(2)(*-)) (nitroblue tetrazolium assay) and hydroxyl radicals (OH(*)) (deoxyribose assay), and lipid peroxidation in rat liver homogenate. In these assays, it was observed that EAF had marked antioxidant potential, especially as a scavenger of the OH(*) radical and in inhibiting lipid peroxidation. The in vivo evaluation of oxidative stress (DNA fragmentation, membrane lipoperoxidation and carbonyl protein formation) and the antioxidant defenses (concentration of reduced glutathione, as well as catalase and glutathione S-transferase activities) were measured in mice pre-treated with EAF (10, 30 or 100 mg/kg, orally) and later exposed to carbon tetrachloride (CCl(4)). The EAF decreased thiobarbituric acid reactive substances levels, DNA damage and carbonyl protein contents, and increased catalase and glutathione S-transferase activities. Based on these results, it is concluded that the EAF from C. phalerata protects liver from oxidative stress induced by CCl(4) in mice and these effects are probably related to the antioxidant activity associated with the free radical scavenging property of this fraction.     

In Vitro. and In Vivo. Evaluation of Free-Radical Scavenging Potential of Cissus quadrangularis.

Abstract

The current study was performed to evaluate the effect of the methanol extract of Cissus quadrangularis. (L.) (CQE) against free-radical damage. The test extract exhibited significant scavenging effect on DPPH free radical, superoxide radical, hydroxyl radical production, and inhibition of lipid peroxide production in erythrocytes. The free-radical scavenging effect of CQE was comparable with that of reference antioxidants. The activities of liver marker enzymes and antioxidant defense enzymes in rat liver homogenate were assessed in CCl₄- and CQE-treated animals. Carbon tetrachloride (CCl₄) caused a significant increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT), alkaline phosphatase (ALP), malondialdehyde (MDL) levels and a decrease in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S.-transferase (GST), and reduced glutathione (GSH) activities, which were reverted by CQE treatment. The results obtained suggest that CQE showed antilipid peroxidative, free-radical scavenging property and ameliorated the liver damage by an increase in antioxidant enzymes activities. It can be concluded that the free-radical scavenging/antioxidant activity of the plant extract may be responsible for the therapeutic action against tissue damage.     

Protective effect of puerariae radix on oxidative stress induced by hydrogen peroxide and streptozotocin

This study evaluated the protective effect of Puerariae radix against the oxidative stress induced by hydrogen peroxide (H2O2) and streptozotocin in vitro and in vivo, respectively. The ethanol extract scavenged intracellular reactive oxygen species (ROS), and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and prevented lipid peroxidation. This radical scavenging activity of the ethanol extract protected the cell viability of Chinese hamster lung fibroblast (V79-4) cells exposed to H2O2. Furthermore, this extract reduced the formation of apoptotic cells induced by H2O2, which was demonstrated by the decreased number of sub G(1) hypo-diploid cells and apoptotic cell body formation. The extract increased the activities of the cellular antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT). Administration of the extract to the streptozotocin induced diabetic rats decreased the blood glucose levels. The diabetic rats showed low activities of superoxide dismutase and catalase in the liver, and the ethanol extract increased the CAT activity. The increased level of lipid peroxidation in the diabetic rats reverted to near normal levels after being treated with the extract. This study showed that Puerariae radix was effective in the amelioration of diabetes, which may be a consequence of its antioxidant potential.     

Hepatoprotective effects of 18beta-glycyrrhetinic acid on carbon tetrachloride-induced liver injury: inhibition of cytochrome P450 2E1 expression.

The protective effects of 18beta-glycyrrhetinic acid (GA), the aglycone of glycyrrhizin (GL) derived from licorice, on carbon tetrachloride-induced hepatotoxicity and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with GA prior to the administration of carbon tetrachloride significantly prevented an increase in serum alanine, aspartate aminotransferase activity and hepatic lipid peroxidation in a dose-dependent manner. In addition, pretreatment with GA also significantly prevented the depletion of glutathione (GSH) content in the livers of carbon tetrachloride-intoxicated mice. However, reduced hepatic GSH levels and glutathione-S-transferase activities were unaffected by treatment with GA alone. Carbon tetrachloride-induced hepatotoxicity was also prevented, as indicated by a liver histopathologic study. The effects of GA on the cytochrome P450 (P450) 2E1, the major isozyme involved in carbon tetrachloride bioactivation, were also investigated. Treatment of mice with GA resulted in a significant decrease of the P450 2E1-dependent hydroxylation of p-nitrophenol and aniline in a dose-dependent manner. Consistent with these observations, the P450 2E1 expressions were also decreased, as determined by immunoblot analysis. GA also showed antioxidant effects upon FeCl(2)-ascorbate-induced lipid peroxidation in mice liver homogenate and upon superoxide radical scavenging activity. These results show that protective effects of GA against the carbon tetrachloride-induced hepatotoxicity may be due to its ability to block the bioactivation of carbon tetrachloride, primarily by inhibiting the expression and activity of P450 2E1, and its free radical scavenging effects.     

