The therapeutic potential of Wild Bitter Melon to ameliorate muscle atrophy in a murine model

Document Type : Original Research Article

Authors

1 Metabolic Disorders Research Center, Department of Biochemistry and Biophysics, Golestan University of Medical Sciences Gorgan, Golestan, Iran

2 Metabolic syndrome Research center, Mashhad University of Medical Sciences, Mashhad, Iran

3 Department of Medical Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

10.22038/ajp.2024.24011

Abstract

Objective: Muscle atrophy due to immobility is a common complication of many diseases and a consequence of therapeutic processes. Immobility and inactivity have been shown to be associated with increased inflammation. The aim of this study was to investigate the therapeutic potential of Wild Bitter Melon (WBM) (Momordica charantia Linn) on muscle atrophy due to immobility in a mouse model.
Materials and Methods: This study was performed in two phases of atrophy and recovery on male BALB/c mice which were divided into 3 groups: control, immobilized, and experimental. The treatment period with WBM at a dose of 400 mg/kg daily by gavage was 17 days, including 7 days of being immobilized and 10 days of recovery. At the end of each phase, half of the mice from each group were examined regarding the four limb grip strength, and then histological and biochemical analyses were done.
Results: The tissue level of malondialdehyde (MDA) oxidative stress index in the atrophy phase in the atrophy group (5.4567±0.522) nmol/g compared to the control group (3.455±0.065) nmol significantly (p 0.001) <) increased. Also, the tissue level of MDA in the WBM group (3.87±0.035) showed a significant decrease compared to the atrophy group (p<0.01). The strength percentage of four limbs in the mice of the treatment group (-23.46±2.45) was significantly higher than that of the atrophy group (-30.60±3.15) at the end of the atrophy phase.
Conclusion: The results suggest that the use of WBM reduces the degree of inflammation, oxidative stress and muscle damage, as well as muscle atrophy, which may improve the muscle atrophy in mice.

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