Hepatoprotective effect ofVitex negundo against carbon tetrachloride-induced liver damage

Alcoholic extract of the seeds of Vitex negundo Linn. was obtained by cold maceration. A dose of 250 mg/kg (1/6 of LD50) of the extract was selected to study the hepatoprotective action against carbon tetrachloride-induced liver damage. The extract was found to be effective in preventing liver damage which was evident by morphological, biochemical and functional parameters.     

Hepatoprotective potentials of Phyllanthus amarus against ethanol-induced oxidative stress in rats

The hepatoprotective effect of methanolic extract of the leaf of Phyllanthus amarus (P. amarus) against ethanol-induced oxidative damage was investigated in adult male Wistar albino rats. P. amarus (250 and 500 mg/kg/day) and ethanol (5 g/kg/day, 20% w/v) were administered orally to animals for 4 weeks and 3 weeks, respectively. Ethanol treatment markedly decreased the level of reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) in the liver, which were significantly enhanced by P. amarus treatment. Glutathione-S transferase (GST), which was increased after chronic ethanol administration, was significantly reduced by P. amarus treatment in the liver. Also, P. amarus significantly increased the activities of hepatic alanine transaminase (ALT) and aspartate transaminase (AST) as well as alkaline phosphatase (ALP), with a concomitant marked reduction in the plasma activity of the transaminases in the ethanol-challenged rats. Lipid peroxidation level, which was increased after chronic ethanol administration, was significantly reduced in the liver by P. amarus co-treatment. Results show that P. amarus leaf extract could protect the liver against ethanol-induced oxidative damage by possibly reducing the rate of lipid peroxidation and increasing the antioxidant defence mechanism in rats.     

Studies on protective effect of DA-9601,Artemisia asiatica extract, on acetaminophen- and CCI4-induced liver damage in rats

The hepatoprotective effect of DA-9601, a quality-controlled extract ofArtemisia asiatica, on liver damage induced by acetaminophen (APAP) and carbon tetrachloride (CCI₄) was investigated by means of serum-biochemical, hepatic-biochemical, and histopathological examinations. Doses of DA-9601 (10, 30, or 100mg/kg) were administered intragastrically to each rat on three consecutive days i.e. 48 h, 24 h and 2 h before a single administration of APAP (640 mg/kg, i.p.) or CCl₄ (2 ml/kg, p.o.). Four h and 24 h after hepatotoxin treatment, the animals were sacrificed for evaluation of liver damage. Pretreatment of DA-9601 reduced the elevation of serum ALT, AST, LDH and histopathological changes such as centrilobular necrosis, vacuolar degeneration and inflammatory cell infiltration dose-dependently. DA-9601 also prevented APAP- and CCl₄-induced hepatic glutathione (GSH) depletion and CCl₄-induced increase of hepatic malondialdehyde (MDA), a parameter of lipid peroxidation, in a dose-dependent manner. These findings suggest that pretreatment with DA-9601 may reduce chemically induced liver injury by complex mechanisms which involve prevention of lipid peroxidation and preservation of hepatic GSH.     

Acanthopanax senticosus reverses fatty liver disease and hyperglycemia in ob/ob mice

Non-alcoholic fatty liver disease (NAFLD) is common in obesity. However, weight reduction alone does not prevent the progression of NAFLD to end-stage disease associated with the development of cirrhosis and liver disease. In a previous experiment, 50% ethanol extract of Acanthopanax senticosus stem bark (ASSB) was found to reduce body weight and insulin resistance in high fat diet-induced hyperglycemic and hyperlipidemic ICR mice. To evaluate the anti-steatosis action of ASSB, insulin-resistant ob/ob mice with fatty livers were treated with ASSB ethanol extract for an 8 week-period. ASSB ethanol extract reversed the hepatomegaly, as evident in reduction of % liver weight/body weight ratio. ASSB ethanol extract also specifically lowered circulating glucose and lipids, and enhanced insulin action in the liver. These changes culminated in inhibition of triglyceride synthesis in non-adipose tissues including liver and skeletal muscle. Gene expression studies confirmed reductions in glucose 6-phosphatase and lipogenic enzymes in the liver. These results demonstrate that ASSB ethanol extract is an effective treatment for insulin resistance and hepatic steatosis in ob/ob mice by decreasing hepatic lipid synthesis.     

