Hepatoprotective activity of Moringa oleifera on antitubercular drug-induced liver damage in rats

Moringa oleifera Lam (Moringaceae), commonly known as "Drumstick," is used in Indian folk medicine for the treatment of various illness. We have evaluated the hepatoprotective effect of an ethanolic extract of M. oleifera leaves on liver damage induced by antitubercular drugs such as isoniazid (INH), rifampicin (RMP), and pyrazinamide (PZA) in rats. Oral administration of the extract showed a significant protective action made evident by its effect on the levels of glutamic oxaloacetic transaminase (aspartate aminotransferase), glutamic pyruvic transaminase (alanine aminotransferase), alkaline phosphatase, and bilirubin in the serum; lipids, and lipid peroxidation levels in liver. This observation was supplemented by histopathological examination of liver sections. The results of this study showed that treatment with M. oleifera extracts or silymarin (as a reference) appears to enhance the recovery from hepatic damage induced by antitubercular drugs.     

Antihyperglycemic property of Tragia cannabina in streptozotocin-induced diabetic rats

The present study was performed to investigate the efficacy of an ethanol extract of the roots of Tragia cannabina for antihyperglycemic and antioxidant effects in streptozotocin (STZ)-induced diabetic rats. Male Wistar rats were administered T. cannabina (250 mg/kg) orally for 21 days, and blood glucose level was measured weekly. At the end of 21 days, concentrations of serum lipids such as total cholesterol, triglycerides, and high-density lipoprotein (HDL) and protein markers such as total protein, albumin, globulin, and albumin:globulin ratio (A:G) were estimated. Also, levels of enzymes such as serum glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), and alkaline phosphatase (ALP) were determined. Antioxidant activity of the extract was evaluated by estimating lipid peroxides (LPO), superoxide dismutase (SOD), and catalase in liver of normal control and STZ- and extract-treated rats. Histopathological changes of liver and kidney were also studied in STZ-induced diabetic animals and normal controls. All these effects produced by the extract were compared with glibenclamide, a standard antidiabetic drug. Oral administration of T. cannabina for 21 days resulted in a significant reduction in blood glucose level, lipid concentration, and SGOT, SGPT, ALP, and LPO levels accompanied by an increase in the levels of SOD and catalase in liver tissues of STZ-induced diabetic rats. Altered levels of protein markers also reverted back to normal. Histopathological changes of liver and kidney were returned to normal. The effects produced by the extract were comparable to that of glibenclamide. In conclusion, the T. cannabina showed significant antihyperglycemic and antioxidant effects in STZ-induced diabetic rats.     

富锗灵芝对四氯化碳诱导大鼠肝损伤保护作用

目的 探讨富锗灵芝胶囊对四氯化碳(CCI₄)所致大鼠肝损伤的保护作用。方法 50只Wistar雄性大鼠,随机分为对照组、模型组、富锗灵芝高、中、低剂量组(分别灌胃给予富锗灵芝胶囊450、230、80 mg/kg),采用CCl₄诱导大鼠急性肝损伤;分别测定血清中谷丙转氨酶(ALT)和谷草转氨酶(AST)活性,肝组织经苏木素-伊红染色,光镜下观察肝组织病理状况,并计算肝损伤指数。结果 与对照组比较,模型组大鼠ALT、AST活性[分别为(258.00±64.81)、(423.60±139.85)IU/L]明显升高,肝脏病变总评分[(194.50±27.71)分]明显升高(P<0.01);与模型组比较,富锗灵芝中、低剂量组大鼠血清ALT、AST活性[分别为(131.30±98.94)、(264.00±187.02)和(138.50±86.08)、(265.70±140.59)IU/L]明显降低(P<0.01),大鼠肝脏病变总评分[分别为(141.40±48.35)和(134.10±25.89)分]明显降低(P<0.01)。结论 富锗灵芝胶囊对CCl4所致大鼠肝损伤具有一定保护作用。     

