نوع مقاله : مقاله پژوهشی
نویسندگان
1 دانشجوی دکتری فیزیولوژی ورزش/ دانشکده تربیت بدنی و علوم ورزشی/ دانشگاه بیرجند
2 دانشیار گروه فیزیولوژی ورزشی/ دانشکده تربیت بدنی و علوم ورزشی/ دانشگاه مازندران
3 استادیار گروه فیزیولوژی ورزشی/ دانشکده تربیت بدنی و علوم ورزشی/ دانشگاه مازندران
چکیده
زمینه وهدف: پروتئین شوک گرمایی 72( HSP72) و ظرفیت آنتی اکسیدانی تام (TAC) دو شاخص مهم در دفاع درونی بدن می باشند. هدف از تحقیق حاضر بررسی تأثیر یک جلسه فعالیت ورزشی تداومی روی نوارگردان بر میزان HSP72 و TAC پلاسمای موش های دیابتی شده توسط استرپتوزوتوسین بود. روش تحقیق: بدین منظور 40 سر موش صحرایی نر نژاد ویستار به وزن 165±1 گرم و سن 6 تا8 هفته، به طور تصادفی در 4 گروه (هر گروه 10 سر)، کنترل دیابت، و 3 گروه دیابتی+تمرین حاد استقامتی (گروه های 1، 2 و 3 که به ترتیب 30 دقیقه، 4 ساعت و 24 ساعت پس از ورزش کشته شدند)، تقسیم شدند. موش های صحرایی با تزریق استروپتوزوتوسین محلول در بافر سیترات 1/ 0 مول (PH = 5/4) به صورت درون صفاقی، دیابتی شدند. پروتکل تمرینی با سرعت 10 متر در دقیقه آغاز شد و به تدریج به 18 متر در دقیقه رسید. مدت دویدن تقریبا 60 دقیقه بود. برای تعیین سطوح HSP72 و TAC به ترتیب از روش الایزا و رنگ سنجی استفاده شد. یافته ها: به دنبال اجرای یک جلسه فعالیت در موش های دیابتی، میزان HSP72 پلاسمای تمام گروه ها افزایش یافت. افزایش HSP72 در گروه 30 دقیقه پس از فعالیت، نسبت به گروه کنترل، غیر معنادار بود؛ اما سطوح این شاخص در گروه 2) 4ساعت( نسبت به گروه کنترل(p=0/03) و در گروه 3(24ساعت) نسبت به گروه کنترل و گروه 30 دقیقه، افزایش معناداری را نشان داد (به ترتیب P=0/001 و P=0/005 ) افزایش ظرفیت آنتی اکسیدانی تام (TAC) فقط در گروه 3 نسبت به گروه کنترل معنی دار بود .(P=0/03) نتیجه گیری: نتایج به دست آمده نشان دهنده اثرات مفید یک جلسه فعالیت استقامتی حاد بر سطوح HSP72 و ظرفیت آنتی اکسیدانی تام در بیماری دیابت می باشد. با توجه به این، احتمالا می توان فعالیت استقامتی حاد را به عنوان یک توصیه درمانی در مقابله با عوارض این بیماری به کار برد.
کلیدواژه‌ها
عنوان مقاله [English]
The effect of continuous treadmill exercise on heat shock protein 72 and total antioxidant capacity level in the plasma of streptozotocin_induced diabetic rats
نویسندگان [English]
- Ali Yaghoubi 1
- Ziya Fallah Mohammadi 2
- Hossein Taheri Chador Neshin 1
- Rozita Fathi 3
1
2
3
چکیده [English]
Background and Aim: HSP72 and TAC are two factors from internal defense of body. The purpose of this study was to investigate the effects of acute treadmill exercise on HSP72 in the plasma of diabetic rats. Materials and Methods: Forty male rats weight 165±1 were assigned randomly into 4 groups: diabetic control group, and 3 diabetic+acute training groups, (included groups 1and 2, and 3 that were killed 30 minute, 4 hours and 24 hours postexercise respectively). Diabetes was induced with injecting streptozotocin (dissolved in 0.1 M citrate buffer, pH 4.5) into the abdominal cavity. Rats were subjected to treadmill exercise, and the speed of the treadmill was 10 m/min, and then gradually increased until 18 m/min (grade 0%). The duration of the treadmill exercise was 60 minutes. For determination of HSP72 and TAC values, respectively sandwich Elisa and decolorization were used. Results: Acute exercise training increased the plasma HSP72 in the groups 2 and 3, but in group 1 no significant changes took place. HSP72 levels significantly increased in the group 2 (P=0.03) and 3 in compared with groups 1 and 2 (P=0.001 and P=0.005 respectively). Increase in TAC levels only in group 3 compared to control group was significant (P=0.03). Conclusion: These results show that acute treadmill exercise improved HSP72 levels and TAC in diabetic’s subjects and have benefit effects. Therefore probably acute exercise treadmill could recommend as a therapeutic strategy for diabetes.
کلیدواژه‌ها [English]
- Rat
- Heat Shock Protein72
- Acute exercise training
- Total antioxidant capacity
2-Atalay M., Laaksonen D.E., 2002. Diabetes, oxidative stress and physical exercise. J Sports Sci Med, vol. 1, pp. 1-14.
3-Banfi G., Dolci A., Verna R., Corsi M.M., 2004. Exercise raises serum heat-shock protein 70 (HSP70) levels. Clin Chem Lab Med, vol. 42, no. 12, pp. 1445-1446.
4-Baydas G., Canatan H., Turkoglu A., 2002. Comparative analysis of the protective effects of melatonin and vitamin E on streptozocin-induced diabetes mellitus. J Pineal Res, vol. 32, no. 4, pp.225-30.
