Swimming alters some proteins of skeletal muscle tissue in rats with Alzheimer-like phenotype

• Published in: Archives of gerontology and geriatrics Vol. 117; p. 105260
• Main Authors: Farsani, Mohammad Soleimani, Fathi, Mohammad, Farsani, Zahra Hemati, Gourgin Karaji, Zinab
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.02.2024
• Subjects: Alzheimer; Alzheimer Disease; Animals; Axons - metabolism; Humans; Male; Muscle, Skeletal - metabolism; NCAM; Nerve Regeneration; Neural Cell Adhesion Molecules - genetics; Neural Cell Adhesion Molecules - metabolism; Neural Cell Adhesion Molecules - pharmacology; Profilin 1; Profilins - pharmacology; Rats; Rats, Wistar; Semaphorin 3; Semaphorin-3A - genetics; Semaphorin-3A - metabolism; Semaphorin-3A - pharmacology; Swimming; Swimming - physiology; Profilin 1; Swimming; Semaphorin 3; NCAM; Alzheimer
• ISSN: 0167-4943; 1872-6976; 1872-6976
• DOI: 10.1016/j.archger.2023.105260

•The results of this study showed that Alzheimer (induced by beta-amyloid hippocampus injection) increase the rate of SEMA3A and decrease the NCAM and PFN1 proteins.•The results of this study showed that swimming increase the rate of NCAM and PFN1 proteins and decrease the SEMA3A proteins in healthy subjects.•The results of this study showed that swimming increase the rate of NCAM and PFN1 proteins and decrease the SEMA3A proteins in Alzheimer's model rats. Exercise training plays a significant role in preventing the destruction of central nerve neurons and muscle atrophy. The purpose of the present study was to investigate the effect of a period of swimming training on the expression of Neural cell adhesion molecule (NCAM), Semaphorin 3A (SEMA3A), and Profilin-1 (PFN1) proteins in the gastrocnemius muscle of Alzheimer-like phenotype rats. 32 Wistar males were (6 weeks of age) divided into four groups: Healthy Control (HC), Alzheimer-like phenotype's Control (AC), Healthy Training (HT), and Alzheimer-like phenotype's Training (AT). Alzheimer-like phenotypes were induced by beta-amyloid injection in the hippocampus. The training program consisted of 20 swimming sessions. Gastrocnemius muscle was removed after the intervention, and NCAM, SEMA3A, and PFN1 proteins were measured by the immunohistoflorescent method. The results showed that SEMA3A was increased (p = 0.001), and NCAM (p = 0.001), and PFN1 (p = 0.001) were decreased in AC compared to the HC group. Also, the results showed that NCAM (p = 0.001) and Pfn1 (p = 0.002) increased in the HT group compared to HC, and the NCAM (p = 0.001) and Pfn1 (p = 0.002) in AT group compared to AC (p = 0.001) increased significantly, while SEMA3A was reduced in the HT group compared to HC (p = 0.001) and AT group compared to AC (p = 0.001) Swimming effectively improves axon regeneration and neuronal formation in motor neurons and, therefore, can be an effective intervention to prevent and control the complications of Alzheimer-like phenotype. [Display omitted]