Comparing the Protective Effects of Curcumin and Ursodeoxycholic Acid after Ethanol-Induced Hepatotoxicity in Rat Liver

BackgroundAlcohol consumption can cause hepatitis and long-term cirrhosis of the liver. The aim of this study was to evaluate the protective effects of curcumin (CUR) and ursodeoxycholic acid (UDCA) alone and together in the prevention and treatment of liver damage caused by overuse of ethanol.MethodsAdult Wistar rats were divided into 8 groups of 5, including the control group and various combinations of ethanol, CUR and UDCA groups. Twenty-eight days after the oral treatment, serum levels of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT) and Arginase I (ArgI) as well as serum levels of Albumin (Alb), total protein (TP) and Blood Urea Nitrogen (BUN) were measured, and liver tissue was evaluated histopathologically.ResultsThe solo administration of CUR, UDCA and CUR+UDCA had no effect on the blood parameters and liver tissue compared to the control group (p>0.05). The solo administration of CUR and UDCA in ethanol-treated rats significantly reduced ALT, AST, ALP, GGT, ArgI and BUN levels (p<0.05), while the solo administration increased Alb and TP levels compared to the ethanol group (p<0.05). In these groups, a significant decrease in cell necrosis and local inflammation of hepatocytes was observed, and the liver damage was mild. However, co-administration of ethanol, CUR and UDCA made significantly greater decrease in ALT, AST, ALP, GGT, ArgI and BUN levels (p>0.05), while the co-administration greatly increased Alb and TP levels compared to the ethanol group (p<0.05). Histopathologically, a decrease in structural changes in liver tissue and inflammation was observed, resulting in the improvement of liver tissue.ConclusionThe solo administration of CUR and UDCA could reduce ethanol-induced liver damage in rats and improve liver''s serum and blood parameters. However, the coadministration of CUR and UDCA has a greater efficacy.     

紫苏提取物对化学性肝损伤保护作用的研究

目的研究紫苏提取物(Perilla frutescens extract,PE)对急性化学性肝损伤的保护作用。方法80只雄性KM小鼠(体重20±2g)随机分为8组:正常对照组(NC),模型对照组(MC),阳性药联苯双酯(DDB)组(200mg/kg),迷迭香酸(rosmarinic acid,RAD)低、高剂量预防组(11、44mg/kg),PE低、中、高剂量预防组(30、60、120mg/kg)。NC、MC组灌胃生理盐水,其它各组灌胃同等容量的相应药物,每天给药1次。实验20d后,用四氯化碳(CCl4 0.05ml/kg)和乙酰氨基酸(APAP 250mg/kg)腹腔注射分别制作急性化学性肝损伤模型。测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性、甘油三酯(TG)含量,肝组织匀浆超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性、丙二醛(MDA)含量,并观察肝脏病理改变。结果PE(120mg/kg)能显著降低CCl4与APAP诱导的肝损伤小鼠血清ALT、AST活性、TG含量,升高肝脏SOD、GSH-Px活性,降低MDA含量能明显减轻肝组织损伤程度;PE对正常小鼠血清ALT、AST、TG无影响。结论PE对CCl4或APAP诱导的小鼠急性化学性肝脏氧化损伤具有显著保护作用。     

Effects of chicken extract on antioxidative status and liver protection under oxidative stress

Chicken extract contains carnosine and anserine, both of which possess some antioxidant abilities. The objective of this study was to investigate the protective effects of chicken extract in male Sprague-Dawley (SD) rats under induced oxidative stress. Carbon tetrachloride was used as the oxidative stress inducer. Glutamic-oxalacetatic transaminase (GOT), glutamic-pyruvic transaminase (GPT), total antioxidant status (TAS), thiobarbituric-reactive substances (TBARS), iron content, and the activities of antioxidant enzymes were determined. We concluded that under oxidative stress, the intake of chicken extract was helpful in promoting the activities of antioxidant enzymes and in protecting the liver from oxidative damage.     