Effect of Azadirachta indica (Neem) leaf aqueous extract on paracetamol-induced liver damage in rats

The effect of aqueous leaf extract of Azadirachta indica (A. indica) was evaluated in paracetamol induced hepatotoxicity in rats. Liver necrosis was produced by administering single dose of paracetamol (2 g/kg, p.o.). The liver damage was evidenced by elevated levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transpeptidase (gamma-GT) and by histopathological observations of liver sections. Aqueous A. indica leaf extract (500 mg/kg, p.o.) significantly (P < 0.01) reduced these elevated levels of AST, ALT and gamma-GT. Paracetamol induced liver necrosis was also found to be reduced as observed macroscopically and histologically.     

蜈蚣提取物对小鼠急性肝损伤的保护作用

目的：研究蜈蚣水提取物和不同体积分数乙醇提取物对小鼠急性肝损伤的保护作用。方法：采用四氯化碳（CCl₄）制备小鼠急性肝损伤模型,测定血清中谷草转氨酶（AST）,谷丙转氨酶（ALT）和肝脏中超氧化物歧化酶（SOD）,丙二醛（MDA）水平;HE染色观察肝脏病理形态改变;RT-PCR检测小鼠肝脏中的肿瘤坏死因子α（TNF-α）,白介素6（IL-6）mRNA表达水平。结果：与CCl₄模型组比较,蜈蚣水提物和30%乙醇提取物可以降低急性肝损伤小鼠ALT,AST和MDA水平,提高SOD水平;减轻小鼠肝脏病理损伤;降低TNF-α及IL-6的mRNA表达。其中水提物的效果更为显著。结论：蜈蚣水提物和30%乙醇提取物对小鼠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以及抑制TNF-α与IL-6的表达有关。     

基于Nrf2/Keap1信号通路探讨金盏银盘水提液对四氯化碳诱导急性肝损伤小鼠抗氧化应激作用

目的 探究金盏银盘Bidens biternata(Lour.)Merr.&Sherff.水提液对四氯化碳诱导的急性肝损伤改善作用及其机制。方法 将60只雄性昆明小鼠随机分为对照组、模型组、水飞蓟素（0.15 g/kg）组和金盏银盘低、高剂量（3.9、7.8 g/kg）组,每组12只。各组小鼠连续ig给予相应药物7 d,末次给药后除对照组外均ip 0.4%四氯化碳构建急性肝损伤小鼠模型。24 h后收集小鼠血清及肝脏组织。用生化试剂盒检测血清中天门冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）、超氧化物歧化酶（SOD）活性及丙二醛（MDA）含量,并取肝组织匀浆检测谷胱甘肽过氧化物酶（GSH-Px）活性。采用苏木精–伊红染色（HE）切片观察小鼠肝脏病理变化。Western blotting测定肝组织中核因子E2相关因子2(Nrf2)、抗体Kelch样ECH相关蛋白1(Keap1)、血红素氧合酶1(HO-1)蛋白的表达情况。结果 与模型组比较,金盏银盘水提液组小鼠组织病理学观察发现肝脏炎症细胞浸润明显减少,血清AST、ALT、MDA水平降低,血清SOD和肝组织GSH-Px活性...     

石榴皮醇提物的急性肝毒性研究

目的 评价石榴皮醇提物对小鼠肝脏的影响。方法 将40只小鼠随机分成阴性对照组、石榴皮醇提物低、中、高剂量组（30,45,60 mg·kg-1）。所有小鼠在禁食12 h后,各剂量组给予相应剂量的石榴皮醇提物,阴性对照组给予等体积的蒸馏水。给药24 h后,所有小鼠麻醉后眼眶取血,麻醉脱臼处死。测定ALT,AST,LDH血清酶指标。留取肝组织测定MDA、GSH、GSSG评价氧化损伤的指标。留取1/2肝大叶经福尔马林溶液固定,HE染色观察小鼠肝脏病理改变。结果 与阴性对照组比较,石榴皮醇提物中、高剂量组体质量、肝重、肝体比明显降低（P〈0.05或P〈0.01）,ALT、LDH、MDA明显升高（P〈0.05）,GSH/GSSG明显降低（P〈0.05）,石榴皮醇提物高剂量组AST明显升高（P〈0.05）。结论 石榴皮醇提物能够引起小鼠肝脏的急性损伤,并且剂量越大,毒性越大。     

