Nigella sativa L. oil protects against induced hepatotoxicity and improves serum lipid profile in rats

The effects of 4 weeks oral intake of Nigella sativa L. (NS) oil on some liver function tests and D-galactosamine- or carbon tetrachloride-induced hepatotoxicity were investigated in male albino rats. In another series of experiments, the effect of the oil on serum lipid profile was examined in male spontaneously hypertensive rats of stroke prone strain and Wistar Kyoto rats. The study showed that daily administration of the oil per se (800 mg/kg orally for 4 weeks) did not adversely effect the serum transaminases (ALT and AST), alkaline phosphatase, serum bilirubin or prothrombin activity in normal albino rats. When the oil was given for 4 weeks prior to induction of hepatotoxicity by D-galactosamine or carbon tetrachloride, it was able to give complete protection against d-galactosamine and partial protection against carbon tetrachloride hepatotoxicity. NS oil showed a favourable effect on the serum lipid pattern where the administration of the oil (800 mg/kg orally for 4 weeks) caused a significant decrease in serum total cholesterol, low density lipoprotein, triglycerides and a significant elevation of serum high density lipoprotein level.     

Inhibition of cytochrome P450 2E1 expression by oleanolic acid: hepatoprotective effects against carbon tetrachloride-induced hepatic injury.

The protective effects of oleanolic acid on carbon tetrachloride-induced hepatotoxicities and the possible mechanisms involved in this protection were investigated in mice. Pretreatment with oleanolic acid prior to the administration of carbon tetrachloride significantly prevented the increase in serum alanine aminotransferase and lactate dehydrogenase activity and liver lipid peroxidation in a dose-dependent manner. Hepatic glutathione levels and glutathione-S-transferase activities were not affected by treatment with oleanolic acid alone but pretreatment with oleanolic acid protects carbon tetrachloride-induced depletion of hepatic glutathione levels. The effects of oleanolic acid on the cytochrome P450 (P450) 2E1, the major isozyme involved in carbon tetrachloride bioactivation were investigated. Treatment of mice with oleanolic acid resulted in a significant decrease of P450 2E1-dependent p-nitrophenol and aniline hydroxylation in a dose-dependent manner. Consistent with these observations, the P450 2E1 expressions were also decreased, as determined by immunoblot analysis. These results show that the protective effects of oleanolic acid against the carbon tetrachloride-induced hepatotoxicity may, at least in part, be due to its ability to block bioactivation of carbon tetrachloride mainly by the inhibition of expression and activities of P450 2E1.     

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.     

Protection against carbon tetrachloride hepatotoxicity by oleanolic acid is not mediated through metallothionein

Oleanolic acid is a triterpenoid compound that has been shown to protect against liver injury produced by some hepatotoxicants. This study was designed to characterize the protective effects of oleanolic acid on carbon tetrachloride-induced hepatotoxicity, and the role of metallothionein in the protection. Oleanolic acid pretreatment (100–400 μmol/kg, sc) protected Sprague–Dawley rats and mice from carbon tetrachloride-induced liver injury in a dose- and time-dependent manner, as evidenced by serum alanine aminotransferase and sorbitol dehydrogenase activities, as well as by histopathology. The protection against carbon tetrachloride hepatotoxicity was not evident until animals were pretreated with oleanolic acid 12 h, and lasted for 72 h after a single injection. This suggests that the protection might be due to induction of some adaptive mechanisms. Metallothionein (MT), an acute-phase protein proposed to decrease carbon tetrachloride-induced liver injury, was dramatically induced following oleanolic acid treatment. To examine whether oleanolic acid protection is mediated through MT, MT-I and II knock-out (MT-null) mice were utilized. Oleanolic acid pretreatment increased MT levels in control mice (20-fold), but not in MT-null mice, however, it protected equally against carbon tetrachloride-induced hepatotoxicity in both control and MT-null mice. These data indicate that oleanolic acid is effective in protecting rats and mice from the hepatotoxicity produced by carbon tetrachloride, and the protection is not mediated through induction of MT.     