Oxidative and nitrosative stress and apoptosis in the liver of rats fed on high methionine diet: Protective effect of taurine

ObjectiveThere are few reports about the direct toxic effects of hyperhomocysteinemia on the liver. We investigated oxidative and nitrosative stresses and apoptotic and necrotic changes in the liver of rats fed a high-methionine (HM) diet (2%, w/w) for 6 mo. We also investigated whether taurine, an antioxidant amino acid, is protective against an HM-diet–induced toxicity in the liver.MethodsLipid peroxide levels, nitrotyrosine formation, and non-enzymatic and enzymatic antioxidants were determined in livers of rats fed an HM diet. In addition, apoptosis-related proteins, proapoptotic Bax and antiapoptotic B-cell lymphoma-2 expressions, apoptotic cell count, histopathologic appearance in the liver, and alanine transaminase and aspartate transaminase activities in the serum were investigated.ResultsPlasma homocysteine levels and serum alanine transaminase and aspartate transaminase activities were increased after the HM diet. This diet resulted in increases in lipid peroxide and nitrotyrosine levels and decreases in non-enzymatic and enzymatic antioxidants in liver homogenates in rats. Bax expression increased, B-cell lymphoma-2 expression decreased, and apoptotic cell number increased in livers of rats fed an HM diet. Inflammatory reactions, microvesicular steatosis, and hepatocyte degeneration were observed in the liver after the HM diet. Taurine (1.5%, w/v, in drinking water) administration and the HM diet for 6 mo was found to decrease serum alanine transaminase and aspartate transaminase activities, hepatic lipid peroxide levels, and nitrotyrosine formation without any change in serum homocysteine levels. Decreases in Bax expression, increases in B-cell lymphoma-2 expression, decreases in apoptotic cell number, and amelioration of histopathologic findings were observed in livers of rats fed with the taurine plus HM diet.ConclusionOur results indicate that taurine has protective effects on hyperhomocysteinemia-induced toxicity by decreasing oxidative and nitrosative stresses, apoptosis, and necrosis in the liver.     

Effects of Sesame Oil Against After the Onset of Acetaminophen‐Induced Acute Hepatic Injury in Rats

Background: Acetaminophen (APAP) is a safe and effective analgesic and antipyretic when used at therapeutic levels. However, an acute or cumulative overdose can cause severe liver injury with the potential to progress to liver failure in humans and experimental animals. Much attention has been paid to the development of an antioxidant that protects against APAP‐induced acute hepatic injury. Hence, we aimed to investigate the effect of sesame oil against after the onset of acute hepatic injury in APAP‐overdosed rats. Methods: Male Wistar rats were first given 2 oral doses (1,000 mg/kg each) of APAP (at 0 and 24 hours) and then 1 oral dose of sesame oil (8 mL/kg at 24 hours). Results: After 48 hours, APAP increased aspartate and alanine aminotransferase levels in the rats' serum and centrilobular necrosis in liver tissue. In addition, APAP significantly decreased the rats' glutathione levels and mitochondrial aconitase activity, but increased superoxide anion, hydroxyl radical, and lipid peroxidation levels. Oral sesame oil (8 mL/kg, given at 24 hours) reversed all APAP‐altered parameters and protected the rats against APAP‐induced acute liver injury. Conclusion: We hypothesize that sesame oil acts as a useful agent that maintains intracellular glutathione levels and inhibits reactive oxygen species, thereby protecting rats against after the onset of APAP‐induced acute oxidative liver injury.     

