The Role of Nicotinamide Mononucleotide Supplementation in Psoriasis Treatment

Psoriasis is one of several chronic inflammatory skin diseases with a high rate of recurrence, and its pathogenesis remains unclear. Nicotinamide mononucleotide (NMN), as an important precursor of nicotinamide adenine dinucleotide (NAD+), has been reported to be a promising agent in treating various...

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Main Authors: Zhengyi Zhang, Baochen Cheng, Wenqian Du, Mengqi Zeng, Ke He, Tingyi Yin, Sen Shang, Tian Su, Dan Han, Xinyi Gan, Ziyang Wang, Meng Liu, Min Wang, Jiankang Liu, Yan Zheng
Format: Article
Language:English
Published: MDPI AG 2024-02-01
Series:Antioxidants
Subjects:
Online Access:https://www.mdpi.com/2076-3921/13/2/186
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author Zhengyi Zhang
Baochen Cheng
Wenqian Du
Mengqi Zeng
Ke He
Tingyi Yin
Sen Shang
Tian Su
Dan Han
Xinyi Gan
Ziyang Wang
Meng Liu
Min Wang
Jiankang Liu
Yan Zheng
author_facet Zhengyi Zhang
Baochen Cheng
Wenqian Du
Mengqi Zeng
Ke He
Tingyi Yin
Sen Shang
Tian Su
Dan Han
Xinyi Gan
Ziyang Wang
Meng Liu
Min Wang
Jiankang Liu
Yan Zheng
author_sort Zhengyi Zhang
collection DOAJ
description Psoriasis is one of several chronic inflammatory skin diseases with a high rate of recurrence, and its pathogenesis remains unclear. Nicotinamide mononucleotide (NMN), as an important precursor of nicotinamide adenine dinucleotide (NAD+), has been reported to be a promising agent in treating various diseases, its positive effects including those induced via its anti-inflammatory and antioxidant properties. For this reason, we have aimed to explore the possible role of NMN in the treatment of psoriasis. Psoriasis models were constructed with imiquimod (IMQ) stimulation for 5 days in vivo and with M5 treatment in keratinocyte cell lines in vitro. NMN treatment during the IMQ application period markedly attenuated excess epidermal proliferation, splenomegaly, and inflammatory responses. According to GEO databases, Sirtuin1 (SIRT1) levels significantly decreased in psoriasis patients’ lesion tissues; this was also the case in the IMQ-treated mice, while NMN treatment reversed the SIRT1 decline in the mouse model. Moreover, NMN supplementation also improved the prognoses of the mice after IMQ stimulation, compared to the untreated group with elevated SIRT1 levels. In HEKa and HaCaT cells, the co-culturing of NMN and M5 significantly decreased the expression levels of proinflammation factors, the phosphorylation of NF-κB, stimulator of interferon genes (STING) levels, and reactive oxygen species levels. NMN treatment also recovered the decrease in mitochondrial membrane potential and respiration ability and reduced mtDNA in the cytoplasm, leading to the inhibition of autoimmune inflammation. The knockdown of <i>SIRT1</i> in vitro eliminated the protective and therapeutic effects of NMN against M5. To conclude, our results indicate that NMN protects against IMQ-induced psoriatic inflammation, oxidative stress, and mitochondrial dysfunction by activating the SIRT1 pathway.
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spelling doaj.art-46f4d74784d14612972c36cd8c3730ed2024-02-23T15:05:25ZengMDPI AGAntioxidants2076-39212024-02-0113218610.3390/antiox13020186The Role of Nicotinamide Mononucleotide Supplementation in Psoriasis TreatmentZhengyi Zhang0Baochen Cheng1Wenqian Du2Mengqi Zeng3Ke He4Tingyi Yin5Sen Shang6Tian Su7Dan Han8Xinyi Gan9Ziyang Wang10Meng Liu11Min Wang12Jiankang Liu13Yan Zheng14Departement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaSchool of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao 266071, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, ChinaCenter for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaDepartement of Dermatology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, ChinaPsoriasis is one of several chronic inflammatory skin diseases with a high rate of recurrence, and its pathogenesis remains unclear. Nicotinamide mononucleotide (NMN), as an important precursor of nicotinamide adenine dinucleotide (NAD+), has been reported to be a promising agent in treating various diseases, its positive effects including those induced via its anti-inflammatory and antioxidant properties. For this reason, we have aimed to explore the possible role of NMN in the treatment of psoriasis. Psoriasis models were constructed with imiquimod (IMQ) stimulation for 5 days in vivo and with M5 treatment in keratinocyte cell lines in vitro. NMN treatment during the IMQ application period markedly attenuated excess epidermal proliferation, splenomegaly, and inflammatory responses. According to GEO databases, Sirtuin1 (SIRT1) levels significantly decreased in psoriasis patients’ lesion tissues; this was also the case in the IMQ-treated mice, while NMN treatment reversed the SIRT1 decline in the mouse model. Moreover, NMN supplementation also improved the prognoses of the mice after IMQ stimulation, compared to the untreated group with elevated SIRT1 levels. In HEKa and HaCaT cells, the co-culturing of NMN and M5 significantly decreased the expression levels of proinflammation factors, the phosphorylation of NF-κB, stimulator of interferon genes (STING) levels, and reactive oxygen species levels. NMN treatment also recovered the decrease in mitochondrial membrane potential and respiration ability and reduced mtDNA in the cytoplasm, leading to the inhibition of autoimmune inflammation. The knockdown of <i>SIRT1</i> in vitro eliminated the protective and therapeutic effects of NMN against M5. To conclude, our results indicate that NMN protects against IMQ-induced psoriatic inflammation, oxidative stress, and mitochondrial dysfunction by activating the SIRT1 pathway.https://www.mdpi.com/2076-3921/13/2/186nicotinamide mononucleotidepsoriasisinflammationSIRT1ROSmitochondria
spellingShingle Zhengyi Zhang
Baochen Cheng
Wenqian Du
Mengqi Zeng
Ke He
Tingyi Yin
Sen Shang
Tian Su
Dan Han
Xinyi Gan
Ziyang Wang
Meng Liu
Min Wang
Jiankang Liu
Yan Zheng
The Role of Nicotinamide Mononucleotide Supplementation in Psoriasis Treatment
Antioxidants
nicotinamide mononucleotide
psoriasis
inflammation
SIRT1
ROS
mitochondria
title The Role of Nicotinamide Mononucleotide Supplementation in Psoriasis Treatment
title_full The Role of Nicotinamide Mononucleotide Supplementation in Psoriasis Treatment
title_fullStr The Role of Nicotinamide Mononucleotide Supplementation in Psoriasis Treatment
title_full_unstemmed The Role of Nicotinamide Mononucleotide Supplementation in Psoriasis Treatment
title_short The Role of Nicotinamide Mononucleotide Supplementation in Psoriasis Treatment
title_sort role of nicotinamide mononucleotide supplementation in psoriasis treatment
topic nicotinamide mononucleotide
psoriasis
inflammation
SIRT1
ROS
mitochondria
url https://www.mdpi.com/2076-3921/13/2/186
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