NFKB1 and metabolic syndrome: In this study, our findings that LUT mitigates inflammation markers in MetS-like mice corroborate previous studies that LUT (1) protects against diabetic cardiomyopathy by inhibiting NFκB-mediated inflammation and activating the NRF2-mediated antioxidant responses in STZ-induced diabetic mice [72] and (2) reverses MetS-induced biochemical dysfunction and related cardiac injury via the suppression of apoptosis, inflammation, and stress in rats with MetS-associated cardiac injury [24].