微囊藻毒素LR对SD大鼠的短期毒效应研究

目的：研究和探讨微囊藻毒素（MCLR）对动物的短期毒效应作用。方法：SD大鼠经腹腔注射不同剂量的MCLR,分别于注射的1、7d和停药后第7天（即第14天）采目力大鼠的血清和肝、肾、心等组织标本,经酶学及病理学检验,观察其损伤效应。结果：122цg/kg剂量组,注射后24h可观察到大鼠心肌细胞肌浆溶解,核变性固缩,肌原纤维局部坏死;血清中天冬氨酸转氨酶(AST)、乳酸脱氢酶（LDH）和磷酸肌酸激酶（CPK）与其他组相比显著升高;肾细胞变性,血清中肌酐（BCr）和尿素氮（BUN）亦显著升高;同时肝细胞片状出血、坏死,注射剂量为50цg/kg和25цg/kg时,仍出现肝细胞重度和轻度颗粒变性。血清中丙氨酸转氨酶（ALT）、碱性磷酸酶（LDH）和AST显著上升。对照组大鼠的肝、肾、心等脏器均正常。结论：MCLR可引起SD大鼠肝、肾、心等脏器的短期毒效应,且随着剂量的增加,损伤效应加重。     

Effects of Picrorrhiza rhizoma water extracts on the subacute liver damages induced by carbon tetrachloride

The hepatoprotective activity of Picrorrhiza rhizoma (PR) water extract was evaluated on carbon tetrachloride (CCl(4))-induced subacute hepatic damage, induced by subcutaneous injection of CCl(4) (0.15 mL/kg of body weight) in pure olive oil (7.92%, vol/vol) three times a week for 10 weeks. Animals were sacrificed 10 weeks after oral administration of PR extracts at 50, 100, or 200 mg/kg or silymarin at 100 mg/kg, which were administered simultaneously with CCl(4); changes in body weight, liver weight, and serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were observed along with differences in liver histopathology and histomorphometry. In addition, liver malondialdehyde as an index for lipid peroxidation, hydoxyproline as an index for collagen synthesis, and protein content were determined. Ten weeks of CCl(4) injections caused subacute hepatic damage, featuring significantly less body weight gain and hepatic protein contents and higher liver weight, serum AST and ALT levels, and hepatic malondialdehyde and hydroxyproline contents with subacute hepatic damage-related histopathology of the liver. However, the CCl(4)-induced toxic effects were dramatically and dose-dependently inhibited by PR extract treatment. Thus oral administration of PR extracts significantly reduced CCl(4)-induced subacute hepatic damage in rats, probably by exerting a protective effect against hepatocellular necrosis via its free radical scavenging ability.     

Hepatoprotective role of ferulic acid: a dose-dependent study

Alcohol use is contributing to an unprecedented decline in life expectancy. Damage to the liver after ethanol administration is a well-known phenomenon. Free radical mechanisms have been proposed to play a part in ethanol-induced liver toxicity. Ingestion of diets rich in polyunsaturated fatty acids (PUFAs) along with alcohol is known to result in enhanced liver damage. The present work is aimed at evaluating the protective role of ferulic acid, a naturally occurring plant component, on alcohol- and PUFA-induced liver toxicity. Three different doses of ferulic acid (10, 20, and 40 mg/kg of body weight) were administered to rats given alcohol, heated PUFA (DeltaPUFA), and alcohol + DeltaPUFA. Influence of ferulic acid on alcohol-and PUFA-induced liver damage was evaluated by analyzing the activities of the liver marker enzymes alkaline phosphatase, gamma-glutamyl transferase, alanine transaminase, and aspartate transaminase. The activities of these liver marker enzymes were increased in the alcohol, DeltaPUFA, and alcohol + DeltaPUFA groups but were decreased significantly on treatment with ferulic acid. The low dose (10 mg/kg of body weight) was not effective, but both 20 mg and 40 mg/kg of body weight were found to be effective. The 20 mg/kg of body weight dose was found to be more effective than 40 mg/kg of body weight (the high dose). The administration of ferulic acid to normal rats did not produce any harmful effects. Thus our results show that ferulic acid is an effective anti-hepatotoxic agent without side effects and may be a good candidate in the current search for a natural hepatoprotective agent.     

