اثر تمرین مقاومتی بر مقدارآنزیم‌های آنتی‌اکسیدانی بافت کبدی در موش صحرایی نر ویستار مبتلا به کبد چرب غیرالکلی

نوع مقاله : مقاله پژوهشی

نویسندگان

1 کارشناس ارشد،گروه فیزیولوژی ورزشی،دانشکده علوم انسانی،دانشگاه آزاد اسلامی واحد ایلام،ایلام،ایران

2 استادیار،گروه فیزیولوژی ورزشی،دانشکده علوم انسانی،دانشگاه آزاد اسالمی واحد ایلام،ایلام،ایران

3 دانشیار، گروه فیزیولوژی ورزشی،دانشکده علوم انسانی،دانشگاه آزاد اسالمی واحد ایلام،ایلام،ایران

چکیده

مقدمه: سازوکار زیربنایی بیماری کبد چرب غیرالکلی و پیشرفت آن به استئوهپاتیت غیرالکلی به ­خوبی شناخته نشده است. هدف از اجرای این پژوهش، تعیین اثر تمرین مقاومتی بر مقدار آنزیم­های آنتی ­اکسیدانی در بافت کبدی موش­ های صحرایی نر نژاد ویستار مبتلا به کبد چرب غیرالکلی بود.
روش کار: در این مطالعه تجربی، 21 سر موش صحرایی نر بالغ نژاد ویستار به ­طور تصادفی به سه گروه تقسیم شدند: گروه کنترل، گروه رژیم پرچرب و گروه رژیم پرچرب+ تمرین مقاومتی. حیوانات گروه­ های رژیم پرچرب به مدت 23 هفته رژیم پرچرب شامل ترکیبی از فروکتوز، کربن تتراکلرید و روغن زیتون دریافت کردند. گروه تمرینی ضمن دریافت رژیم پرچرب، هشت هفته پایانی پروتکل تمرین مقاومتی فزاینده شامل حمل وزنه معادل 30 تا 100 درصد وزن بدن را سه جلسه در هفته اجرا کرد. در پایان مداخله، مقدار آنزیم ­های سوپراکسید دیسموتاز (SOD) و گلوتاتیون پراکسیداز (GPX) در بافت کبد به روش رنگ ­سنجی آنزیمی اندازه ­گیری شد. هم­ چنین، آسیب ­شناسی کبد برای تأیید نتایج بیوشیمیایی انجام شد. آزمون­ های تحلیل واریانس یک­ طرفه و تعقیبی توکی برای تجزیه و تحلیل داده ­های جمع ­آوری شده استفاده شد.
یافته ­ها: مقدار آنزیم SOD کبدی گروه رژیم پرچرب + تمرین مقاومتی در مقایسه با گروه رژیم پرچرب به­ طور معناداری افزایش داشت (0.035 = p)، اما مقدار آنزیم GPX کبدی در هر سه گروه تغییر معناداری نداشت (0.085 = p). بررسی آسیب­ شناسی کبد نیز تغییرات ناشی از رژیم پرچرب و آثار محافظتی تمرین مقاومتی را تأیید کرد.
نتیجه ­گیری: بر اساس نتایج مطالعه حاضر می­ توان گفت اجرای تمرین مقاومتی می‌تواند اختلال آنزیم­های آنتی­ اکسیدانی و استئاتوز بافت کبدی ناشی از دریافت رژیم غذایی پرچرب در موش­ های صحرایی نژاد ویستار مبتلا به کبد چرب غیر الکلی را به ­طور معناداری بهبود بخشد.

کلیدواژه‌ها

عنوان مقاله [English]

The effect of resistance training on the level of liver antioxidant enzymes of male Wistar rats with non-alcoholic fatty liver

نویسندگان [English]

  • Sara Kianitabar 1
  • Abdolhossein Taheri Kalani 2
  • Mahmoud Nikseresht 3

1 Master of Exercise Physiology, Department of Exercise Physiology, Faculty of Humanities, Ilam Branch, Islamic Azad University, Ilam, Iran

2 Assistant Professor, Department of Exercise Physiology, Faculty of Humanities, Ilam Branch, Islamic Azad University, Ilam, Iran

3 Associated Professor, Department of Exercise Physiology, Faculty of Humanities, Ilam Branch, Islamic Azad University, Ilam, IraIran

چکیده [English]

