Effect of High Intensity Interval Training with Curcumin on Gene Expression of Bax, Bcl- 2, and Caspase- 3 in Aged Female Rat Hepatocytes
محورهای موضوعی : Report of Health Care
Solmaz shirpour
1
(Department of Exercise Physiology, Islamic Azad University, Central Branch)
Mohammad Ali Azarbayjani
2
(Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran)
Maghsod Peeri
3
(Department of Exercise Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran)
Parvin Farzanegi
4
(Department of Exercise Physiology, Sari Branch, Islamic Azad University, Sari, Iran)
کلید واژه: Training, Curcumin, Apoptosis, Hepatocyte,
چکیده مقاله :
Introduction: Apoptosis is a type of cell death that is essential for homeostasis. Findings on the impact of physical activity on apoptosis are contradictory. The aim of this study was to investigate the effect of high intensity interval training with curcumin on gene expression of Bax, Bcl- 2, and Caspase- 3 in aged female rat hepatocytes. Methods: In this experimental study, 35 aged female, postmenopausal Wistar rats (2-year-old), were randomly assigned to five groups including control, curcumin, high intensity interval training (HIIT), curcumin with HIIT and sham. Curcumin was given at 30 mg/kg by gavage in experimental groups 3 days a week. The HIIT protocol consisted of three sessions of high intensity treadmill training per week for 8 weeks. Forty-eight hours after the last training session and gavage, the Bax, Bcl- 2, and Caspase-3 genes expression were measured in the hepatocytes. Results: The expression of Bax (P = 0.0003) and Caspase- 3 (P = 0.0006) genes increased significantly due to HIIT, while curcumin reduced this increase (P≤0.05). Bcl- 2 gene decreased due to HIIT (P = 0.001), and Curcumin with HIIT increased Bcl- 2 (P≤0.05). Conclusion: HIIT and curcumin had an antagonistic effect on expression of apoptosis-regulating genes in hepatocytes.
1. Finkel T. Radical medicine: treating ageing to cure disease. Nat Rev Mol Cell Biol. 2005; 12: 971- 976.
2. Fabbrini E, Sullivan S, Kliein S. Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical applications. Hepatology. 2010; 51 (2): 679- 689.
3. Schmucker D. Age-related changes in liver structure and function: implications for disease? Exp Gerontol. 2005; 40: 650- 659.
4. Dinenno FA, Seals DR, DeSouza CA, Tanaka H. Age- related decreases in basal limb blood flow in humans: time course, determinants and habitual exercise effects. J Physiol. 2001; 531: 573- 579.
5. Strasser A. Deciphering the rules of programmed cell death to improve therapy of cancer and other diseases. EMBO J. 20111; 30: 3667- 3683.
6. Czabotar PE. Control of apoptosis by the Bcl- 2 protein family: implications for physiology and therapy. Nat Rev Mol CellBiol. 2014; 15: 49- 63.
7. Delbridge ARD. Thirty years of Bcl- 2: translating cell death discoveries in to novel cancer therapies. Nat Rev Cancer. 2016; 16: 99- 109.
8. Frith J, Jones D, Newton JL. Chronic liver disease in an ageing population. Age Ageing. 2009; 38 (1): 11- 18.
9. Lee JY, Kim KM, Lee SG, Yu E, Lim YS, Lee HC, et al. Prevalence and risk factors of non-alcoholic fatty liver disease in potential living liver donors in Korea: a review of 589 consecutive liver biopsies in a single center. J Hepatol. 2007; 47 (2): 239- 244.
10. Hilmer SN, Shenfield GM, Le Couteur DG. Clinical implications of changes in hepatic drug metabolism in older people. Ther Clin Risk Manag. 2005; 1 (2): 151- 156.
11. Zsolt R, Hae YC, Hisashi N, Ryoya T, Kyung JJ, Hyon- Jeen K, et al. Age-
associated increases in oxidative stress and nuclear transcription factor κB activation are attenuated in rat liver by regular exercise. FASEB. 2004; 18 (6): 749- 750
12. Hallsworth K, Thoma C, Hollingsworth KG, Cassidy S, Anstee QM, Day CP, et al. Modified high-intensity interval training reduces liver fat and improves cardiac function in non-alcoholic fatty liver disease: a randomized controlled trial. Clin Sci. 2015; 129: 1097- 1105.