山豆根水提组分大鼠长期毒性实验研究

目的 观察连续给予山豆根水提组分导致大鼠慢性毒性的损伤表现、程度及可逆性.方法 连续27天分别给80只大鼠灌胃高、中、低剂量的山豆根水提组分样品,除观察一般状况外,检测血常规、血生化指标,剖杀大鼠,精密称取心、肝、脾、肺、肾脏,计算脏体比值,进行常规病理检查.停药后进行恢复期观察.结果 连续给予不同剂量山豆根水提组分可致使大鼠体重下降,饮食、饮水不佳;血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)增高,肝体比值升高,病理检查可见不同程度的肝损伤,对血常规无明显影响.肝毒性损伤程度与给药剂量呈现一定的剂量依赖相关性.停药后,部分病理改变不可逆.结论 山豆根水提组分长期给药的长期毒性表现为血清ALT、.AST、ALP活性及尿素氮(BuN)、肌酐(CRE)含量的变化,且部分病变为不可逆性损伤.     

香加皮不同组分大鼠长期毒性研究

目的 观察连续给予香加皮不同组分导致大鼠慢性毒性的损伤表现、程度及可逆性.方法 分别给140只大鼠灌胃高、中、低剂量的香加皮水提组分和醇提组分样品,除观察一般状况外,检测血常规、血生化指标,剖杀大鼠,精密称取心、肝、脾、肺、肾脏等重要脏器,计算脏、体比值,进行常规病理检查.停药后,进行恢复期观察.结果 连续20天给予不同剂量的香加皮水提组分和连续9天给予不同剂量的醇提组分样品均可导致大鼠体重下降,饮食、饮水不佳,血ALT、AST、AKP、TPC增高,ALB、CR降低、A/G比值降低,肝脏重量和肝体比值、肾脏重量和肾体比值增大,病理检查可见不同程度的肝脏、肾脏病理组织损伤;对血常规影响不明显;肝、肾毒性损伤程度与给药剂量呈现一定的剂量依赖相关性;经过恢复期观察,上述部分病变不可逆.结论 香加皮水提组分给药20天、醇提组分给药9天造成的慢性毒性损伤部位以肝、肾损伤为主,且部分病变为不可逆性损伤.     

Protective effect of Artin M from extract of Artocarpus integrifolia seeds by Th1 and Th17 immune response on the course of infection by Candida albicans

The immunoregulatory effect of Artin M and jacalin from extract of Artocarpus integrifolia seeds (jack extract) against infection with Candida albicans was investigated. Swiss mice received jack extract containing 500 μg protein/ml PBS intraperitoneally (i.p.) or PBS alone and after 72 h were infected i.p. with C. albicans CR15 (10⁷) and sacrificed after 30 min, 2, 6, 24, and 72 h. ELISA analysis revealed that in jack extract-treated mice IFN-γ was predominantly produced versus IL-10 in control mice. These results suggest that jack extract induced a protective immune response, since C. albicans clearance was complete at 72 h postinfection. Jack extract presents two lectins (Artin M and jacalin) with distinct biological properties. Artin M was able to induce IL-12 production by macrophages. Also, Artin M in different concentrations, associated with jacalin or in jack extract induced both IFN-γ and IL-17 production. As a consequence, phagocytic and candidacidal activity increased significantly. Alanine aminotransferase activity (ALT) was used as parameter for damage of the liver. The activity of ALT correlated with inoculum size that increased significantly in control group, however, mice pretreated with jack extract 3 days before infection presented normal ALT. Mice pretreated with jack extract that received a lethal inoculum of Candida presented 90% survival versus 20% among controls or mice pretreated with jacalin. Thus, the results suggest that Artin M by itself, associated with jacalin or present in jack extract is able to induce protective Th1 and Th17 immune responses against Candida albicans infection.     