Influence of N-acetylcysteine against dimethylnitrosamine induced hepatotoxicity in rats

This study evaluates the hepatoprotective and antioxidant properties of N-acetylcysteine (NAC) on dimethylnitrosamine (DMN) induced hepatotoxicity in male Wistar albino rats. A single intraperitoneal dose of DMN (5 mg/kg b.w.) caused a significant increase in the levels of the serum marker enzymes (aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), glutamyl transpeptidase (γ-GT)) and a subsequent decrease in AST, ALT, ALP and increase in LDH and γ-GT in the liver tissue indicating hepatocellular damage. Elevation in the status of lipid peroxidation, fall in the activities of the enzymic (superoxide dismutase, catalase) and non-enzymic antioxidants (vitamin C, vitamin E) in the liver tissue further confirms oxidative stress and hepatocellular damage induced on DMN administration. Oral administration of NAC (50 mg/kg b.w.) for 7 days significantly prevented the above alterations in the status of the marker enzymes of hepatotoxicity and antioxidant parameters and restored them towards normalcy, which was further substantiated by the histopathological studies of the liver tissue. These results suggest that NAC offers hepatoprotection by ameliorating DMN-induced oxidative stress and hepatotoxicity and this protective effect was attributed to its antioxidant and free radical scavenging properties.     

三氯乙烯急性染毒对大鼠肝脂质过氧化的影响

用抗氧化剂维生素E预处理后,观察三氯乙烯(3000mg/kg B.W.)一次性经口染毒24小时大鼠肝脏的超氧化物歧化酶、谷胱甘肽过氧化物酶等抗氧化酶活力及丙二醛含量的变化.结果表明,三氯乙烯染毒组肝脏中丙二醛含量、超氧化物歧化酶活力及血清谷丙转氨酶、谷草转氨酶活力均高于对照组(P<0.01),同时,肝细胞出现脂肪变与坏死;而维生素E干预组的丙二醛含量、超氧化物歧化酶活力及血清谷丙转氨酶、谷草转氨酶活力均分别低于三氯乙烯染毒组(P<0.01),肝细胞脂肪变与坏死程度有所改善,说明三氯乙烯急性染毒可引起肝脏脂质过氧化反应及肝损害,肝脏超氧化物歧化酶活力升高可能是机体受自由基及脂质过氧化反应刺激而诱导产生的一种适应性反应,维生素E对三氯乙烯所致的肝损害有一定的保护作用.     

Nitric oxide synthase inhibitor attenuates intestinal damage induced by zinc deficiency in rats

A nitric oxide synthase (NOS) inhibitor, NG-nitro-L -arginine methyl ester (L-NAME), was given to zinc-deficient (ZD) rats to determine whether it prevents the intestinal damage usually observed under these conditions. Weanling male rats were given free access to a ZD diet (2 mg zinc/kg), whereas control rats including pair-fed (PF) and ad libitum consumption (AL) groups were given a zinc-supplemented (50.8 mg zinc/kg) diet for 4 wk. Half of the ZD rats received L-NAME (0.3 g/L in drinking water) for 3 wk starting at the wk 2 of the deficient period. Plasma zinc concentration in ZD rats was significantly lower (P < 0.05) than that of AL and PF rats. Administration of L-NAME did not alter this concentration. Intestinal zinc concentration did not differ among groups. However, metallothionein-1 (MT-1) mRNA level was significantly lower in the intestine of ZD rats than in AL or PF rats. Treatment of ZD rats with L-NAME did not affect this level. Intestinal microvascular permeability evaluated by Evans blue showed significantly higher extravasation in ZD rats than in AL rats, whereas L-NAME administration inhibited the extravasation. Expression of inducible NOS mRNA was observed in intestine of ZD but not of AL or PF rats, and there was no significant difference between ZD rats, regardless of L-NAME treatment. The activity ratio of inducible NOS to total NOS in ZD rats not receiving L-NAME was significantly higher than that in AL rats or ZD rats treated with L-NAME (P < 0.05). The number of apoptotic-positive and goblet cells in intestinal villi was significantly higher in ZD rats compared with AL or PF rats. L-NAME administration in ZD rats reversed this effect. These results indicate that inhibition of NOS ameliorates zinc deficiency-induced intestinal damage in rats.     

