title: Effects of aqueous extract of Portulaca oleracea L. on oxidative stress and liver, spleen leptin, PARα and FAS mRNA expression in high-fat diet induced mice.
abstract: We reported that an aqueous extract of Portulaca oleracea L. inhibited high-fat-diet-induced oxidative injury in a dose-dependent manner. Male kunming mice (5-weeks-old, 24 g) were used in this experiment. After a 4-day adaptation period, animals were randomly divided into four groups (n = 10 in each group); Group 1: animals received normal powdered rodent diet; Group 2: animals received high fat diet; Groups 3 and 4: animals received high fat diet and were fed by gavage to mice once a day with aqueous extract at the doses of 100 and 200 mg/kg body weight, respectively. In mice fed with high-fat diet, blood and liver lipid peroxidation level was significantly increased, whereas antioxidant enzymes activities were markedly decreased compared to normal control mice. Administration of an aqueous extract of P. oleracea L. significantly dose-dependently reduced levels of blood and liver lipid peroxidation and increased the activities of blood and liver antioxidant enzymes activities in high fat mice. Moreover, administration of an aqueous extract of P. oleracea L. significantly dose-dependently increase liver Leptin/β-actin (B), and Liver PPARα/β-actin, decrease liver, spleen FAS mRNA, p-PERK and p-PERK/PERK protein expression levels. Taken together, these data demonstrate that aqueous extract of P. oleracea L. can markedly alleviate high fat diet-induced oxidative injury by enhancing blood and liver antioxidant enzyme activities, modulating Leptin/β-actin (B), and Liver PPARα/β-actin, decrease liver, spleen FAS mRNA, p-PERK and p-PERK/PERK protein expression levels in mice.
authors.affiliation: Department of the Fifth Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200438, China.
authors.forename: Bendong
authors.initials: B
authors.lastname: Chen
authors.forename: Haining
authors.initials: H
authors.lastname: Zhou
authors.forename: Wenchao
authors.initials: W
authors.lastname: Zhao
authors.forename: Wenyan
authors.initials: W
authors.lastname: Zhou
authors.forename: Quan
authors.initials: Q
authors.lastname: Yuan
authors.forename: Guangshun
authors.initials: G
authors.lastname: Yang
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D059305:Diet, High-Fat; D005786:Gene Expression Regulation / Q000187:drug effects*; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D020738:Leptin / Q000235:genetics*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D018384:Oxidative Stress / Q000187:drug effects*; D047493:PPAR alpha / Q000235:genetics*; D010936:Plant Extracts / Q000494:pharmacology*; D031822:Portulaca / Q000737:chemistry*; D013154:Spleen / Q000187:drug effects / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014158:Transcription, Genetic / Q000187:drug effects; D014280:Triglycerides / Q000097:blood; D019892:eIF-2 Kinase / Q000378:metabolism; D019014:fas Receptor / Q000235:genetics*
chemical_list: D002374:Catalase; D002784:Cholesterol; D005978:Glutathione; D005979:Glutathione Peroxidase; D020738:Leptin; D047493:PPAR alpha; D010936:Plant Extracts; D013482:Superoxide Dismutase; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D019892:eIF-2 Kinase; D019014:fas Receptor