Role of Formoterol on Myogenic Regulatory Factor to Ameliorate Statin-induced Myopathy

Abdullah  Qamar; Arsalan Manzoor Mughal; Humaira  Ali; Tayyaba Faisal; Maria Iram; Sana Malik

doi:10.35787/jimdc.v13i1.1022

Abdullah Qamar Department of Anatomy, Army Medical College, Rawalpindi
Arsalan Manzoor Mughal Department of Anatomy, Rawalpindi Medical University, Rawalpindi
Humaira Ali Department of Anatomy, Swat Medical College, Saidu Shareef, Swat
Tayyaba Faisal Department of Anatomy, Army Medical College, Rawalpindi
Maria Iram Department of Anatomy, Rawal Institute of Health Sciences, Islamabad
Sana Malik Department of Anatomy, Federal Medical College, Islamabad

DOI: https://doi.org/10.35787/jimdc.v13i1.1022

Keywords: Statin, Formoterol, Myopathy, Myogenin, Muscle regeneration

Abstract

Objective: To investigate the effects of β2-adrenergic agonist formoterol on expression of myogenic regulatory factor myogenin in statin-induced myopathies in rats

Methods: Adult male Sprague-Dawley rats were randomized into control (A), statin-only (B), and statin + formoterol groups (C) (n=30 per group). The control group A received no treatment. B group received simvastatin at 60 mg/kg/day by oral gavage for 12 weeks to induce myotoxicity. C group received simvastatin at 60 mg/kg/day plus formoterol at 3 μg/kg/day by oral gavage for 12 weeks. After 12 weeks, extensor digitorum longus muscles were dissected and 5 μm transverse sections were immunostained for myogenin expression. One cross section was selected from each of the specimen for study. Myogenin-positive nuclei were quantified in 8 random 40x magnification fields per muscle section by a blinded investigator. Data was analyzed using IBM SPSS.

Results: Myogenin-positive nuclei were minimal in the control (A) group and statin-only (B) groups. In contrast, the statin + formoterol (C) group exhibited a significant increase in myogenin-positive nuclei compared to both control and statin-only groups (p<0.001), indicating enhanced muscle regeneration.

Conclusion: Formoterol treatment augmented skeletal muscle repair pathways in a rat model of statin-induced myopathy, potentially via activation of quiescent muscle satellite cells and upregulation of myogenic regulatory factor myogenin in group C.