Chemoprotection of garlic extract toward cyclophosphamide toxicity in mice

The effect of the administration of an extract of garlic (Allium sativum) was studied in mice that were treated with a chronic lethal dose of cyclophosphamide (50 mg/kg body wt, 14 days). The intraperitoneal administration of garlic (50 mg/animal, 14 days) along with cyclophosphamide reduced the toxicity of the latter considerably with an increase in life span of more than 70%. The administration of garlic extract did not improve the lymphopenia produced by cyclophosphamide or liver alkaline phosphatase, but there was a significant reduction in liver glutamic-pyruvic transaminase. Moreover, garlic extract reduced the level of lipid peroxidation induced in the liver by cyclophosphamide administration. Administration of garlic extract did not interfere with the tumor-reducing activity of cyclophosphamide.     

A water extract of Artemisia capillaris prevents 2,2'-azobis(2-amidinopropane) dihydrochloride-induced liver damage in rats

A water extract of Artemisia capillaris Thunberg (Compositae) was investigated for protective effects against oxidative stress induced by 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) in Sprague-Dawley male rats. Rats were orally administered A. capillaris water extract (ACWE; 7.5 g/kg) for 7 days before AAPH treatment (60 mg/kg). AAPH intoxication significantly elevated enzyme markers of liver injury (glutamic oxaloacetic transaminase and glutamic pyruvic transaminase). The pre-administration of ACWE significantly reduced the liver-damaging effects of AAPH as indicated by the low levels of these enzymes. Moreover, the ACWE administration significantly attenuated the accumulation of thiobarbituric acid-reactive substances in both plasma and liver tissues compared with those of rats administered AAPH alone. Furthermore, ACWE administration slightly improved the liver reduced glutathione levels and enhanced the production of antioxidant enzymes like catalase. A. capillaris contained 10.1 mg of catechin in 100 g of dried sample; the high-performance liquid chromatography results showed catechin composition in the ACWE to be 28% (-)-epigallocatechin gallate, 49% (-)- epigallocatechin, and 23% other catechins. These observations clearly indicate that ACWE contains antioxidant catechins capable of ameliorating the AAPH-induced hepatic injury by virtue of its antioxidant activity.     

Dietary Fish Oil Aggravates Paracetamol‐Induced Liver Injury in Mice

Background: Paracetamol (APAP) hepatotoxicity remains the leading cause of drug‐induced liver failure. Fish oil, which contains ω‐3 fatty acids, has demonstrated therapeutic efficacy in several models of liver disease. Evidence for its use in APAP intoxication, however, is conflicting. The effects of fish oil supplementation on APAP‐induced liver failure were investigated. Methods: Ten C57BL6/J mice were fed a diet based on menhaden fish oil (MEN) or soybean oil (SOY) for 3 weeks followed by APAP intoxication. In a second experiment, the prefeeding period was reduced to 5 days. In a third experiment, 10 mice received the study diets for 3 weeks, after which they received chronic, low‐dose APAP administration for another 4 weeks. Finally, 10 mice received oral parenteral nutrition supplemented with either intravenous (IV) soybean‐based or fish oil–based lipid emulsion for 19 days, followed by APAP intoxication. Results: The extent of hepatocellular necrosis (3.8 ± 0.2 vs 2.8 ± 0.2; P = .021) and serum alanine aminotransferase values (2807 ± 785 vs 554 ± 141 IU/L; P = .048) were significantly elevated in mice fed a MEN diet compared with SOY‐diet fed controls. Long‐term, low‐dose APAP administration did not lead to liver injury irrespective of study diet. Pretreatment with soybean‐ or fish oil–based IV lipid emulsions followed by APAP intoxication demonstrated no significant differences in hepatic injury between groups. Conclusion: Within therapeutic ranges, APAP is harmless to the liver irrespective of dietary fat composition. IV use of fish oil did not increase APAP‐induced hepatotoxicity, but animals fed a fish oil–based diet were more susceptible, rather than resistant, to APAP‐induced hepatotoxicity.     

