Anti-inflammatory effects of Calebin A on metabolic syndrome via NF-κB signaling pathway modulation.

Abstract

Metabolic syndrome is a complex disorder characterized by a combination of events such as insulin resistance, obesity, dyslipidemia, and hypertension, and chronic low-level inflammation plays a major role in its development. The nuclear factor kappa B (NF-κB) signaling pathway plays a critical role in mediating inflammatory responses leading to metabolic dysregulation and progression. Calbin A, a bioactive compound derived from turmeric, exhibited significant anti-inflammatory effects that occur primarily through modulation of the NF-κB pathway. Calbin A is a diarylheptanoid characterized by distinct electrophilic centers that facilitate direct interactions with intracellular signaling molecules, leading to inhibition of NF-κB nuclear translocation and subsequent expression of proinflammatory cytokines. Recent preclinical evidence suggests that Calbin A effectively reduces inflammatory markers, increases insulin sensitivity, and modulates lipid metabolism in both cellular and animal models of metabolic syndrome. Calbin A suppresses NF-κB activation and affects interconnected pathways, including AMP-activated protein kinase and phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), thereby enhancing metabolic homeostasis. These findings suggest that Calbin A may serve as a potential candidate for therapeutic intervention in metabolic syndrome and related disorders. Future research should prioritize comprehensive molecular characterization, increased bioavailability, and clinical translation to effectively utilize Calbin A in the management of metabolic diseases.