Introduction: The pathogenic mechanism underlying non-alcoholic fatty liver disease (NAFLD) and progression from non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH) is not entirely understood. The purpose of this study was to determine the effect of resistance training on the level of antioxidant enzymes in liver tissue of male Wistar rats with non-alcoholic fatty liver.
Materials and Methods: In the present experimental study, 21 adults male Wistar rats were purchased and randomly divided into three groups: control, high fat diet and high fat diet+ resistance training groups. Animals in the high-fat diet groups received a high-fat diet including a combination of fructose, carbon tetrachloride and olive oil for 23 weeks. The training group while receiving a high-fat diet, in the final 8 weeks performed the progressive resistance training protocol including carrying weights equivalent to 30 to 100 percent of body weight three sessions a week. At the end of the intervention, level of superoxide dismutase (SOD) and glutathione peroxidase (GPX) enzymes in liver tissue were measured by enzyme colorimetric method. Also, liver histopathology was performed to confirm the biochemical results. The data collected were analyzed using statistical tests of one-way analysis of variance and Tukey's follow-up test.
Results: Liver SOD enzyme level in the high-fat diet+ resistance training group showed significant increase in compared to the high-fat diet group (p = 0.035), but liver GPX enzyme level did not change significantly in the three groups (p = 0.085). The histopathological examination of the liver also confirmed the changes caused by the high-fat diet and the protective effects of resistance training.
Conclusion: According to the results of this study, it can be said that resistance training can significantly improve the disorder of antioxidant enzymes and liver tissue steatosis caused by high-fat diet in male Wistar rats with non-alcoholic fatty liver.

کلیدواژه‌ها [English]

