β-Nicotinamide Mononucleotide (NMN) Administrated by Intraperitoneal Injection Mediates Protection Against UVB-Induced Skin Damage in Mice

Abstract

Ultraviolet light is an important environmental factor that induces skin oxidation, inflammation, and other diseases. Nicotinamide mononucleotide (NMN) has the effect of antioxidation and improving various physiological processes. This study explores the protective effect of NMN monomers given via intraperitoneal injection on UVB-induced photodamage. Methods:We used a murine model of UVB-induced photodamage to evaluate the effect of an NMN monomer on photoaging skin by assessing skin and liver tissue sections, serum and skin oxidative stress levels, inflammatory markers, mRNA expression, and protein expression of skin-and liver-related genes. Results:The results showed that NMN treatment blocked UVB-induced photodamage in mice, maintaining normal structure and amount of collagen fibers, normal thickness of epidermis and dermis, reducing the production of mast cells, and maintaining complete organized skin structure. NMN intraperitoneal injection also maintained the normal morphology of the mouse liver after UVB exposure. Meanwhile, NMN intraperitoneal injection was found to increase antioxidant ability and regulate the proinflammatory response of the skin and liver to UVB irradiation by enhancing the activity of antioxidant enzymes, release of anti-inflammatory cytokines, reduction of hydrogen peroxide production (H 2 O 2 ), and decreased inflammatory cytokines. Furthermore, RT-qPCR results indicated that NMN reduced oxidative stress of skin and liver by promoting the activation of the AMP-activated protein kinase (AMPK) signaling pathway and further increasing the expression of downstream antioxidant genes of AMPK. RT-qPCR results also revealed that NMN treatment could downregulate the mRNA expression of interleukin (IL)-6, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α, and upregulate NF-kappa-B inhibitor-α (IκB-α) and interleukin (IL)-10 by inhibiting the activation of nuclear factor-κBp65 (NFκB-p65). Finally, NMN upregulated AMPK, IκB-α, SOD1, and CAT in the skin and downregulated NF-κBp65 protein expression, which is in line with the RT-qPCR results. Conclusion: Based on the above results, NMN monomer treatment with intraperitoneal injection also block the photodamage caused by UVB irradiation in mice by regulating the oxidative stress response and inflammatory response.

Nicotinamide mononucleotide supplementation protects the intestinal function in aging mice and d-galactose induced senescent cells

“…45 In addition, D-gal treated cells showed upregulated gene expression of pro-inflammatory factors such as IL-1β, IL-6, and TNF-α, and cellular senescence associated genes P53 and P21. 46 In the present study, the cellular transcriptome demonstrated that D-gal up-regulated the gene expression of IL6ST, IL-1A, and NF-κB1, which have been identified as SASPs in the intestine of old rats. 47 Treatment of 500 μM NMN down-regulated these inflammatory SASPs in D-gal treated IPEC-J2 cells.…”

“…Previously, a study also reported the enhancing effect of NMN treatment on the antioxidant capacity. 46 Han and his colleagues have investigated the supplementary effects of different doses of d -gal ranging from 5–20 g kg −1 on weaned piglets. 48 The results showed that d -gal did not cause a significant change in serum SOD, but a specific dose-dependent increase in the GSH-Px activity and MDA content and a decrease in the CAT activity were observed.…”

Supplementation of nicotinic acid and its derivatives up-regulates cellular NAD+ level rather than nicotinamide derivatives in cultured normal human epidermal keratinocytes

“…The in vivo studies of NMN treatment are administered mainly by oral gavage and intraperitoneal injection. Zhou et al demonstrated that both types of administration of NMN protect against UVBinduced skin damage in mice [23]. Contrary, NMN supplementation in the medium did not up-regulate NAD + levels directly in our study.…”

Preparation and Evaluation of Liposomes and Niosomes Containing Total Ginsenosides for Anti-Photoaging Therapy

“…A cascade of reactions is triggered after UV exposure, with ROS triggering inducing the release of IL-6, IL-1β, and TNF-α ( Zhou et al, 2021 ). ELISA kits were used to determine IL-6, IL-1β, and TNF-α expression in the rat skin tissue homogenate.…”

“…MMPs degrade collagen and elastin in the extracellular matrix in vivo . MMP-1 breaks down intact type I and III fibrillar collagen, ultimately leading to progressive senescence of fibroblasts ( Rui-Zhen et al, 2004 ; Zhang and Tian, 2007 ; Zhou et al, 2021 ). Additionally, MMP-1 upregulates the expression of IL-6, IL-1β, and TNF-α by activating nuclear factor-κB (NF-κB), which can lead to the inflammatory infiltration of neutrophils and further production of ROS ( Xiao et al, 2016 ; Ighodaro and Akinloye, 2018 ).…”