垂盆草对四环素所致非酒精性脂肪性肝病的保护作用

目的 探讨垂盆草对四环素所致非酒精性脂肪性肝病的作用,以及抗非酒精性脂肪肝作用的有效部位。方法 采用不同极性溶剂提取分离垂盆草的不同部位,即醇提部位、水提部位、正丁醇提取部位、乙酸乙酯提取部位,利用四环素所致非酒精性脂肪肝小鼠模型,采用生化法检测小鼠肝功能和血脂指标、HE染色检测病理组织学改变、生化法测定氧化损伤指标等,从而确证垂盆草的有效部位。结果 小鼠腹腔注射四环素24 h后,小鼠血清谷丙转氨酶（ALT）升高、甘油三酯（TG） 和胆固醇（CHO）显著降低,肝组织丙二醛（MDA）显著升高,超氧化物歧化酶（SOD）活性显著下降,肝脏的中央静脉和小叶间静脉周围出现肝细胞肿胀、水样变性等病理改变;与模型组比较,正丁醇提取部位能显著抑制血清转氨酶的升高,缓解血脂的降低;醇提部位和正丁醇提取部位可明显减轻上述病理改变;正丁醇提取部位对超氧化物歧化酶作用显著;此外,正丁醇提取部位中黄酮的含量高于醇提部位的黄酮量。结论 垂盆草的不同部位可显著缓解四环素所致小鼠脂肪肝的作用,尤其是正丁醇提取部位作用更强,其作用与其成分中含黄酮量高有关,其作用机制主要与增强其抗氧化损伤有关。     

Ligularia fischeri extract attenuates liver damage induced by chronic alcohol intake

Context Ligularia fischeri (Ledebour) Turcz. (Compositae) has been used as a leafy vegetable and in traditional medicine to treat hepatic disorder in East Asia.

Objective The present study explores the antioxidant activity of LF aqueous extract on EtOH-induced oxidative stress accompanied by hepatotoxicity both in vitro and in vivo.

Materials and methods In vitro study using the mouse liver NCTC-1469 cell line was conducted to estimate the cytotoxicity as well as the inhibitory effect of LF extract against alcohol-treated cell damage. In vivo study used an alcohol-fed Wister rat model orally administered EtOH (3.95?g/kg of body weight/d) with or without LF extract (100 or 200?mg/kg body weight) for 6 weeks. Serum and liver tissue were collected to evaluate hepatic injury and antioxidant-related enzyme activity.

Results The EC₅₀ value for the DPPH radical scavenging capacity of LF extract was 451.5?μg/mL, whereas the IC₅₀ value of LF extract in terms of EtOH-induced reactive oxygen species (ROS) generation was 98.3?μg/mL without cell cytotoxicity. LF extract (200?mg/kg body weight) significantly reduced the triglyceride content of serum (33%) as well as hepatic lipid peroxidation (36%), whereas SOD activity was elevated three-fold. LF extract suppressed expression of CYP2E1 and TNF-α, and attenuated alcohol-induced abnormal morphological changes.

Discussion and conclusion LF extract attenuated liver damage induced by alcoholic oxidative stress through inhibition of ROS generation, down-regulation of CYP2E1, and activation of hepatic antioxidative enzymes. Homeostasis of the antioxidative defence system in the liver by LF extract mitigated hepatic disorder following chronic alcohol intake.     

Toxicological evaluation and hepatoprotective potential of Clerodendron glandulosum.Coleb leaf extract

This inventory evaluates toxicological effects and hepatoprotective potential of Clerodendron glandulosum.Coleb (CG) aqueous extract. Acute and subchronic toxicity tests were performed using Swiss albino mice as per the guideline of Organisation for Economic Cooperation and Development (OECD). Also, hepatoprotective potential of CG extract was examined in experimental model of carbon tetrachloride (CCl( 4))-induced hepatotoxicity. Acute and subchronic toxicity tests revealed that CG extract is non-toxic and its median lethal dose (LD(50)) value is >5000 mg/kg bodyweight. Also, rats pretreated with CG extract followed by administration of CCl(4) recorded significant decrement in plasma marker enzymes of hepatic damage, total bilirubin content and hepatic lipid peroxidation. While, hepatic reduced glutathione, ascorbic acid content, activity levels of superoxide and catalase and plasma total protein content were significantly increased. Microscopic examination of liver showed that pretreatment with CG extract prevented CCl(4)-induced hepatic damage in CG + CCl( 4) group. CG extract has hepatoprotective potential by modulating activity levels of enzymes and metabolites governing liver function and by helping in maintaining cellular integrity of hepatocytes that is comparable with that of standard drug silymarin. CG extract exhibits potent hepatoprotective activity against CCl(4)-induced hepatic damage but does not exhibit any toxic manifestations.     