The protective effects of PMC against chronic carbon tetrachloride-induced hepatotoxicity in vivo.

In this study, PMC (2,2,5,7,8-pentamethyl-6-hydroxychromane), a derivative of alpha-tocopherol, dose-dependently (1-10 mg/kg) ameliorated the increase in plasma aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) levels caused by chronic repeated carbon tetrachloride (CCl4) intoxication in mice. Moreover, PMC significantly improved the CCl4-induced increase of hepatic glutathione peroxidase, reductase, and superoxide dismutase activities. PMC also restored the decrement in the glutathione content of hepatic tissues in CCl4-intoxicated mice. Furthermore, it also dose-dependently inhibited the formation of lipid peroxidative products during carbon tetrachloride treatment. Histopathological changes of hepatic lesions induced by carbon tetrachloride were significantly improved by treatment with PMC in a dose-dependent manner. These results suggest that PMC exerts effective protection in chronic chemical-induced hepatic injury in vivo.     

Protective effects of echinacoside on carbon tetrachloride-induced hepatotoxicity in rats

The aim of this study was to investigate the possible protective effects of echinacoside, one of the phenylethanoids isolated from the stems of Cistanches salsa, a Chinese herbal medicine, on the free radical damage of liver caused by carbon tetrachloride in rats. Treatment of rats with carbon tetrachloride produced severe liver injury, as demonstrated by dramatic elevation of serum ALT, AST levels and typical histopathological changes including hepatocyte necrosis or apoptosis, haemorrhage, fatty degeneration, etc. In addition, carbon tetrachloride administration caused oxidative stress in rats, as evidenced by increased reactive oxygen species (ROS) production and MDA concentrations in the liver of rats, along with a remarkable reduction in hepatic SOD activity and GSH content. However, simultaneous treatment with echinacoside (50mg/kg, intraperitoneally) significantly attenuated carbon tetrachloride-induced hepatotoxicity. The results showed that serum ALT, AST levels and hepatic MDA content as well as ROS production were reduced dramatically, and hepatic SOD activity and GSH content were restored remarkably by echinacoside administration, as compared to the carbon tetrachloride-treated rats. Moreover, the histopathological damage of liver and the number of apoptotic hepatocytes were also significantly ameliorated by echinacoside treatment. It is therefore suggested that echinacoside can provide a definite protective effect against acute hepatic injury caused by CCl(4) in rats, which may mainly be associated with its antioxidative effect.     

Hepatotoxic interactions of ethanol with allyl alcohol or carbon tetrachloride in rats.

To assess whether potential toxic interactions occur between ethanol and allyl alcohol or carbon tetrachloride following subacute, concurrent chemical exposure, male Fischer 344 rats, approximately 70 d of age, were given ethanol at 0, 0.05, 0.1, 0.2, or 0.5 ml/kg in corn oil daily by gavage for 14 d (ETOH group), or the same levels of ethanol with 21 mg allyl alcohol/kg (ALAC group), or the same levels of ethanol with 20 mg carbon tetrachloride/kg (CCL4 group). Hepatic response was assessed 24 h after the last dose. Interactions were evaluated by comparing the ETOH group with either the ALAC group or the CCL4 group using multivariate analysis of variance procedures. No statistically significant interaction was seen between the ETOH group and the ALAC group at the dosages used. Although an interaction between ethanol and carbon tetrachloride given simultaneously was not statistically significant, a small interactive effect on weight gain from d 0 to termination was apparent (p = .057). Exposure to ethanol alone resulted in a concentration-dependent decrease in absolute and relative liver weight, with a threshold between 0.05 and 0.1 ml/kg. There was no histopathological evidence of hepatic damage with ethanol alone, and no effect on hepatic cytochrome P-450 and glutathione levels or on serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALK). Exposure to allyl alcohol alone resulted in significant increases in absolute and relative liver weights, liver glutathione, and periportal hepatocellular vacuolar degeneration. Exposure to carbon tetrachloride alone resulted in significant increases in absolute and relative liver weight, serum levels of ALT, AST, and ALK, and centrilobular hepatocellular vacuolar degeneration and necrosis. These observations indicate that subacute, concurrent exposure of ethanol with carbon tetrachloride or allyl alcohol at ethanol levels comparable to those reported in gavage vehicles did not result in interactive toxicity.     

