Sulforaphane Promotes the Skeletal Muscle Postinjury Regeneration by Up-Regulating the Transcription of Prl2c2 through JAK2/STAT3 Signaling

Sulforaphane (SFN), a lipophilic small-molecule compound, can be rapidly and completely absorbed upon entering the body. It has garnered extensive research attention for its potential as an antiaging, anticancer, antidiabetic, and antibacterial agent. However, its role and mechanisms of SFN on skeletal muscle postinjury regeneration have not been reported. This research demonstrated that SFN enhanced the regeneration after skeletal muscle injury and up-regulated the proliferation of mouse C2C12 myoblasts. RNA-transcriptome sequencing data revealed that SFN increased Prl2C2 transcription and JAK/STAT signaling pathway activity. CHIP and dual-luciferase reporter gene assays verified that STAT3 binds to the Prl2C2 promoter and regulates its transcription. Consequently, SFN influenced the JAK2/STAT3 signaling activity. Finally, the transcription of Prl2C2 and the proliferation of mouse C2C12 myoblasts were detected by adding JAK2 inhibitor and SFN. The results showed that the JAK2 inhibitor blocked the up-regulation of SFN on the transcription of Prl2C2 and the proliferation of mouse C2C12 myoblasts. The discovery of this phenomenon and its mechanism offer guidance for treating skeletal muscle injuries and supporting animal nutrition research. SFN shows great potential in muscle repair, and future clinical trials could confirm its safety and efficacy, paving the way for new SFN-based treatments and providing new options for patients.