Potential antioxidant properties and hepatoprotective effects of an aqueous extract formula derived from three Chinese medicinal herbs against CCl4-induced liver injury in rats

The hepatoprotective effects of an aqueous extract formula (AEF) derived from Artemisia capillaris, Lonicera japonica and Silybum marianum (ratio 1:1:1) were evaluated by its antioxidant properties and its attenuation of carbon tetrachloride (CCl₄)-induced liver damage in rats. The antioxidant analyses revealed that the AEF showed higher 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and superoxide anion radical scavenging activities as well as ferric reducing antioxidant potential (FRAP) and Trolox equivalent antioxidant capacity (TEAC) compared with the individual herbs, suggesting a synergism in antioxidation between the three herbs. The animal experiments showed that the CCl₄ treatment increased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, but decreased triglyceride (TG) and glutathione (GSH) levels as well as glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT) activities. However, AEF administration can successfully lower serum ALT and AST activities, restore the GSH level, ameliorate or restore GPx and CAT activities as well as improve SOD action depending on AEF dosage. Histological examination of liver showed that CCl₄ increased the extent of bile duct proliferation, necrosis, fibrosis and fatty vacuolation throughout the liver, but AEF can improve bile duct proliferation, vacuolation and fibrosis, and restore necrosis. The present study demonstrated the hepatoprotective potential of AEF as an alternative to the traditional silymarin.     

Free radical scavenging: a possible mechanism of action for the anti-inflammatory activity of <Emphasis Type="Italic">Russelia equisetiformis</Emphasis> (Schlect &; Chan) (Scrophulariacae)

The methanol extract of Russelia equisetiformis (MRE), which exhibited significant antiinflammatory activity, was evaluated for the possible mode of action by studying its antioxidant potential in adjuvant- induced arthritic rats. 1, 1 diphenyl-2-picrylhydrazyl (DPPH) radical scavenging effect was determined by spectrophotometric method. The enzymatic activity of the superoxide dismutase, glutathione peroxidase, showed a significant increase, while the lipid peroxide content was found to decrease to a large extent in MRE and indomethacin-treated rats. There was also significant and concentration-dependent increase in the percentage inhibition of DPPH, comparable to that of vitamin E and butylated hydroxyanisole (BHA) which are natural and synthetic antioxidants, respectively. The results obtained in the present study indicate that MRE possesses free radical scavenging and antioxidant properties.     

Protective effect of Platycodi radix on carbon tetrachloride-induced hepatotoxicity.

The protective effects of a Platycodi radix (Changkil: CK), the root of Platycodon grandiflorum A. DC (Campanulaceae) on carbon tetrachloride (CC14)-induced hepatotoxicity and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with CK prior to the administration of CC14 significantly prevented the increased serum enzymatic activities of alanine and aspartate aminotransferase in a dose-dependent manner. In addition, pretreatment with CK also significantly prevented the elevation of hepatic malondialdehyde formation and the depletion of reduced glutathione content in the liver of CC14-intoxicated mice. However, hepatic reduced glutathione levels and glutathione S-transferase activities were not affected by treatment with CK alone. CC14-induced hepatotoxicity was also essentially prevented, as indicated by a liver histopathologic study. The effects of CK on the cytochrome P450 (P450) 2E1, the major isozyme involved in CC14 bioactivation were also investigated. Treatment of mice with CK resulted in a significant decrease of P450 2E1-dependent p-nitrophenol and aniline hydroxylation in a dose-dependent manner. CK showed antioxidant effects in FeCl2-ascorbate-induced lipid peroxidation in mice liver homogenate and in superoxide radical scavenging activity. Our results suggest that the protective effects of CK against CC14-induced hepatotoxicity possibly involve mechanisms related to its ability to block P450-mediated CC14 bioactivation and free radical scavenging effects.     

