Sodium butyrate, a HDAC inhibitor ameliorates eNOS, iNOS and TGF-β1-induced fibrogenesis, apoptosis and DNA damage in the kidney of juvenile diabetic rats

The role of butyrate, a histone deacetylase inhibitor in diabetes mellitus: experimental evidence for therapeutic intervention

“…Further, children with β-cell autoimmunity have shown low abundance of butyrate-producing bacteria in the gut [44,45]. Apart from this, butyrate have several other pharmacological activities such as anti-inflammatory, anticancer, antioxidant and immunomodulatory, which in part responsible for its beneficial effects across different experimental and clinical studies [46,47]. From the recent literature, it can be deduced that butyrate can modulate the expression of various regulatory genes and/or proteins, which are directly and/or indirectly involved in the glucose metabolism as well as pathogenesis of DM.…”

“…Suppression of NF-κB activation by HDAC inhibition is the most frequently investigated anti-inflammatory mechanism of butyrate [59,60]. NF-κB modulates the expression of genes encoding the proinflammatory cytokines, chemokines, inducible nitric oxide synthase, COX-2 and adhesion molecules [47]. The anti-inflammatory effect of butyrate is mainly exerted by the inhibition of NF-κB, decreased myeloperoxidase and COX-2 expression [61,62].…”

Sodium butyrate reduces insulin-resistance, fat accumulation and dyslipidemia in type-2 diabetic rat: A comparative study with metformin

“…Besides, butyrate have several other pharmacological activities such as antiinflammatory, anti-cancer, anti-oxidant and immunomodulatory, which in part contribute for its beneficial effects in different experimental and clinical studies [27e29]. Recently, we have also reported the protective role of NaB on beta-cell damage and apoptosis as well as attenuate the renal fibrogenesis and DNA damage in type-1 diabetic rats [30,31]. Thus, the present study aimed to investigate the comparative role of NaB and metformin on insulin-resistance, fat deposition, dyslipidemia and gluconeogenesis in type-2 diabetic rat.…”

Valproate attenuates the proteinuria, podocyte and renal injury by facilitating autophagy and inactivation of NF-κB/iNOS signaling in diabetic rat

“…Capsular space was determined by difference between parietal and visceral layer area of glomeruli. The shortest and longest diameters of each glomerular were measured using free hand selection tool and average of diameter was used for GV calculation as described previously [18].…”

“…Diabetes activates the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), which regulates the expression of several genes involved in the inflammatory response and cellular stress such as inducible nitric oxide synthase (iNOS) [13][14][15]. Further, HDACs control the transcription and translation of the iNOS by histone acetylation, thereby modulate the production of nitric oxide (NO) [16][17][18]. Moreover, HDAC2 could augment the induction of iNOS promoter activity [17].…”