The use of medicinal plants in treating illnesses has been reported since ancestral times.In the case of hepatic diseases,several species such as Silybum marianum,Phyllanthus niruri,and Panus giganteus(Berk.)have been...The use of medicinal plants in treating illnesses has been reported since ancestral times.In the case of hepatic diseases,several species such as Silybum marianum,Phyllanthus niruri,and Panus giganteus(Berk.)have been shown to ameliorate hepatic lesions.Silymarin is a natural compound derived from the species Silybum marianum,which is commonly known as Milk thistle.This plant contains at least seven flavoligands and the flavonoid taxifolin.The hepatoprotective and antioxidant activity of silymarin is caused by its ability to inhibit the free radicals that are produced from the metabolism of toxic substances such as ethanol,acetaminophen,and carbon tetrachloride.The generation of free radicals is known to damage cellular membranes and cause lipoperoxidation.Silymarin enhances hepatic glutathione and may contribute to the antioxidant defense of the liver.It has also been shown that silymarin increases protein synthesis in hepatocytes by stimulating RNA polymerase I activity.A previous study on humans reported that silymarin treatment caused a slight increase in the survival of patients with cirrhotic alcoholism compared with untreated controls.展开更多
AIM: To evaluate the effect of an extract of Geranium schiedeanum(Gs) as a hepatoprotective agent against ethanol(Et OH)-induced toxicity in rats. METHODS: Male Wistar rats weighing 200-230 g were subjected to a 70% p...AIM: To evaluate the effect of an extract of Geranium schiedeanum(Gs) as a hepatoprotective agent against ethanol(Et OH)-induced toxicity in rats. METHODS: Male Wistar rats weighing 200-230 g were subjected to a 70% partial hepatectomy(PH); they were then divided into three groups(groups 1-3). During the experiment, animals in group 1 drank only water. The other two groups(2-3) drank an aqueous solution of Et OH(40%, v/v). Additionally, rats in group 3 received a Gs extract daily at a dose of 300 mg/kg body weight intragastically. Subsequently, to identify markers of liver damage in serum, alanine aminotransferase, aspartate aminotransferase, albumin and bilirubin were measured by colorimetric methods. Glucose, triglyceride and cholesterol concentrations were also determined. In addition, oxidative damage was estimated by measuring lipid peroxidation [using thiobarbituric-acid reactive substances(TBARS)] in both plasma and the liver and by measuring the total concentration of antioxidants in serum and the total antioxidant capacity in the liver. In addition, a liver mass gain assessment, total DNA analysis and a morpho-histological analysis of the liver from animals in all three groups were performed and compared. Finally, the number of deaths observed in the three groups was analyzed.RESULTS: Administration of the Geranium shiedeanum extract significantly reduced the unfavorable effect of ethanol on liver regeneration(restitution liver mass: PHEt OH group 60.68% vs PH-Gs-Et OH group 69.22%). This finding was congruent with the reduced levels of hepatic enzymes and the sustained or increased levels of albumin and decreased bilirubin in serum. The extract also modified the metabolic processes that regulate glucose and lipid levels, as observed from the serum measurements. Lower antioxidant levels and the liver damage induced by Et OH administration appeared to be mitigated by the extract, as observed from the TBARs(PH-Et OH group 200.14 mmol/mg vs PH-Gs-Et OH group 54.20 mmol/mg; P < 0.05), total status of antioxidants(PH-Et OH group 1.43 mmol/L vs PH-Gs-Et OH group 1.99 mmol/L; P < 0.05), total antioxidant capacity values, liver mass gain and total DNA determination(PH-Et OH group 4.80 mg/g vs PH-Gs-Et OH 9.10 mg/g; P < 0.05). Overall, these processes could be related to decreased mortality in these treated animals.CONCLUSION: The administered extract showed a hepatoprotective effect, limiting the Et OH-induced hepatotoxic effects. This effect can be related tomodulating oxido-reduction processes.展开更多
文摘The use of medicinal plants in treating illnesses has been reported since ancestral times.In the case of hepatic diseases,several species such as Silybum marianum,Phyllanthus niruri,and Panus giganteus(Berk.)have been shown to ameliorate hepatic lesions.Silymarin is a natural compound derived from the species Silybum marianum,which is commonly known as Milk thistle.This plant contains at least seven flavoligands and the flavonoid taxifolin.The hepatoprotective and antioxidant activity of silymarin is caused by its ability to inhibit the free radicals that are produced from the metabolism of toxic substances such as ethanol,acetaminophen,and carbon tetrachloride.The generation of free radicals is known to damage cellular membranes and cause lipoperoxidation.Silymarin enhances hepatic glutathione and may contribute to the antioxidant defense of the liver.It has also been shown that silymarin increases protein synthesis in hepatocytes by stimulating RNA polymerase I activity.A previous study on humans reported that silymarin treatment caused a slight increase in the survival of patients with cirrhotic alcoholism compared with untreated controls.
基金Supported by SIP Project,No.20140856 and No.2014092,ESM-IPN
文摘AIM: To evaluate the effect of an extract of Geranium schiedeanum(Gs) as a hepatoprotective agent against ethanol(Et OH)-induced toxicity in rats. METHODS: Male Wistar rats weighing 200-230 g were subjected to a 70% partial hepatectomy(PH); they were then divided into three groups(groups 1-3). During the experiment, animals in group 1 drank only water. The other two groups(2-3) drank an aqueous solution of Et OH(40%, v/v). Additionally, rats in group 3 received a Gs extract daily at a dose of 300 mg/kg body weight intragastically. Subsequently, to identify markers of liver damage in serum, alanine aminotransferase, aspartate aminotransferase, albumin and bilirubin were measured by colorimetric methods. Glucose, triglyceride and cholesterol concentrations were also determined. In addition, oxidative damage was estimated by measuring lipid peroxidation [using thiobarbituric-acid reactive substances(TBARS)] in both plasma and the liver and by measuring the total concentration of antioxidants in serum and the total antioxidant capacity in the liver. In addition, a liver mass gain assessment, total DNA analysis and a morpho-histological analysis of the liver from animals in all three groups were performed and compared. Finally, the number of deaths observed in the three groups was analyzed.RESULTS: Administration of the Geranium shiedeanum extract significantly reduced the unfavorable effect of ethanol on liver regeneration(restitution liver mass: PHEt OH group 60.68% vs PH-Gs-Et OH group 69.22%). This finding was congruent with the reduced levels of hepatic enzymes and the sustained or increased levels of albumin and decreased bilirubin in serum. The extract also modified the metabolic processes that regulate glucose and lipid levels, as observed from the serum measurements. Lower antioxidant levels and the liver damage induced by Et OH administration appeared to be mitigated by the extract, as observed from the TBARs(PH-Et OH group 200.14 mmol/mg vs PH-Gs-Et OH group 54.20 mmol/mg; P < 0.05), total status of antioxidants(PH-Et OH group 1.43 mmol/L vs PH-Gs-Et OH group 1.99 mmol/L; P < 0.05), total antioxidant capacity values, liver mass gain and total DNA determination(PH-Et OH group 4.80 mg/g vs PH-Gs-Et OH 9.10 mg/g; P < 0.05). Overall, these processes could be related to decreased mortality in these treated animals.CONCLUSION: The administered extract showed a hepatoprotective effect, limiting the Et OH-induced hepatotoxic effects. This effect can be related tomodulating oxido-reduction processes.