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1.
Arch Physiol Biochem ; 128(4): 938-944, 2022 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32216601

RESUMO

Inhibition of adipogenesis is crucial and is a key area of research to develop antiobesity drugs. In this study, 3-O-glucoside of kaempferol (astragalin) was isolated from Moringa oleifera leaves and evaluated for its lipolytic and antiadipogenic activity in 3T3-L1 adipocytes. Astragalin has substantially reduced the triglycerides content and lipid accumulation in 3T3-L1 adipocytes and enhanced the glycerol release in a dose dependent manner. The assay for secreted adipocytokines confirmed that, astragalin at a concentration of 20 µg/mL significantly (p < .01) increased the secretion of adiponectin, but decreased leptin secretion in 3T3-L1 adipocytes. In molecular studies, both the mRNA expression and corresponding protein expression of PPAR-γ, C/EBP-α, FAS, and leptin genes were downregulated while that of adiponectin was upregulated in astragalin treated groups. Taken together, astragalin of M. oleifera promotes lipolysis, suppresses adipogenesis in 3T3-L1 adipocytes, and may be considered as an effective candidate to treat obesity aliments.


Assuntos
Adipogenia , Moringa oleifera , Células 3T3-L1 , Adipócitos/metabolismo , Adipogenia/genética , Adiponectina/genética , Adiponectina/metabolismo , Animais , Diferenciação Celular , Glucosídeos/metabolismo , Glucosídeos/farmacologia , Quempferóis/metabolismo , Quempferóis/farmacologia , Leptina/metabolismo , Camundongos , Moringa oleifera/metabolismo , Folhas de Planta
2.
Front Pharmacol ; 12: 704074, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34366856

RESUMO

Objective: To evaluate the therapeutic efficacy and underlying molecular mechanisms of Bauhiniastatin-1 (BSTN1) to alleviate adiposity in diet-induced obese rodent model and in 3T3-L1 cells. Methods: BSTN1 was purified and confirmed through HPLC. In-vitro experiments such as MTT assay, Oil Red-O (ORO) stain, cellular lipid content, glycerol release and RT-PCR analysis were performed in 3T3-L1 cells in the presence and absence of BSTN1. In animal experiments, rats were divided into Group-I: normal pellet diet-fed, Group-II: HFD-fed, Groups-III, IV and V: HFD-fed BSTN1 (1.25, 2.5, and 5 mg/kg.b.wt./day/rat)-treated and Group-VI: HFD-fed Orlistat-treated. The rats were fed either normal diet or high fat diet (HFD) for 18 weeks and water ad-libitum. BSTN1 was orally administered from 13th week onwards to the selected HFD-fed groups. Body composition parameters, biochemical assays, histopathology examination and western blot analysis were performed to identify the predicted targets related to obesity. Molecular docking studies threw light on the binding interactions of BSTN1 against PPAR-γ, FAS and AMPK. Results: BSTN1 at 20 µM significantly (p < 0.001) inhibited adipocyte differentiation and lipid accumulation in 3T3-L1 cells. A conspicuous down-regulation in the mRNA expression levels of PPAR-γ, FAS and SREBP1 was observed but AMPK expression remained unchanged in BSTN1 treated 3T3-L1 cells. A substantial decrease in body weight gain, fat percent, total body fat, serum and liver lipid profile (except high-density lipoprotein), glucose, insulin and insulin resistance in BSTN1 treated rats was noticed in a dose dependent manner. In BSTN1 (5 mg/kg.b.wt.)-treated groups significantly (p < 0.01) elevated plasma adiponectin level but reduced leptin level as well as fall in serum AST and ALT were noticed. Further, the disturbed structural integrity and architecture of adipose and hepatic tissues due to high fat diet feeding were considerably recovered with BSTN1 treatment. Down-regulation in the protein expression level of PPAR-γ and activation of AMPK through phosphorylation was observed in BSTN1 treated rats than the untreated. Molecular docking studies revealed strong binding interactions of BSTN1 against PPAR-γ and AMPK and thus supported the experimental results. Conclusion: Taken together, the results suggest that BSTN1 could be a promising pharmacological molecule in the treatment of obesity and dyslipidemia.

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