Nicotinamide mononucleotide attenuates renal fibrosis in mice with Al-port syndrome through TGFβ/Smad3 signaling pathway
10.3969/j.issn.1000-4718.2025.03.012
- VernacularTitle:烟酰胺单核苷酸通过TGFβ/Smad3信号通路减轻Alport综合征小鼠肾纤维化
- Author:
Mo LI
1
;
Xingxing WANG
;
Shangming LI
;
Xiaomei LI
;
Xiufen ZHANG
;
Xiao HAN
;
Xifei YANG
Author Information
1. 山西医科大学公共卫生学院,山西 太原 030000;深圳市疾病预防控制中心深圳市现代毒理学重点实验室,深圳市卫生毒理学医学重点学科,广东 深圳 518055
- Publication Type:Journal Article
- Keywords:
nicotinamide mononucleotide;
Alport syndrome;
renal fibrosis;
TGFβ/Smad3 signaling pathway
- From:
Chinese Journal of Pathophysiology
2025;41(3):518-523
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To study the effect of nicotinamide mononucleotide(NMN)on renal fibrosis in mice with Al-port syndrome(AS)through TGFβ/Smad3 pathway.METHODS:SPF grade female X-linked AS(COL4A5 KI)mice were divided into model group(AS group)and model drug administration group(AS+NMN group).while female C57BL/6 mice served as the wild-type(WT)group,with 7 to 8 mice in each group.The mice in the administration group were given oral administration at 8 weeks of age for 8 weeks to 16 weeks of age.The remaining mice were given saline intragastric ad-ministration.The ratio of urinary microalbumin to urinary creatinine(UACR)was measured by biochemical method.After sampling,the renal fibrosis was analyzed by Masson staining.The expression levels of desmin and α-smooth muscle actin(α-SMA)were detected by immunohistochemistry.The expressions of fibrosis-related proteins desmin,α-SMA,trans-forming growth factor β(TGFβ),Smad3,p-Smad3,and fibronectin were detected by Western blot.RESULTS:Com-pared with the model group,UACR(13 weeks,P＜0.01;15 weeks,P＜0.01)and fibrosis-related protein expression(P＜0.05)in AS mice were significantly decreased after NMN treatment.CONCLUSION:Treatment with NMN attenuates renal fibrosis in AS mice through TGFβ/Smad3 signaling pathway.