Potentiation of carbon tetrachloride hepatotoxicity by phenylpropanolamine

Hepatic necrosis produced by carbon tetrachloride (0.02, 0.06, or 0.20 ml/kg, ip) in mice was found to be potentiated by simultaneous cotreatment with phenylpropanolamine (200 mg/kg, ip), a drug with catecholamine-like pharmacologic effects. The ability to potentiate carbon tetrachloride-induced hepatic necrosis was shared by a compound with agonist effects relatively selective for alpha 2-adrenoreceptors (clonidine, 5 mg/kg, ip), but not by specific alpha 1-adrenoreceptor agonists (phenylephrine, up to 100 mg/kg, ip and methoxamine, up to 50 mg/kg, ip) or by the beta-adrenoreceptor agonist isoproterenol (up to 100 mg/kg, ip). Yohimbine (5 mg/kg, ip), a selective alpha 2-adrenoreceptor antagonist, completely blocked the potentiating effect of phenylpropanolamine on carbon tetrachloride hepatotoxicity, providing further evidence that the increased hepatotoxic response with phenylpropanolamine cotreatment was mediated through alpha 2-adrenoreceptor stimulation. Four potential mechanisms for phenylpropanolamine potentiation of liver injury from carbon tetrachloride were examined: (1) increased concentrations of carbon tetrachloride in the liver from greater absorption or altered distribution; (2) diminished food consumption leading to a starvation-like increase in responsiveness to carbon tetrachloride; (3) impaired detoxification through a depletion of hepatic glutathione content; and (4) enhanced toxicity produced by elevated core body temperature. None of these potential mechanisms was supported by the experimental results. It is concluded that phenylpropanolamine and related compounds potentiate carbon tetrachloride hepatotoxicity through a mechanism involving alpha 2-adrenoreceptor stimulation that has yet to be identified.     

Effects of adenosine on liver cell damage induced by carbon tetrachloride

Adenosine administration delayed the fatty liver and cell necrosis induced by carbon tetrachloride without affecting the action of the hepatotoxin on protein synthesis and liver triacylglycerol release. Adenosine produced a drastic antilipolytic effect accompanied by a decrease in the incorporation of [1-14C]palmitic acid into triacylglycerols and free fatty acids of the liver. Furthermore, a decrease in the serum levels of ketone bodies was observed at early times. The nucleoside also avoided the release of intracellular enzymes and prevented the lipid peroxidation produced by carbon tetrachloride during the 4 hr of treatment. The protective action of adenosine was transient, lasting 3-4 hr, probably the time required to be metabolized. The results suggest that the antilipolytic effect of the nucleoside, the inhibition of hepatic fatty acid metabolism, and the decrease in carbon tetrachloride-induced lipoperoxidation that it produced are involved in the delayed acute hepatotoxicity induced by carbon tetrachloride.     

六味五灵片对四氯化碳致大鼠肝纤维化的保护作用

目的研究六味五灵片对四氯化碳(CCl4)所致大鼠肝纤维化的保护作用。方法用CCl4-植物油溶液腹腔注射造模,将造模成功的大鼠随机分为5组,每组12只,分别为模型组、复方鳖甲软肝片组、六味五灵片低剂量组(4 g.kg-1)、六味五灵片中剂量组(8 g.kg-1)、六味五灵片高剂量组(16 g.kg-1)。以血清中谷草转氨酶(AST)、谷丙转氨酶(ALT)、透明质酸(HA)、层粘连蛋白(LN)及羟脯氨酸(HyP)和肝组织中还原型谷胱甘肽(GSH)、超氧化物歧化酶(SOD)及丙二醛(MDA)为评价指标,以肝组织Masson染色追踪其肝纤维化程度。结果六味五灵片能明显降低CCl4所致的大鼠血清中ALT、AST、HA、LN和HyP的含量(P<0.05),降低肝组织中的MDA含量(P<0.05),明显升高肝组织中的GSH和SOD含量(P<0.05),肝组织纤维化变性明显减轻,肝组织结构比较完好。结论六味五灵片对四氯化碳所致大鼠肝纤维化具有保护作用。     

