Volume 11, Issue 2 (December 2025)                   Elderly Health Journal 2025, 11(2): 135-141 | Back to browse issues page


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Mehdipouryan S, Bostani M. Effects of an Eight-Week Aerobic Training Program on Plasma cPLA2 Levels in Sedentary Elderly Men. Elderly Health Journal 2025; 11 (2) :135-141
URL: http://ehj.ssu.ac.ir/article-1-365-en.html
Department of Physical Education, Ahv.C., Islamic Azad University, Ahvaz, Iran , mehdi.boustani@iau.ac.ir
Abstract:   (53 Views)
Introduction: Aging is a gradual, time-dependent process marked by a decline in physiological functions, reduced organ performance, and increased susceptibility to disease. Adopting an active lifestyle can substantially influence both the trajectory and pace of aging. Cytosolic Phospholipase A2 (cPLA2) is an enzyme involved in cell signaling and inflammation through the release of arachidonic acid from membrane phospholipids. The present study aimed to investigate the effects of an eight-week aerobic training program on plasma cPLA2 levels in sedentary elderly men.
Methods: In this quasi-experimental study, twenty elderly men aged 60–74 years were recruited through convenience sampling and randomly assigned to an aerobic training group or a control group. The training group completed an eight-week aerobic exercise program consisting of three sessions per week at 50–75% of heart rate reserve, following the principle of progressive overload. The control group did not engage in any structured physical activity. Blood samples were collected from both groups 48 hours before and after the intervention. Plasma cPLA2 levels were measured using an ELISA kit. Analysis of covariance was used to compare outcomes between groups. Data were analyzed using SPSS version 23 at a significance level of 0.05.
Results: Eight weeks of aerobic training resulted in a significant reduction in plasma cPLA2 levels compared with the control group (p < 0.05).
Conclusion: These findings suggest that regular aerobic exercise may reduce inflammatory markers such as cPLA2 in elderly individuals and may contribute to the management of inflammation-related conditions in older age.

 
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Type of Study: Research | Subject: General
Received: 2025/10/8 | Accepted: 2025/11/30 | Published: 2025/12/19