益生汤抗氧化活性研究

目的:研究益生汤抗氧化作用.方法:用体外化学模拟体系研究了益生汤清除DPPH自由基、羟基(·OH)自由基和超氧阴离子(O2-)自由基的能力以及益生汤总的还原能力、抑制亚油酸过氧化作用进行了测定;通过D-半乳糖诱导的衰老小鼠研究益生汤对小鼠心肌线粒体超氧化物歧化酶(SOD)活性,丙二醛(MDA)含量及肝组织中谷胱甘肽过氧化物酶(GSH-Px)活性的影响.结果:益生汤清除DPPH自由基、·OH自由基和O2-自由基的IC50值分别为0.547 0、0.209 1和0.300 9 mg·ml-1;总还原力的IC50为0.506 2 mg·ml-1;益生汤可明显抑制亚油酸的氧化.体内研究显示,与模型组相比,益生汤可剂量依赖性提高小鼠心肌线粒体中SOD的活性(P＜0.01)和肝组织GSH-Px活性(P＜0.01),降低心肌线粒体中MDA的含量(P＜0.01).结论:益生汤有一定的抗氧化功能,具有良好的开发前景.     

Antioxidant and drug detoxification potentials of Hibiscus sabdariffa anthocyanin extract

The antioxidant and drug metabolizing potentials of Hibiscus anthocyanin extract in CCl(4)- induced oxidative damage of rat liver was investigated. Hibiscus anthocyanin extract effectively scavenge α-diphenyl-β-picrylhydrazyl (DPPH) radical, superoxide ion, and hydrogen peroxide. It produced a 92% scavenging effect of DPPH radical at a concentration of 2.0 mg/mL. Hibiscus anthocyanin extract produced a 69 and 90% scavenging effect on superoxide ion and hydrogen peroxide, respectively, at 1.0 mg/mL, which compared favorably with the synthetic antioxidant (butylated hydroanisole and α-tocopherol). A reducing power of this anthocyanin was examined using K(3)Fe(CN)(6). Hibiscus anthocyanin extract has reducing power that is approximately 2-fold that of the synthetic antioxidant, butylated hydroanisole. Hibiscus anthocyanin extract produced a significantly increase and completely attenuated the CCl(4)-mediated decrease in antioxidant enzymes (e.g., catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase). However, the level of nonenzymic antioxidant molecules (i.e., vitamins C and E) were significant preserved by Hibiscus anthocyanin extract. There was an induction of phase II drug-detoxifying enzymes: glutathione S-transferase, NAD(H):quinone oxidoreductase, and uridyl diphosphoglucuronosyl transferase by 65, 45, and 57%, respectively. In view of these properties, Hibiscus sabdariffa anthocyanin extract can act as a prophylactic by intervening as a free radical scavenger both in vitro and in vivo as well as inducing the phase II drug detoxification enzymes.     

(−)Epigallocatechin-gallate (EGCG) prevents mitochondrial damage in isoproterenol-induced cardiac toxicity in albino Wistar rats: A transmission electron microscopic and in vitro study

Altered mitochondrial function and free radical-mediated tissue damage have been suggested as important pathological events in isoproterenol (ISO)-induced cardiotoxicity. This study was undertaken to know the preventive effect of (-)epigallocatechin-gallate (EGCG) on mitochondrial damage in ISO-induced cardiotoxicity in male Wistar rats. Rats were pretreated with EGCG (30 mg/kg) orally using an intragastric tube daily for a period of 21 days. After that, ISO (100mg/kg) was subcutaneously injected to rats at intervals of 24h for 2 days. ISO-induced rats showed significant increase in mitochondrial lipid peroxidation products (thiobarbituric acid reactive substances and lipid hydroperoxides) and significant decrease in mitochondrial antioxidants (superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and reduced glutathione). Also, significantly decreased activities of tricarboxylic acid cycle enzymes such as isocitrate, succinate, malate and alpha-ketoglutarate dehydrogenases and respiratory chain marker enzymes such as NADH-dehydrogenase and cytochrome-c-oxidase were observed in mitochondrial heart of myocardial infarcted rats. Prior treatment with EGCG (30mg/kg body weight) significantly prevented these alterations and restored normal mitochondrial function. Transmission electron microscopic findings also correlated with these biochemical parameters. In vitro studies on the effect of EGCG on scavenging 1,1-diphenyl-2-picrylhydrazyl (DPPH), 2,2'-azinobis-(3-ethyl-benzothiazoline-6-sulfonic acid) (ABTS(+)), superoxide anion (O(-)), and hydroxyl (OH) radicals also confirmed the free radical scavenging and antioxidant activity of EGCG. Thus, the observed effects are due to the free radical scavenging and antioxidant potential of EGCG. Thus, this study confirmed the preventive effect of EGCG on isoproterenol-induced mitochondrial damage in experimentally induced myocardial infarction in Wistar rats.