asiatic acid/vefjadrep

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Asiatic acid ameliorates hepatic lipid accumulation and insulin resistance in mice consuming a high-fat diet.

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Effects of asiatic acid (AA) at 10 or 20 mg/kg/day upon hepatic steatosis in mice consuming a high-fat diet (HFD) were examined. AA intake decreased body weight, water intake, feed intake, epididymal fat, and plasma and hepatic triglyceride levels in HFD-treated mice (P < 0.05). HFD enhanced

Asiatic acid alleviates hemodynamic and metabolic alterations via restoring eNOS/iNOS expression, oxidative stress, and inflammation in diet-induced metabolic syndrome rats.

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Asiatic acid is a triterpenoid isolated from Centella asiatica. The present study aimed to investigate whether asiatic acid could lessen the metabolic, cardiovascular complications in rats with metabolic syndrome (MS) induced by a high-carbohydrate, high-fat (HCHF) diet. Male Sprague-Dawley rats

The anti-inflammatory effects of asiatic acid in lipopolysaccharide-stimulated human corneal epithelial cells.

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OBJECTIVE To investigate the anti-inflammatory effects of asiatic acid (AA) on lipopolysaccharide (LPS)-induced inflammatory response in human corneal epithelial cells (HCECs). METHODS Cell viability was measured using a cell counting kit-8 (CCK-8) assay. Quantitative real-time polymerase chain

Antiobesity efficacy of asiatic acid: down-regulation of adipogenic and inflammatory processes in high fat diet induced obese rats.

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In the current study, we evaluated the effects of Asiatic acid (AA) on lipid metabolic markers in HFD-induced obese Sprague-Dawley rat model. AA (20 mg/kg BW) was administered orally to HFD-fed rats for 42 days. Changes in body composition, glucose, insulin resistance (IR) and lipid profiles of

Anti-Cancer Effects of Asiatic Acid, A Triterpene From Centilla Asiatica L: A Literature Review.

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Centilla asiatica L is a medicinal herb that has been widely used in folk medicine to treat various diseases. Asiatic Acid (AA), a triterpene and a known component of this herb, has been shown to display important biological activities, including anti-inflammatory, antibacterial,

Anti-glycative effects of asiatic acid in human keratinocyte cells.

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Background: Human skin keratinocyte (HaCaT) cells served to examine effects of asiatic acid (AA) at 1, 2, 4 and 8 μM against advanced glycative endproduct (AGE)-modified bovine serum albumin (BSA) induced glycative stress. Results: AGE-BSA treatment reduced cell viability; and increased reactive

Barrier protective effect of asiatic acid in TNF-α-induced activation of human aortic endothelial cells.

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BACKGROUND Endothelial cell activation is characterized by increased endothelial permeability and increased expression of cell adhesion molecules (CAMs). This allows monocyte adherence and migration across the endothelium to occur and thereby initiates atherogenesis process. Asiatic acid is a major

Neuroprotective effect of asiatic acid against spinal cord injury in rats.

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OBJECTIVE The present study investigated the therapeutic efficacy of asiatic acid (AA) on spinal cord injury (SCI) as well as the underlying mechanisms. METHODS Sprague-Dawley rats (n=150) were randomly assigned to five groups: sham, SCI, SCI+methylprednisolone (30mg/kg), SCI+AA (30mg/kg), and

Protective effect of asiatic acid in an experimental cerulein-induced model of acute pancreatitis in mice.

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Asiatic acid (AA), a triterpenoid derived from the medicinal plant Centella asiatica, is considered to have anti-inflammatory, anti-fibrotic and anti-tumor effects, but its effects in acute pancreatitis (AP) are unknown. Our purpose of this study was to investigate the effects of AA in a mouse model

Asiatic acid from Potentilla chinensis attenuate ethanol-induced hepatic injury via suppression of oxidative stress and Kupffer cell activation.

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This study examined the effect of Asiatic acid from Potentilla chinensis (AAPC) on chronic ethanol-induced hepatic injury. Rats underwent intragastric administration of ethanol (5.0–9.0 g/kg) once a day for 12 weeks. A subset of rats were also intragastrically treated with AAPC (2, 4 or 8 mg/kg)

Asiatic acid stabilizes cytoskeletal proteins and prevents TNF-α-induced disorganization of cell-cell junctions in human aortic endothelial cells.

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Endothelial hyperpermeability represents an initiating step in early atherosclerosis and it often occurs as a result of endothelial barrier dysfunction. Asiatic acid, a major triterpene isolated from Centella asiatica (L.) Urban, has previously been demonstrated to protect against tumor necrosis

Asiatic acid alleviates cardiovascular remodelling in rats with L-NAME-induced hypertension.

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A previous study demonstrated the antihypertensive effect of asiatic acid. The current study investigates the effect of asiatic acid on cardiovascular remodelling and possible mechanisms involved in Nω -nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats. Male

Combination of carnosine and asiatic acid provided greater anti-inflammatory protection for HUVE cells and diabetic mice than individual treatments of carnosine or asiatic acid alone.

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The purpose of present HUVE cells and mice study was to investigate the combined effects of carnosine and asiatic acid (AA) against diabetic progression. In HUVE cells, high glucose decreased cell viability, reduced Bcl-2 mRNA expression and increased Bax mRNA expression. The co-treatment of 0.5 μM

Antioxidative and antiinflammatory activities of asiatic acid, glycyrrhizic acid, and oleanolic acid in human bronchial epithelial cells.

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Protective effects of triterpenic acids, asiatic acid (AA), glycyrrhizic acid (GA), or oleanolic acid (OA), for two human bronchial epithelial cells, 16HBE and BEAS-2B cells, against hydrogen peroxide (H2O2) induced injury were examined. Cells were pretreated by triterpenic acid at 4 or 8 μmol/L and

Anti-apoptotic and anti-glycative effects of asiatic acid in the brain of D-galactose treated mice.

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Protection of asiatic acid (AA) in mice brain against D-galactose (DG) induced aging was examined. AA at 5, 10 or 20 mg kg(-1) per day was supplied to DG treated mice for 8 weeks. AA intake at 10 or 20 mg kg(-1) per day increased its deposit in brain. DG treatment increased Bax, cleaved caspase-3

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