Evidence for carbon tetrachloride-induced lipid peroxidation in mouse liver

The involvement of lipid peroxidation in the mechanism of carbon tetrachloride-induced hepatotoxicity has been a point of controversy. Previous investigators have reported an absence of lipid peroxidative degradation products in mice after exposure to carbon tetrachloride and have used this evidence against the hypothesis that lipid peroxidation is an integral part of the events that cause tissue damage. We have compared the extent of lipid peroxidation caused by carbon tetrachloride between Sprague-Dawley rats and three strains of mice (A/J, BALB/cJ, and C57B1/6J) in in vitro and in vivo systems. Hepatic microsomes isolated from fasted mice of each strain produced more malondialdehyde (a degradation product of lipid peroxidation) per mg microsomal protein than those isolated from fasted rats at all times of incubation with CCl₄. In vivo lipid peroxidation was estimated by the lipid conjugated diene content in hepatic microsomes from the rat and three strains of mice. Increased conjugated diene formation was observed in microsomal lipids of these animals after intraperitoneal injection of CCl₄ (1 ifml/kg as a 20% solution in corn oil) when compared to animals given only corn oil, but no differences were found in the amount of conjugated dienes between mice and rats. Our observations show that the CCl₄-treated mouse undergoes hepatic lipid peroxidation at least as well as the rat, and indicate that lipid peroxidation cannot be excluded as a mechanism of carbon tetrachloride hepatotoxicity as has been claimed on the basis of its ineffectiveness in the mouse.     

Hepatoprotective Effect of Methanol Extracts of Zingiber officinale and Cichorium intybus

The present work was carried out to investigate the hepatoprotective effect of ginger, chicory and their mixture against carbon tetrachloride intoxication in rats. Carbon tetrachloride treatment significantly elevated the alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and gamma glutamyltransferase activities and the serum triglycerides and cholesterol concentration as compared to control group. It also increased RBCs counts and Hb concentration, total or differential leucocytes counts. However it decreased platelet counts, platelet distribution width, mean platelet volume, platelet larger cell ratio. Methanol extract of ginger (250 and 500 mg/kg) and chicory (250 and 500 mg/kg) given alone or mixed (1:1 wt/wt) significantly restored the carbon tetrachloride-induced alterations in the biochemical and cellular constituents of blood. No toxic symptoms were reported in doses up to 5 g/kg. Alkaloids and/or nitrogenous bases, carbohydrates and/or glycosides, tannins, flavonoids, saponins and unsaturated sterols and/or triterpenes are the main active constituents of their methanol extract. The hepatoprotective effect of ginger and chicory was also confirmed by the histopathological examination of liver tissue.     

大蒜油对大鼠实验性脂肪肝的预防作用

目的观察大蒜油对长期喂食高脂饲料引起的大鼠脂肪肝的预防作用。方法于实验第一天一次性注射小剂量四氯化碳并长期喂食高脂饲料复制大鼠脂肪肝模型,大蒜油低、中、高组分别灌胃相应浓度大蒜油,正常对照组、模型组同时灌胃等体积蒸馏水、玉米油,1次/d,连续8周,测定血脂和肝脂,以肝脏的重量、肝脂质含量和肝细胞的脂变程度为主要衡量指标,观察大蒜油预防脂肪肝效果。结果大蒜油各组与模型组相比,肝组织中三酰甘油(TG)、总胆固醇(TC)、游离脂肪酸(FFA)、血清中的葡萄糖(GLU)、TC、TG、FFA、低密度脂蛋白(LDL)含量和谷丙转氨酶(ALT)活力显著降低,病理检查苏丹Ⅲ染色肝细胞脂变减轻。结论大蒜油对大鼠实验性脂肪肝的形成具有预防作用。     

