Nicotinamide Prevents Diabetic Brain Inflammation via NAD+-Dependent Deacetylation Mechanisms

This study investigated the effect of nicotinamide (NAM) supplementation on development brain inflammation and microglial activation in a mouse model type 1 diabetes mellitus. C57BL/6J male mice, which were made diabetic with five consecutive, low-dose (55 mg/kg i.p.) streptozotocin (STZ) injections. Diabetic mice randomly distributed different experimental groups challenged to doses NAM (untreated, low-dose, LD, 0.1%; high-dose, HD, 0.25%) for 25 days. A control, non-diabetic group was used as reference. The NAD+ content increased brains NAM-treated compared untreated (NAM LD: 3-fold; HD: 3-fold, p-value < 0.05). Immunohistochemical staining revealed that markers (TNFα: −35%; −46%; 0.05) (IBA-1: −29%; −50%; 0.05; BDKRB1: −36%; −37%; from significantly decreased non-treated T1D mice. finding accompanied by concomitant alleviation nuclear NFκB (p65) signaling treated (NFκB (p65): −38%; −53%, Notably, acetylated form NAM-treated, −48%; −63%, inversely correlated (r = −0.50, 0.03), suggesting activity NAD+-dependent deacetylases Thus, dietary prevented via deacetylation mechanisms, an action sirtuin signaling.