  • Diet
  • Resistance Training
  • Antioxidant
  • Oxidative Stress
  • Fatty Liver
1.Woo Baidal JA, Lavine JE. The intersection of
nonalcoholic fatty liver disease and obesity. Sci Transl
Med 2016; 8 (323): 323rv1.
2.Pais R, Giral P, Khan JF, Rosenbaum D, Housset C,
Poynard T, et al. Fatty liver is an independent predictor
of early carotid atherosclerosis. J Hepatol 2016; 65 (1):
95-102.
3.Mohajeri D, Rezaie A, Mosavi S. Histopathological
study on the effects of Crocin on prevention of fatty liver
disease in the rats fed with high fat diet. Veteri Clin
Pathol 2011; 5 (3): 1295-1304.
4.Wen S, Jadhav KS, Williamson DL, Rideout TC.
Treadmill exercise training modulates hepatic cholesterol
metabolism and circulating PCSK9 concentration in
high-fat-fed mice. J Lipids 2013; 2013.
5.Hawley JA, Yeo WK. Metabolic adaptations to a high‐fat
diet. Encycl Sports Med 2013; 19: 166-73.
6.Köroğlu E, Canbakan B, Atay K, Hatemi İ, Tuncer M,
Dobrucalı A, et al. Role of oxidative stress and insulin
resistance in disease severity of non-alcoholic fatty liver
disease. Turk J Gastroenterol 2016; 27 (4): 361-6.
7.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 Radic Res
2019; 53 (5): 497-521.
8.Malhi H, Gores GJ. Molecular mechanisms of
lipotoxicity in nonalcoholic fatty liver disease. Semin
Liver Dis 2008; 28: 360-9.
9.Browning JD, Horton JD. Molecular mediators of hepatic
steatosis and liver injury. J Clin Invest 2004; 114 (2):
147-52.
10. Bergamini CM, Gambetti S, Dondi A, Cervellati C.
Oxygen, reactive oxygen species and tissue damage. Curr
Pharm Des 2004; 10 (14): 1611-26.
11. Yesilova Z, Yaman H, Oktenli C, Ozcan A, Uygun A,
Cakir E, et al. Systemic markers of lipid peroxidation and
antioxidants in patients with nonalcoholic fatty liver
disease. Am J Gastroenterol 2005; 100 (4): 850-5.
12. Powers SK, Deminice R, Ozdemir M, Yoshihara T,
Bomkamp MP, Hyatt H. Exercise-induced oxidative
stress: Friend or foe? J Sport Health Sci 2020; 9 (5): 415-
25.
13. Radak Z, Ishihara K, Tekus E, Varga C, Posa A, Balogh
L, Boldogh I, Koltai E. Exercise, oxidants, and
antioxidants change the shape of the bell-shaped
hormesis curve. Redox Biol 2017; 12: 285-90.
14. Azizbeigi K, Stannard SR, Atashak S, Haghighi MM.
Antioxidant enzymes and oxidative stress adaptation to
exercise training: Comparison of endurance, resistance,
and concurrent training in untrained males. J Exer Sci
Fitness 2014; 12 (1): 1-6.
15. Strauss RS. Comparison of serum concentrations of α-
tocopherol and β-carotene in a cross-sectional sample of
obese and nonobese children (NHANES III). J Pediatr
1999; 134 (2): 160-5.
16. Furukawa S, Fujita T, Shimabukuro M, Iwaki M,
Yamada Y, Nakajima Y, et al. Increased oxidative stress
in obesity and its impact on metabolic syndrome. J Clin
Invest 2017; 114 (12): 1752-61.
17. Day CP. From fat to inflammation. Gastroenterology
2006; 130 (1): 207-10.
18. Barbuio R, Milanski M, Bertolo MB, Saad MJ, Velloso
LA. Infliximab reverses steatosis and improves insulinsignal transduction in liver of rats fed a high-fat diet. J
Endocrinol 2007; 194 (3): 539-50.
19. Venditti P, Napolitano G, Barone D, Di Meo S. Effect
of training and vitamin E administration on rat liver
oxidative metabolism. Free Radic Res 2014; 48 (3): 322-
32.
20. Kalvandi F, Azarbayjani MA, Azizbeigi R, Azizbeigi
K. Elastic resistance training is more effective than
vitamin D3 supplementation in reducing oxidative stress
and strengthen antioxidant enzymes in healthy men. Eur
J Clin Nutr 2021; 10: 1-6.
21. da Palma RK, Moraes-Silva IC, da Silva Dias D,
Shimojo GL, Conti FF, Bernardes N, et al. Resistance or
aerobic training decreases blood pressure and improves
cardiovascular autonomic control and oxidative stress in
hypertensive menopausal rats. J Appl Physiol 2016; 121
(4): 1032-8.
22. Arazi H, Rahmati S, Ghafoori H. The interaction
effects of resistance training and sustanon abuse on liver
antioxidant activities and serum enzymes in male rats.
Interv Med Appl Sci 2017; 9 (3): 178-83.
23. Rodrigues MF, Stotzer US, Domingos MM, Deminice
R, Shiguemoto GE, Tomaz LM, et al. Effects of
ovariectomy and resistance training on oxidative stress
markers in the rat liver. Clinics (Sao Paulo) 2013; 68 (9):
1247-54.
24. Rahmani A, Gorzi A, Ghanbari M. The effects of high
intensity interval training and strenuous resistance
training on hippocampal antioxidant capacity and serum
levels of malondialdehyde and total antioxidant capacity
in male rats. SJKU 2019; 23 (6): 47-58. [Persian]
25. Eslami Z, Mirghani SJ, Moghanlou AE, Norouzi A,
Naseh H, Joshaghani H, et al. An efficient model of non-
alcoholic fatty liver disease (NAFLD) versus current
experimental models: effects of fructose, fat, and carbon
tetrachloride on NAFLD. Hep Month 2021; 21 (8).
26. Safarzade A, Gharakhanlou R, Hedayati M, Talebi-
Garakani E. Effects of 3 resistance training programs on
serum vaspin, hs-CRP and TNF-α concentrations in the
streptozotocin-induced diabetic rats. J Appl Exer Physiol
2012; 8 (16): 87-100. [Persian]
27. Tan Y, Sun LQ, Kamal MA, Wang X, Seale JP, Qu X.
Suppression of retinol-binding protein 4 with RNA
oligonucleotide prevents high-fat diet-induced metabolic
syndrome and non-alcoholic fatty liver disease in mice.
Biochimica et Biophysica Acta 2011; 1811: 1045–1053.
28. Brunt EM, Janney CG, Di Bisceglie AM,
Neuschwander-Tetri BA, Bacon BR. Nonalcoholic
steatohepatitis: a proposal for grading and staging the
histological lesions. Am J Gastroenterol 1999; 94 (9):
2467-74.
29. Hovanloo F, Hedayati M, Ebrahimi M, Abednazari H.
Effect of various time courses of endurance training on
alterations of antioxidant enzymes activity in rat liver
tissue. Res Med 2011; 35 (1): 14-19. [Persian]
30. Smith LL, Miles MP. Exercise-induced muscle injury
and inflammation. In: Garret WE, Kirkendall DT, eds.
Exercise and Sport Science. Philadephia, PA: Lippincott
Williams and Wilkins; 2000: 401-411.
31. Inal M, Akyu¨z F, Turgut A, et al. Effect of aerobic and
anaerobic metabolism on free radical generation
swimmers. Med Sci Sports Exer 2001; 33: 564-67.
32. Ogonovszky H, Sasvári M, Dosek A, Berkes I, Kaneko
T, Tahara S, et al The effects of moderate, strenuous, and
overtraining on oxidative stress markers and DNA repair
in rat liver. Can J Appl Physiol 2005; 30 (2): 186-95.
33. Sriram KI, Lakshmi CJ. Endurance exercise-induced
alterations in antioxidant enzymes of old albino male rats.
Curr Sci 2001; 80 (8): 921-23.
34. Schneider CD, Barp J, Ribeiro JL, Belló-Klein A,
Oliveira AR. Oxidative stress after three different
intensities of running. Can J Appl Physiol 2005; 30 (6):
723-34.
35. Radak Z, Chung HY, Goto S. Systemic adaptation to
oxidative challenge induced by regular exercise. Free
Radic Biol Med 2008; 44 (2): 153-9.
36. Liu Y, Palanivel R, Rai E, Park M, Gabor TV, Scheid
MP, et al. Adiponectin stimulates autophagy and reduces
oxidative stress to enhance insulin sensitivity during
high-fat diet feeding in mice. Diabetes 2015; 64 (1): 36-
48.
37. Ming M, Guanhua L, Zhanhai Y, Guang C, Xuan Z.
Effect of the Lycium barbarum polysaccharides
administration on blood lipid metabolism and oxidative
stress of mice fed high-fat diet in vivo. Food Chem 2009;
113 (4): 872-7.
38. Mayer M, Bukau B. Hsp70 chaperones: cellular
functions and molecular mechanism. Cell Mol Life Sci
2005; 62 (6): 670-9