Protective effects of Ziziphora tenuior extract against chlorpyrifos induced liver and lung toxicity in rat: Mechanistic approaches in subchronic study

Chlorpyrifos (CPF) is one of the most widely used organophosphorus, which has spurred renewed interest. This study was conducted to investigate the protective effect of ziziphora tenuior extract against CPF‐induced liver and lung toxicity. This study conducted 8‐week rat sub‐chronic toxicity study and then the effect of ziziphora tenuior extract in 3 different doses (40, 80, 160 mg/kg) was determined. We administrated maximum tolerated dose of CPF (6.75 mg/kg) by gavage for 8 weeks (5 times in week) to male rats. Rats were sacrificed 24 h after last dose and the biochemical analysis, which confirms involvement of oxidative stress in the pathogenesis of CPF toxicity in liver including increased in lipid peroxidation, protein carbonyl content, and ROS formation, glutathione depletion, decreased of antioxidant effect via frap oxidation and cytochrome c expulsion. In addition, pathological lesions confirm the dysfunction of the organs (liver and lung). In addition, using of ziziphora extract as an antioxidant is resulted in amelioration of oxidative stress marker in liver and lung damage. In conclusion, the current study revealed that CPF toxicity is related to oxidative stress and induction of cell death signaling and cotreatment with ziziphora extract is recommended in the routine therapy for the protection against CPF induced liver and lung tissue damage.     

Antifibrotic effect ofStephania tetrandra on experimental liver fibrosis induced by bile duct ligation and scission in rats

We examined the antifibrotic effect of a methanol extract from Stephania tetrandra (ST) on experimental liver fibrosis. Liver fibrosis was induced by bile duct ligation and scission (BDL/S) in rats. In BDL/S rats, activity levels of aspartate transaminase (AST), alanine transaminse (ALT), alkaline phosphatase (ALP), concentration of total bilirubin in serum, and hydroxyproline content of the liver were significantly increased. The ST treatment (either 100 mg/kg/day or 200 mg/kg/day, p.o. for 4 weeks) in BDL/S rats reduced the serum AST, ALT and ALP activity levels significantly (p< 0.01). Similarly, when compared to the control group, the concentration of hydroxyproline in the livers of the BDL/S rats treated with 100mg or 200mg ST treated rats decreased by 40% and 33% respectively, when compared to the BDL/S control group (p<0.01). The morphological characteristics of fibrotic liver that were observed in the BDL/S control group, improved in the ST treated BDL/S group. In the fibrotic liver of BDL/S rats treated with ST, a marked reduction in the numbers of alpha smooth muscle cell actin positive stellate cells was observed. These results indicate that doses of either 100 or 200 mg/kg/day of methanol extract from S. tetrandra, had an antifibrotic effect in rats with liver fibrosis induced by bile duct ligation and scission.     

Hepatoprotective effect of flavonol glycosides rich fraction from egyptianVicia calcarata desf. Against CCI4-induced liver damage in rats

The hepatoprotective activity of flavonol glycosides rich fraction (F-2), prepared from 70% alcohol extract of the aerial parts of V. calcarata Desf., was evaluated in a rat model with a liver injury induced by daily oral administration of CCl4 (100 mg/kg, b.w) for four weeks. Treatment of the animals with F-2 using a dose of (25 mg/kg, b.w) during the induction of hepatic damage by CCl4 significantly reduced the indices of liver injuries. The hepatoprotective effects of F-2 significantly reduced the elevated levels of the following serum enzymes: alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and lactate dehydrogenase (LDH). The antioxidant activity of F-2 markedly ameliorated the antioxidant parameters including glutathione (GSH) content, glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), plasma catalase (CAT) and packed erythrocytes glucose-6-phosphate dehydrogenase (G6PDH) to be comparable with normal control levels. In addition, it normalized liver malondialdehyde (MDA) levels and creatinine concentration. Chromatographic purification of F-2 resulted in the isolation of two flavonol glycosides that rarely occur in the plant kingdom, identified as quercetin-3, 5-di-O-beta-D-diglucoside (5) and kaempferol-3, 5-di-O-beta-D-diglucoside (4) in addition to the three known compounds identified as quercetin-3-O-alpha-L-rhamnosyl- (1-->6)-beta-D-glucoside [rutin, 3], quercetin-3-O-beta-D-glucoside [isoquercitrin, 2] and kaempferol-3-O-beta-D-glucoside [astragalin, 1]. These compounds were identified based on interpretation of their physical, chemical, and spectral data. Moreover, the spectrophotometric estimation of the flavonoids content revealed that the aerial parts of the plant contain an appreciable amount of flavonoids (0.89%) calculated as rutin. The data obtained from this study revealed that the flavonol glycosides of F-2 protect the rat liver from hepatic damage induced by CCl4 through inhibition of lipid peroxidation caused by CCl4 reactive free radicals.     