Interaction between ethanol and carbohydrate on the metabolism in rat liver of aromatic and chlorinated hydrocarbons

Metabolic rates of eight hydrocarbons (benzene, toluene, styrene, chloroform, carbon tetrachloride, 1,2-dichloroethane, 1,1-dichloroethylene, and trichloroethylene) were measured in vitro with the livers from rats that had consumed ethanol for 3 weeks in combination with various diets. Ethanol and carbohydrate antagonized each other in connection with activity of hepatic drug-metabolizing enzymes (mixed-function oxidases); the former increased and the latter decreased these enzymes. A decrease (increase) in carbohydrate intake augmented (suppressed) the action of ethanol in a dose-related manner. In particular, a combination of ethanol with a low-carbohydrate diet (DeCarli and Lieber diet) enhanced enzyme activity and potentiated carbon tetrachloride-induced hepatotoxicity. Enhancement of metabolism and potentiation of toxicity were due to the combination rather than to ethanol per se.     

Protective role of dietary butylated hydroxyanisole against chemical-induced acute liver damage in mice

Prior consumption of a diet containing the food antioxidant, butylated hydroxyanisole (BHA), by female mice prevented the development of or minimized the acute liver damage caused by monocrotaline, acetaminophen, or bromobenzene. In contrast, neither the incidence nor the severity of carbon tetrachloride-induced hepatotoxicity was affected by dietary BHA. Hepatotoxicity was judged by plasma alanine aminotransferase and aspartate aminotransferase levels, hepatic cytochrome P-450 content, and liver histology. The protective effect of BHA against acetaminophen-induced hepatotoxicity was not demonstrated in male mice. The observed protection by dietary BHA against acetaminophen- and bromobenzene-induced hepatotoxicity was associated with the increase of liver glutathione. It is concluded that the protective action of BHA is dependent upon the nature of the toxic agent.     

Mechanism for the protective effects of silymarin against carbon tetrachloride-induced lipid peroxidation and hepatotoxicity in mice. Evidence that silymarin acts both as an inhibitor of metabolic activation and as a chain-breaking antioxidant

Administration of silymarin (800 mg/kg i.p.) 30 min before carbon tetrachloride (18 microL/kg i.p.) did not modify total hepatic levels of CCl4 and metabolites in mice, but decreased by 40% the in vivo covalent binding of CCl4 metabolites to hepatic lipids at 2 hr. This pretreatment decreased by 60% the exhalation of ethane during the first hour after CCl4, and decreased by 50% the incidence of liver cell necrosis. In vitro, silymarin (800 micrograms/mL) decreased by 50 to 70% various monooxygenase activities, and decreased by 20% the covalent binding of CCl4 metabolites to microsomal proteins. Silymarin (800 micrograms/mL) decreased by 70% in vitro lipid peroxidation mediated by CCl4 metabolites, and decreased by 90% peroxidation mediated by NADPH alone. Silibinin, one of the three isomers composing silymarin, also decreased carbon tetrachloride-induced lipid peroxidation; this effect, however, was less than that of silymarin in vitro, and was more transient in vivo. Pretreatment with silibinin (800 mg/kg i.p.) 30 min before CCl4 (18 microL/kg i.p.) did not improve SGPT activity or liver histology at 24 hr. We conclude that silymarin prevents carbon tetrachloride-induced lipid peroxidation and hepatotoxicity in mice, firstly, by decreasing the metabolic activation of CCl4, and, secondly, by acting as a chain-breaking antioxidant.     

