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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 tissues, plasma and the pattern of gene expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) and its target genes fatty-acid synthase (FAS), adipocyte protein-2 (aP2) and uncoupling protein-2 (UCP-2) and pro-inflammatory factor tumor necrosis factor (TNF)-α were observed in experimental rats. Oral administration of AA exerts therapeutic effects similar to orlistat in attenuating body weight gain, glucose, IR, plasma and tissue lipids and mRNA levels of PPAR-γ, FAS, aP2 and inflammatory factor TNF-α and increasing UCP-2 expression in HFD-fed rats. Hence, these findings concluded that AA attenuate HFD-induced obesity by modulating PPAR-γ and its target genes and regulate lipid metabolism, suggesting their possible antiobesity effects.

Aim: In the present study, we evaluated the therapeutic potentiality of S-allylcysteine (SAC) in streptozotocin (STZ)-nicotinamide (NAD)-induced diabetic nephropathy (DN) in experimental rats., Methods: SAC was orally administered for 45 days to rats with STZ-NAD-induced DN; a metformin-treated group was included for comparison. Effect of SAC on body weight, organ weight, blood glucose, levels of insulin, glycated haemoglobin, and renal biochemical markers was determined. Body composition by total body electrical conductivity (TOBEC) and dual-X ray absorptiometry (DXA), kidney antioxidant analysis, real-time polymerase chain reaction, and western blot analysis of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), nuclear factor kappa B (NF-κB), interleukin (IL)-6, and tumor necrosis factor (TNF)-α; histopathological and scanning electron microscope (SEM) analysis of the kidneys were performed in both control and experimental rats., Results: SAC treatment showed significantly decreased levels of blood glucose, glycated haemoglobin, creatinine, albumin, AST, ALT, creatinine kinase, lactate dehydrogenase, and expressions of NF-κB, IL-6, and TNF-α compared with DN control rats. Furthermore, SAC administration to DN rats significantly improved body composition and antioxidant defense mechanism which was confirmed by the upregulation of mRNA and protein expressions of antioxidant genes., Conclusions: Thus, SAC showed adequate therapeutic effect against DN by downregulation of inflammatory factors and attenuation of oxidative stress. Histological and SEM observations also indicated that SAC treatment notably reverses renal damage and protects the kidneys from hyperglycemia-mediated oxidative damage.

In the present study, we evaluated the effect of biochanin A (BCA) on high-fat diet (HFD)-induced obesity cardiomyopathy. BCA (10 mg/kg body weight) was administered to HFD-induced obese rats for 30 days, and its effect on anthropometrical, morphological, plasma cardiac, and inflammatory biomarkers, along with cardiac lipid profiles was assessed. Supplementation of HFD to rats significantly increased body mass index, obesity index parameters, and cardiac lipid profile along with notable oxidative stress and inflammation. Additionally, BCA treatment in obese rats demonstrated a superior therapeutic action by restoring the altered parameters to almost normal levels. Simultaneously, BCA increased the activities and mRNA expressions of enzymatic antioxidants by upregulating the Nrf-2 pathway and inhibiting the NF-κB cascade. BCA may attenuate obesity and its associated cardiomyopathy by suppressing oxidative stress and inflammation through activation of the Nrf-2 pathway and inhibition of NF-κB activation. [ABSTRACT FROM AUTHOR]