Protective effect of Rumex patientia (English Spinach) roots on ferric nitrilotriacetate (Fe-NTA) induced hepatic oxidative stress and tumor promotion response.

In this communication, we document the antioxidant potential of ethanolic extract of Rumex patientia L. (Polygonaceae) roots and its chemopreventive effects against Fe-NTA mediated hepatic oxidative stress, hepatotoxicity and tumor promotion response. The extract exhibited high polyphenolic content, potent reducing power and significantly scavenged free radicals (including several reactive oxygen species (ROS) and reactive nitrogen species (RNS)). The extract also significantly and dose dependently protected against oxidative damage to lipids and DNA. These results indicated R. patientia root extract to exert a potent antioxidant activity in vitro. The efficacy of extract was also evaluated in vivo and it was found to exert a potent protective affect in acute oxidative tissue injury animal model: ferric nitrilotriacetate (Fe-NTA) induced hepatotoxicity in mice. Administration of Fe-NTA (9 mg/kg body weight, i.p.) to mice led to a significant oxidative stress and allied damage in liver tissues and induced hyperproliferation. A significant depletion was observed in GSH content and enzymes implicated in its metabolism. Attenuation also occurred in activities of other hepatic antioxidant enzymes including SOD, CAT, and GPX. Fe-NTA also incited hyperproliferation response elevating ornithine decarboxylase activity and [(3)H]-thymidine incorporation into DNA. Histopathological investigations and liver function tests (LFT) indicated Fe-NTA to cause extensive hepatic damage. However, prophylactic treatment with R. patientia root extract at a dose regimen of 100-200mg/kg body weight for a week not only restored hepatic antioxidant armory close to normal, but also significantly precluded oxidative damage restoring normal hepatic architecture and levels of hepatic damage markers. The data obtained in the present study illustrates R. patientia roots to possess potent antioxidant and free radical scavenging activities and thwart oxidative damage and hyperproliferation in hepatic tissues.     

Antigenotoxic effects ofSatureja hortensis L. on rat lymphocytes exposed to oxidative stress

The protective properties of Satureja hortensis L. on the rat lymphocytes DNA lesions were tested. Lymphocytes were isolated from blood samples taken from healthy rats. DNA breaks and resistance to H2O2-induced damage were measured with the comet assay. Rat lymphocytes were incubated in S. hortensis ethanolic extract (SHE) (0.05, 0.1, 0.5, 1.0, and 2.5 mg/ mL), essential oil (SHEO)(0.05, 0.1, 0.5, 1.0, and 2.5 microL/mL), H2O2 (50, 100, and 200 microM), a combination of H2O2 (200 mM) with either SHE (1.0, 2.5 mg/mL) or SHEO (1.0, 2.5 microL/mL) at 4 degrees C for 30 min, and the extent of DNA migration was measured using a single-cell microgel electrophoresis technique under alkaline conditions. Treatment of rat lymphocytes with SHE or SHEO resulted in significant reduction of H2O2-induced DNA damage compared to controls. SHE exhibited a significant (P < 0.01) inhibitory effect on oxidative DNA damage at 2.5 mg/mL. SHEO (1.0 and 2.5 microL/mL) also showed significant inhibitory effects (P < 0.01) on H2O2 induced chromosomal damage. In conclusion both the ethanolic extract and the essential oil of the plant reversed the oxidative damage to rat lymphocytes induced by hydrogen peroxide.     

‘Okra’ Hibiscus esculentus L.: A study of its hepatoprotective activity

In the present study, an attempt has been made to validate the claimed uses of ‘Okra’ Hibiscus esculentus in liver diseases. The preventive action of ethanolic extract of okra (EEO) against liver injury was evaluated in rodents using carbon tetrachloride-induced hepatotoxicity model. EEO, at 250 and 500 mg/kg body weight, exerted significant dose-dependent hepatoprotection by decreasing the CCl₄-induced elevation of serum SGOT, SGPT, ALP, GGT, cholesterol, triglycerides and malondialdehyde (MDA) non-protein sulfhydryls (NP-SH) and total protein (TP) levels in the liver tissue. A significant reduction was also observed in pentobarbital-induced sleeping time in mice. The hepatoprotective and antioxidant activities of the extract are being comparable to standard silymarin. These findings were supported by histological assessment of the liver biopsy. The ability of okra extract to protect chemically induced liver damage may be attributed to its potent antioxidant property.