Protective role of Raphanus sativus root extract on paracetamol-induced hepatotoxicity in albino rats

The methanol extract of Raphanus sativus root extract showed a protective effect on paracetamol-induced hepatotoxicity in a dose-dependent manner. Degree of lipid peroxidation caused by paracetamol was measured in terms of thiobarbituric acid reactive substances (TBARS) and protection was measured in reference to serum glutamate oxaloacetate transaminase (SGOT), serum glutamate aspartate transaminase (SGPT), and blood and hepatic levels of antioxidants like glutathione and catalase. Administration of extract along with paracetamol showed significant protection. Levels of TBARS were found to be low, activities of SGOT and SGPT were low, while hepatic glutathione levels were significantly higher in experimental rats that received the mixture of paracetamol and the extract as compared to rats that received paracetamol only. Activities of catalase were also high in all experimental groups. Thus this study indicates the involvement of Raphanus sativus root extract with antioxidants like glutathione and catalase in rendering protection against paracetamol-induced lipid peroxidation and hepatotoxicity.     

Antihepatotoxic nature of Ulva reticulata (Chlorophyceae) on acetaminophen-induced hepatoxicity in experimental rats

Ulva reticulata, a marine edible green alga, is a known source of proteins, vitamins, and sulfated polysaccharides. Though there are many reports in the literature regarding the composition and antiviral property of Ulva sp., studies of the antihepatotoxic property of green seaweeds in animal model are scarce. We have studied the antihepatotoxic nature of this marine green edible alga, U. reticulata, in a hot water extract (150 mg/kg of body weight for a period of 15 days) against acetaminophen- induced hepatotoxicity in experimental albino rats. The acetaminophen-induced rats showed significant elevation in levels of the serum marker enzymes aspartate transaminase and alanine transaminase and of lipid peroxides in liver tissue with decreased levels of antioxidant enzymes such as superoxide dismutase and catalase. The levels of reduced glutathione and vitamins (E and C) were also decreased in the liver tissue of acetaminophen-intoxicated rats. The oral pretreatment with a hot water extract of U. reticulata reduced the hepatotoxicity triggered by acetaminophen considerably by improving the antioxidant status in experimental animals with depleted levels of lipid peroxides. These results indicate that the oral pretreatment with a hot water extract of U. reticulata in rats is effective in reducing the hepatic oxidative stress via free radical scavenging properties, suggesting an antihepatotoxic activity.     

X射线全身照射对大鼠血清氨基转移酶活性和肝脏结构的影响

[目的]观察不同剂量X射线全身照射对大鼠血清氨基转移酶活性及肝脏结构的影响. [方法] Wistar大鼠40只,随机分为4组:对照组、2Gy组、4Gy组、6Gy组.除对照组外,其余3组大鼠按处理剂量行X射线全身单次照射.照射后第2天,经腹主动脉取血、分离血清,测量谷氨酸氨基转移酶(alanine transaminase,ALT)、天冬氨酸氨基转移酶(aspartate transaminase,AST);取肝脏组织制作病理切片,观察肝脏的光学显微镜、电子显微镜结构.[结果]4Gy、6Gy组ALT水平升高,与对照组相比,差异具有统计学意义(P＜0.01);各照射组AST值与对照组相比,差异无统计学意义(P＞0.05).光镜结果显示,各照射组未见明显异常;电镜结果显示,6Gy组细胞器的改变多见于内质网,其结构松散,出现大量空泡. [结论] 4Gy、6GyX射线全身照射可对大鼠血清氨基转移酶活性造成影响,6GyX射线照射可对肝脏结构造成损害.