References
1. Singh A, Schurman SH, Bektas A, Kaileh M, Roy R, Wilson DM, et al. Aging and inflammation. Cold Spring Harbor Perspectives in Medicine. 2024; 14(6): 1-26.
2. Sun GY, Geng X, Teng T, Yang B, Appenteng MK, Greenlief CM, et al. Dynamic role of phospholipases A2 in health and diseases in the central nervous system. Cells. 2021; 10(11): 1-23.
3. Khan SA, Ilies MA. The phospholipase A2 superfamily: structure, isozymes, catalysis, physiologic and pathologic roles. International Journal of Molecular Sciences. 2023; 24(2): 1-35.
4. Hugo C, Asante I, Sadybekov A, Katritch V, Yassine HN. Development of calcium-dependent phospholipase a2 inhibitors to target cellular senescence and oxidative stress in neurodegenerative diseases. Antioxidants & Redox Signaling. 2024; 41(16-18): 1100-16.
5. Mukherjee AK. Correlation between the phospholipids domains of the target cell membrane and the extent of Naja kaouthia PLA2-induced membrane damage: evidence of distinct catalytic and cytotoxic sites in PLA2 molecules. Biochimica et Biophysica Acta (BBA)-General Subjects. 2007; 1770(2): 187–95.
6. Czapski GA, Czubowicz K, Strosznajder JB, Strosznajder RP. The lipoxygenases: their regulation and implication in Alzheimer’s disease. Neurochemical Research. 2016; 41(1): 243–57.
7. Strokin M, Sergeeva M, Reiser G. Docosahexaenoic acid and arachidonic acid release in rat brain astrocytes is mediated by two separate isoforms of phospholipase A2 and is differently regulated by cyclic AMP and Ca2+. British Journal of Pharmacology. 2003; 139(5): 1014-22.
8. Chao CC, Gutiérrez-Vázquez C, Rothhammer V, Mayo L, Wheeler MA, Tjon EC, et al. Metabolic control of astrocyte pathogenic activity via cPLA2-MAVS. Cell. 2019; 179(7): 1483–98.
9. Chuang DY, Simonyi A, Kotzbauer PT, Gu Z, Sun GY. Cytosolic phospholipase A2 plays a crucial role in ROS/NO signaling during microglial activation through the lipoxygenase pathway. Journal of Neuroinflammation. 2015; 12(1): 1-20.
10. Lee JCM, Simonyi A, Sun AY, Sun GY. Phospholipases A2 and neural membrane dynamics: implications for Alzheimer’s disease. Journal of Neurochemistry. 2011; 116(5): 813–9.
11. Gentile MT, Reccia M, Sorrentino P, Vitale E, Sorrentino G, Puca AA, et al. Role of cytosolic calcium-dependent phospholipase A2 in Alzheimer's disease pathogenesis. Molecular Neurobiology. 2012; 45(3): 596–604.
12. Gynther M, Estrada ML, Loppi S, Korhonen P, Kanninen KM, Malm T, et al. Increased expression and activity of brain cortical cPLA2 due to chronic lipopolysaccharide administration in mouse model of familial alzheimer’s disease. Pharmaceutics. 2022; 14(11): 1-12.
13. Ma QL, Ebright B, Li B, Li J, Galvan J, Sanchez A, et al. Evidence for cPLA2 activation in Alzheimer’s disease synaptic pathology. BioRxiv. 2025; 1: 1-43.
14. Kregel KC, Zhang HJ. An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 2007; 292(1): 18– 36.
15. Sun GY, Chuang DY, Zong Y, Jiang J, Lee JC, Gu Z, et al. Role of cytosolic phospholipase A2 in oxidative and inflammatory signaling pathways in different cell types in the central nervous system. Molecular Neurobiology. 2014; 50(1): 6–14.
16. Sanchez-Mejia RO, Newman JW, Toh S, Yu GQ, Zhou Y, Halabisky B, et al. Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's disease. Nature Neuroscience. 2008; 11(11): 1311–8.
17. Bostani M, Noaein SA. The effect of continuous aerobic training on bax/bcl2 ratio in pancreatic tissue diabetic rats. Iranian Journal of Diabetes and Obesity. 2021.
18. Cerqueira É, Marinho DA, Neiva HP, Lourenço O. Inflammatory effects of high and moderate intensity exercise—a systematic review. Frontiers in Physiology. 2020; 10: 1-14.
19. de Sousa CV, Sales MM, Rosa TS, Lewis JE, de Andrade RV, Simoes HG. The antioxidant effect of exercise: a systematic review and meta-analysis. Sports Medicine. 2017; 47(2): 277–93.
20. de Souza DC, Matos VA, Dos Santos VO, Medeiros IF, Marinho CS, Nascimento PR, et al. Effects of high-intensity interval and moderate-intensity continuous exercise on inflammatory, leptin, IgA, and lipid peroxidation responses in obese males. Frontiers in Physiology. 2018; 9: 1-9.
21. Pillon Barcelos R, Freire Royes LF, Gonzalez-Gallego J, Bresciani G. Oxidative stress and inflammation: liver responses and adaptations to acute and regular exercise. Free Radical Research. 2017; 51(2): 222–36.
22. Bushman B, Medicine ACoS. ACSM's Complete Guide to Fitness & Health, 2E: Human Kinetics .2017.
23. Gómez-Rubio P, Trapero I. The beneficial effect of physical exercise on inflammatory makers in older individuals. Endocrine, Metabolic & Immune Disorders-Drug Targets . 2021; 21(6): 1008-16.
24. Buyukyazi G, Ulman C, Taneli F, Esen H, Gozlukaya F, Ozcan I, et al. The effects of different intensity walking programs on serum blood lipids, high-sensitive C-reactive protein, and lipoprotein-associated phospholipase A2 in premenopausal women. Science & Sports. 2010; 25(5): 245–52.
25. Thijssen DH, Cable NT, Green DJ. Impact of exercise training on arterial wall thickness in humans. Clinical Science. 2012; 122(7): 311–22.
26. Lavi S, McConnell JP, Rihal CS, Prasad A, Mathew V, Lerman LO, et al. Local production of lipoprotein-associated phospholipase A2 and lysophosphatidylcholine in the coronary circulation: association with early coronary atherosclerosis and endothelial dysfunction in humans. Circulation. 2007; 115(21): 2715–21.
27. Vina J, Borras C, Abdelaziz KM, Garcia-Valles R, Gomez-Cabrera MC. The free radical theory of aging revisited: the cell signaling disruption theory of aging. Antioxidants & Redox Signaling. 2013; 19(8): 779–87.
28. Kruk J, Aboul-Enein HY, Kładna A, Bowser JE. Oxidative stress in biological systems and its relation with pathophysiological functions: the effect of physical activity on cellular redox homeostasis. Free Radical Research. 2019; 53(5): 497–521.
29. Webb R, Hughes MG, Thomas AW, Morris K. The ability of exercise-associated oxidative stress to trigger redox-sensitive signalling responses. Antioxidants. 2017; 6(3): 1-21.
30. Deleidi M, Jäggle M, Rubino G. Immune aging, dysmetabolism, and inflammation in neurological diseases. Frontiers in Neuroscience. 2015;9: 1-14.
31. Wang S, Zhou H, Zhao C, He H. Effect of exercise training on body composition and inflammatory cytokine levels in overweight and obese individuals: a systematic review and network meta-analysis. Frontiers in Immunology. 2022; 13: 1-13.
32. Scheele C, Nielsen S, Pedersen BK. ROS and myokines promote muscle adaptation to exercise. Trends in Endocrinology & Metabolism. 2009; 20(3): 95–9.

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