Protective effect of curcumin in rat liver injury induced by carbon tetrachloride

This study was carried out to investigate the protective effects of curcumin on acute or subacute carbon tetrachloride-induced liver damage in rats. Acute hepatotoxicity was induced by intraperitoneal injection of carbon tetrachloride after 4 consecutive days of curcumin treatment. Subacute hepatotoxicity was induced by oral administration of carbon tetrachloride twice a week during 4 weeks of curcumin treatment. In rats with acute liver injury, curcumin (100 and 200 mg kg(-1)) lowered the activity of serum alanine aminotransferase to 52-53% (P < 0.05) and aspartate aminotransferase to about 62% (P < 0.05) those of control rats. In rats with subacute liver injury, curcumin (100 mg kg(-1)) lowered the activity of serum alanine aminotransferase to 34% (P < 0.01) and alkaline phosphatase to 53% (P < 0.05) of control rats. The liver hydroxyproline content in the curcumin (100 mg kg(-1))-treated group was reduced to 48% of the carbon tetrachloride control group (P < 0.01). Malondialdehyde levels in curcumin (100 mg kg(-1)) treated rat liver was decreased to 67% of the control rat liver (P < 0.01) in subacute injury. It was concluded that curcumin improved both acute and subacute liver injury induced by carbon tetrachloride in rats.     

Hepatoprotective activity of aqueous extract of Portulaca oleracea in combination with lycopene in rats

Objective:

To investigate the hepatoprotective activity of the aqueous extract of the aerial parts of Portulaca oleracea (P. oleracea) in combination with lycopene against carbon tetrachloride induced hepatotoxicity in rats.

Materials and Methods:

Hepatotoxicity was induced in male Wistar rats by intraperitoneal injection of carbon tetrachloride (0.1 ml/kg b.w for 14 days). The aqueous extract of P. oleracea in combination with lycopene (50 mg/kg b.w) was administered to the experimental animals at two selected doses for 14 days. The hepatoprotective activity of the combination was evaluated by the liver function marker enzymes in the serum [aspartate transaminases (AST), alanine transaminases (ALT), alkaline phosphatase (Alk.P), total bilirubin (TB), total protein (TP) and total cholesterol (TC)], pentobarbitone induced sleeping time (PST) and histopathological studies of liver.

Results:

Both the treatment groups showed hepatoprotective effect against carbon tetrachloride induced hepatotoxicity by significantly restoring the levels of serum enzymes to normal which was comparable to that of silymarin group. Besides, the results obtained from PST and histopathological results also support the study.

Conclusions:

The oral administration of P. oleracea in combination with lycopene significantly ameliorates CCl₄ hepatotoxicity in rats.     

The ethanol-soluble part of a hot-water extract from Artemisia iwayomogi inhibits liver fibrosis induced by carbon tetrachloride in rats

This study was carried out to investigate the protective effects of the hot-water extract from Artemisia iwayomogi (Compositae) on carbon tetrachloride-induced liver fibrosis in rats. Liver injury was induced by oral administration of carbon tetrachloride (1 mL kg(-1)) twice a week during 4 weeks of A. iwayomogi treatment. Extracts from A. iwayomogi were prepared and administered to rats orally (2 g kg(-1) as A. iwayomogi for 4 weeks) as follows: group 1, hot-water extract; group 2, ethanol-soluble part of hot-water extract; group 3, ethanol-insoluble part of hot-water extract; and group 4, methanol extract. In rats treated with the ethanol-soluble part of the hot-water extract, liver hydroxyproline content was reduced to 74% that of carbon tetrachloride control rats (P < 0.05). Protein expression of alpha smooth muscle cell like actin was also decreased in rats treated with the ethanol-soluble part of the hot-water extract, which indicates inhibition of hepatic stellate cell activation. Liver malondialdehyde levels were significantly lowered in rats treated with the ethanol-soluble part of hot-water extract (P < 0.05). Serum cholesterol levels in rats treated with hot-water extract, ethanol-soluble or -insoluble parts of hot-water extract or methanol extract were significantly reduced when compared with those of carbon tetrachloride control rats (P < 0.05). The ethanol-soluble part of the hot-water extract from A. iwayomogi inhibited fibrosis and lipid peroxidation in rats with liver fibrosis induced by carbon tetrachloride. Both hot-water extract (either ethanol-soluble or -insoluble) and methanol extract of A. iwayomogi also lowered serum cholesterol levels in fibrotic rats.     

‘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.