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Hydroalcoholic extract from Sechium edule (Jacq.) S.w. root reverses oleic acid-induced steatosis and insulin resistance in vitro

Steatosis is characterized by fat accumulation and insulin resistance (IR) in hepatocytes, which triggers a pro-oxidant, pro-inflammatory environment that may eventually lead to cirrhosis or liver carcinoma. This work was aimed to assess the effect of Sechium edule root hydroalcoholic extract (rSe-H...

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Published in:Heliyon 2024-01, Vol.10 (2), p.e24567-e24567, Article e24567
Main Authors: Aziel Alvarado-Ojeda, Zimri, Zamilpa, Alejandro, Costet-Mejia, Alejandro, Méndez-Martínez, Marisol, Trejo-Moreno, Celeste, Jiménez-Ferrer, Jesús Enrique, Salazar-Martínez, Ana Maria, Cruz-Muñoz, Mario Ernesto, Fragoso, Gladis, Rosas-Salgado, Gabriela
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Language:English
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Summary:Steatosis is characterized by fat accumulation and insulin resistance (IR) in hepatocytes, which triggers a pro-oxidant, pro-inflammatory environment that may eventually lead to cirrhosis or liver carcinoma. This work was aimed to assess the effect of Sechium edule root hydroalcoholic extract (rSe-HA) (rich in cinnamic and coumaric acid, among other phenolic compounds) on triglyceride esterification, lipid degradation, AMPK expression, and the phosphorylation of insulin receptor in a Ser312 residue, as well as on the redox status, malondialdehyde (MDA) production, and the production of proinflammatory cytokines in an in vitro model of steatosis induced by oleic acid, to help develop a phytomedicine that could reverse this pathology. rSe-HA reduced triglyceride levels in hepatocyte lysates, increased lipolysis by activating AMPK at Thr172, and improved the redox status, as evidenced by the concentration of glycerol and formazan, respectively. It also prevented insulin resistance (IR), as measured by glucose consumption and the phosphorylation of the insulin receptor at Ser312. It also prevented TNFα and IL6 production and decreased the levels of MDA and nitric oxide (ON). Our results indicate that rSe-HA reversed steatosis and controlled the proinflammatory and prooxidant environment in oleic acid-induced dysfunctional HepG2 hepatocytes, supporting its potential use to control this disorder. [Display omitted]
ISSN:2405-8440
2405-8440
DOI:10.1016/j.heliyon.2024.e24567