Nicotinamide Riboside Enhances Endothelial Precursor Cell Function to Promote Refractory Wound Healing Through Mediating the Sirt1/AMPK Pathway

Abstract

Lack of vascularization is directly associated with refractory wound healing in diabetes mellitus (DM). Enrichment of endothelial precursor cells (EPCs) is a promising but challenging approach for the treatment of diabetic wounds. Herein, we investigate the action of nicotinamide riboside (NR) on EPC function for improved healing of diabetic wounds. Db/db mice that were treated with NR-supplemented food (400 mg/kg/d) for 12 weeks exhibited higher wound healing rates and angiogenesis than untreated db/db mice. In agreement with this phenotype, NR supplementation significantly increased the number of blood EPCs and bone marrow (BM)-derived EPCs of db/db mice, as well as the tube formation and adhesion functions of BM-EPCs. Furthermore, NR-supplemented BM-EPCs showed higher expression of sirtuin 1 (Sirt1), phosphorylated adenosine monophosphate–activated protein kinase (p-AMPK), and lower expression of acetylated peroxisome proliferator–activated receptor γ coactivator (PGC-1α) than BM-EPCs isolated from untreated db/db mice. Knockdown of Sirt1 in BM-EPCs significantly abolished the tube formation and adhesion function of NR as well as the expression of p-AMPK and deacetylated PGC-1a. Inhibition of AMPK abolished the NR-regulated EPC function but had no effect on Sirt1 expression, demonstrating that NR enhances EPC function through the Sirt1-AMPK pathway. Overall, this study demonstrates that the oral uptake of NR enhances the EPC function to promote diabetic wound healing, indicating that NR supplementation might be a promising strategy to prevent the progression of diabetic complications.

Application Effect of Silver-Containing Dressings in the Repair of Chronic Refractory Wounds

“…Once in contact with wound exudate, the hydrocolloid particle (CMC sodium carboxymethylcellulose) in the dressing swells after absorbing the exudate, forms a soft, cohesive hydrogel that allows it to absorb the wound exudate while locking it in within the gel, avoiding the risk of exudate leakage as well as the wound skin. Intrasite gel also creates a moist environment conducive to wound healing [20][21][22]. e results of this study showed that after treatment, the positive rate of wound bacterial culture in the observation group was significantly lower than that in the control group.…”

“…Once in contact with wound exudate, the hydrocolloid particle (CMC sodium carboxymethylcellulose) in the dressing swells after absorbing the exudate, forms a soft, cohesive hydrogel that allows it to absorb the wound exudate while locking it in place within the gel, avoiding the risk of exudate leakage as well as macerating the wound skin. Intrasite gel also creates a moist environment conducive to wound healing [ 20 – 22 ].…”

Nicotinamide riboside ameliorates high-fructose-induced lipid metabolism disorder in mice via improving FGF21 resistance in the liver and white adipose tissue

“…41 There is plenty of evidence supporting the metabolic benefits of NR provided by SIRT1. 40,42 In addition, the activation of SIRT1 can alleviate a multitude of NF-κB-driven inflammation, which have been confirmed by a series of in vitro and in vivo studies. 43 SIRT1 is able to bind to the RelA/p65 subunit of NF-κB and deacetylate RelA/p65 at lysine 310, a key site for NF-κB transcriptional activity.…”

AMPK/SIRT1 Deficiency Drives Adjuvant-Induced Arthritis in Rats by Promoting Glycolysis-Mediated Monocytes Inflammatory Polarization

“…Meanwhile, it significantly inhibited the expression of hypoxia-inducible factor 1-Alpha (HIF-1α) as well as its downstream TPI1 (Figure 5G). 23,24 These results partially explained the declined glycolysis levels in those AIA monocytes overexpressing SIRT1. Besides, phosphorylation of STAT3 (a transcriptional factor controlling M2 polarization) was inhibited in AIA monocytes compared to normal control, which was restored by SIRT1 overexpression (Figure 5G).…”