Fig. 7: Dimenhydrinate exhibits muscle regeneration capability in a toxin-induced muscle damage model.

a Schematic of the muscle damage model induced by cardiotoxin (CTX, 1 μg) or BaCl₂ (1.2% w/v). PBS or 30 mpk DH was administered to each mouse by intraperitoneal injection. b Representative immunohistochemistry image of gastrocnemius muscle sections from the CTX-induced model. Pax7 was used as a marker of MuSCs, while MyoD and myogenin were used as markers of muscle differentiation. Scale bars = 100 μm. c, d Locomotor test of CTX-treated PBS- or DH-treated mice. c Time (s) taken for the “T-turn” in the pole; n = 3 for each group. d Longest time (s) spent hanging wire with four limbs. The maximum time was set at 600 s. n = 3 for each group. e Representative image of the gastrocnemius muscle in BaCl₂-induced muscle damage model mice. The measured area was calculated using ImageJ. f Comparison of fiber diameter in BaCl₂-induced muscle damage model mice with or without DH administration; n = 5 for each group. g Representative hematoxylin and eosin (H&E) staining image of the BaCl₂-induced model. Scale bars = 200 μm. h–j Muscle satellite cells were isolated from 8-week-old MDX mice. The cells were incubated in differentiation media for 1 day with or without DH. h Representative microscopy image of primary myoblasts isolated from MDX mice with or without DH (10 μM). i Relative number of myoblasts isolated from MDX mice with or without DH (10 μM). j Relative mRNA expression of PAX7, MYOD, and MYOG. n = 3 for each group. ns not significant, *p < 0.05, **p < 0.01, ***p < 0.005. Error bars: standard deviation (SD). DH dimenhydrinate, MuSC muscle satellite cell.