13. Shehzad A, Lee J, Lee YS. Curcumin in various cancers. Biofactors. 2013; 39 (1): 56- 68.
14. Shehzad A, Lee YS. Molecular mechanisms of curcumin action: signal transduction. Biofactors. 2013; 39 (1): 27- 36.
15. Shishodia S. Molecular mechanisms of curcumin action: Gene expression. Biofactors. 2013; 39: 37- 55.
16. Hilchie AL, Furlong SJ, Sutton K, Richardson A, Robichaud MR, Giacomantonio CA, et al. Curcumin-induced apoptosis in PC3 prostate carcinoma cells is caspase-independent and involves cellular ceramide accumulation and damage to mitochondria. Nutr Cancer. 2010; 62: 379- 389.
17. Yu T, Li J, Qiu Y, Sun H. 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) facilitates curcumin-induced melanoma cell apoptosis by enhancing ceramide accumulation, JNK activation, and inhibiting PI3K/AKT activation. Molecular Cell Biochem. 2012; 361 (1- 2): 47- 54.
18. Mythri R, Srinivas Bharath M. Curcumin: a potential neuroprotective agent in Parkinson's disease. Current Pharm Design. 2012; 18 (1): 91- 99.
19. Merrell JG, McLaughlin SW, Tie L, Laurencin CT, Chen AF, Nair LS. Curcumin loaded poly (ε caprolactone) nanofibres: Diabetic wound dressing with antioxidant and antiinflammatory properties. Clin Exper Pharm Physiol. 2009; 36 (12): 1149- 1156.
20. Antunes LH, DarinNde JD, Bianchi L. Effects of the antioxidants curcumin or selenium on cisplatin-induced nephrotoxicity and lipid peroxidation in rats. Pharmacol Res. 2001; 43 (2): 145- 150.
21. Zhong W, Qian K, Xiong J, Ma K, Wang A, Zou Y. Curcumin alleviates lipopolysaccharide induced sepsis and liver failure by suppression of oxidative stress-related inflammation via PI3K/AKT and NF-κB related signaling. Biomed Pharm. 2016; 83: 302- 313.
22. Begriche K, Massart J, Robin MA, Bonnet F, Fromenty B. Mitochondrial adaptations and dysfunctions in nonalcoholic fatty liver disease. Hepatology. 2013; 58 (4): 1497- 1507.
23. John M, Aniko H, Alice K, Brett J, Catriona M, Sarah J. et al. The effect of aging on mitochondrial and cytosolic hepatic intrinsic death pathway and apoptosis associated proteins in Fischer 344 rats. Exp Ger. 2015; 67: 54- 61.
24. Kruger K, Mooren FC. Exercise- induced leukocyte apoptosis. Exerc Immunol Rev. 2014; 20: 117- 134.
25. Fernandes T, Magalhaes FC, Everton CC. Aerobic exercise training inhibits skeletal muscular apoptotic signaling mediated by vegf-vegr2 in spontaneously hypertensive rats. Exerc & Sports Sci. 2012; 18 (6): 412- 418.
26. Quadrilatero J, Hoffman-Goetz L. N-Acetyl-L-cysteine prevents exercise-induced intestinal lymphocyte apoptosis by maintaining intracellular glutathione levels and reducing mitochondrial membrane depolarization. Biochem Biophys Res Commun. 2004; 319 (3): 894- 901.
27. Mooren FC, Krüger K. Exercise, autophagy, and apoptosis. Pro Molecular Biol Trans Sci. 2015; 135: 407- 422.
28. Venditti P, Di Meo S. Antioxidants, tissue damage, and endurance in trained and untrained young male rats. Arch Biochem Biophys. 1996; 331: 63- 68.
29. Venditti P, De Rosa R, Caldarone G, DiMeo S. Effect of prolonged exercise on oxidative damage and susceptibility to oxidants of rat tissues in severe hyperthyroidism. Arch Biochem Biophys. 2005; 442: 229- 237.
30. Ascensão A, Martins MJ, Antos- Alves E, Gonçalves O, Portincasa PJ, Oliveira P, et al. Modulation of hepatic redox status and mitochondrial metabolism by exercise: therapeutic strategy for liver diseases. Mitochondrion. 2013; 13: 862- 870.
