Effect of nicotinamide ribose on sarcopenia in Marfan syndrome mice

Hong Shiyao; Zhang Yanhong; Yao Kexin; Jin Shuhui; Zhang Fan; Han Yingchun; Zhang Congcong

doi:10.3760/j.issn.1673-4777.2025.05.007

Abstract：Objective To investigate the effects of nicotinamide ribose(NR)supplementation on mitochondrial synthesis and sarcopenia in Marfan syndrome(MFS)mice.Methods Ten 3-month-old male wild type and 10 FBN1C1039G/+transgenic(FBN1 TG)mice were selected to establish a skeletal muscle injury model by intramuscular injection of cardiotoxin into the tibial anterior muscle.The area of neonatal muscle fiber,the number and volume of mitochondria were analyzed,and the expression levels of mitochondrial function-related genes were detected.NR(NR group)or equal volume of phosphate buffer(control group)was added to the culture medium of induced C2C12 myoblasts.The expression of myogenin gene,the area of muscle fiber and the content of mitochondria in cells were observed.The area of newly formed muscle fibers was analyzed on the 15th day after operation.Results The ratios of gastrocnemius muscle mass to muscle length and tibialis anterior muscle mass to muscle length of FBN1 TG mice were lower than those of wild type mice,and the cross-sectional areas of muscle fibers before and after cardiac toxin injury were smaller than those of wild type mice(all P＜0.001).It was manifested as sarcopenia.On day 10 after surgery,the number of mitochondria and the expression of mitochondria-related genes in the newborn skeletal muscle of FBN1 TG mice were less/lower than those of wild type mice(all P＜0.001).The expression of myogenin,the positive area of myofibers and the content of mitochondria in C2C12 myoblasts in NR group were higher than those in control group(all P＜0.001).On postoperative day 15,the cross-sectional area of muscle fibers in skeletal muscle of NR-treated FBN1 TG mice was larger than that of FBN1 TG mice treated with 0.9％sodium chloride injection[(836±52)μm2 vs(550±36)μm2](t=9.017,P＜0.001).Conclusion NR can improve the phenotype of sarcopenia in MFS mice by promoting mitochondrial synthesis and muscle fiber formation.