5-Baydas G., Nedzvetskii VS., Nerush PA., Kirichenko SV., et al. 2003. Altered expression of NCAM in hippocampus and cortex may underlie memory and learning deficits in rats with streptozotocininduced diabetes mellitus. Life Sci, 73:1907–16
6-Benjamin I.J., McMillan D.R., 1998. Stress (heat shock) proteins: molecular chaperones in cardiovascular biology and disease. Circ Re, vol. 27, no. 83(2), pp. 117–132.
7-Bruce C.R., Carey A.L., Hawley J.A., Febbraio MA., 2003. Intramuscular heat shock protein 72 and heme oxygenase-1 mRNA are reduced in patients with type 2 diabetes. Evidence that insulin resistance is associated with a disturbed antioxidant defense mechanism. Diabetes, vol. 52, no. 9, pp. 2338–2345.
8-Davison G.W., George L., Jackson S.K., Young I.S., et al., 2002. Exercise, free radicals, and lipid peroxidation in type 1 diabetes mellitus. Free Radic Biol Med, vol. 33, no. 11: pp. 1543-51.
9-Febbraio M.A., Ott P., Nielsen H.B., Steensberg A., et al., 2002. Exercise induces hepatosplanchnic release of heat shock protein 72 in humans. J Physiol, vol. 544, no. 1(Pt 3), pp. 957-62.
10-Fehrenbach E., Niess A.M., Veith R., Dickhuth H.H., Northoff H., 2001. Changes of HSP72 expression in leukocytes are associated with adaptation to exercise under conditions of high environmental temperature. J Leukoc Biol, vol. 69, no. 5, pp. 747-54.
11-Gething M.J., Sambrook J., 1992. Protein folding in the cell. Nature, vol. 355, no. 6355, pp. 33–45.
12-Gispen W.H., Biessels G.J., 2000. Cognition and synaptic plasticity in diabetes mellitus. Trends Neurosci, vol. 23, no 11, pp.542–9.
13-Hooper P.L., Hooper P.L., 2009. Inflammation, heat shock proteins, and type 2 diabetes. Cell Stress Chaperones, vol. 14, no. 2, pp. 113–5.
14-Ji L.L., Radak Z., Goto S., 2008. Hormesis and exercise: how the cell copes with oxidative strss. Am J Pharmacol Toxicol, vol. 3, no. 1, pp. 41-55.
15-Kavanagh K., Zhang L., Wagner J.D., 2009. Tissue-specific regulation and expression of heat shock proteins in type 2 diabetic monkeys. Cell Stress and Chaperones, vol. 14, no. 3, pp. 291–299.
16-Khanna S., Atalay M., Laaksonen DE., Gul M., et al., 1999. Alpha-lipoic acid supplementation: tissue glutathione homeostasis at rest and after exercise. J Appl Physiol, vol. 86, no. 4, pp. 1191-1196.
17-Khassaf M., Child R.B., McArdle A., Brodie D.A., et al., 2001. Time course of responses of human skeletal muscle to oxidative stress induced by nondamaging exercise. J Appl Physiol, vol. 90, no. 3, pp. 1031–5.
18-Kregel KC., 2002. Invented Review: Heat shock proteins: Modifying factors in physiological stress responses and acquired thermotolerance. J Appl Physiol, vol. 92, no. 5, pp. 2177-2186.
19-Kurucz I., Morva A., Vaag A., Eriksson K.F., et al., 2002. Decreased expression of heat shock protein 72 in skeletal muscle of patients with type 2 diabetes correlates with insulin resistance. Diabetes, vol. 51, no. 4, pp. 1102–1109.
20-Laaksonen D.E., Atalay M., Niskanen L.K., Mustonen J., et al., 2000. Aerobic exercise and the lipid profile in type1 diabetic men: a randomized controlled trial. Med Sci Sports Exerc, vol. 32, no.9, pp. 1541-8.
21-Locke M., Noble E.G., Atkinson B.G., 1990. Exercising mammals synthesize stress proteins. Am J Physiol, vol. 258, no. 4, pp.723-9.
22-Mohamadi M., Salehi I., Farajnia S.A., 2008. Effect of swimming exercise on oxidative stress in the hippocampus of male diabetic rats. Med J Tabriz Univ Med Sci, vol. 30, no. 2, pp. 111-118.
23-Powers S.K., Demirel H.A., Vincent H.K., Coombes J.S., et al., 1998. Exercise training improves myocardial tolerance to in vivo ischemia-reperfusion in the rat. Am J Physiol, vol. 275, no. 5 (Pt 2), pp.1468–77.
24-Powers S.K., Locke M., Demirel HA., 2001. Exercise, heat shock proteins, and myocardial protection from I-R injury. Med Sci Sports Exerc, vol. 33, no. 3, pp. 386–392.
25-Smolka M.B., Zoppi C.C., Alves A.A., Silveira L.R., et al., 2000. HSP72 as a complementary protection
against oxidative stress induced by exercise in the soleus muscle of rats. Am J Physiol Regul Integr Comp Physiol, vol. 279, no. 5, pp. 1539–545.
26-Walsh R.C., Koukoulas I., Garnham A., Moseley P.L., et al., 2001. Exercise increases serum HSP72 in humans. Cell Stress Chaperones, vol. 6, no. 4, pp. 386–93.
27-Welsh N., Margulis B., Borg L.A., Wiklund H.J., et al., 1995. Differences in the expression of heat-shock proteins and antioxidant enzymes between human and rodent pancreatic islets: implications for the pathogenesis of insulin-dependent diabetes mellitus. Mol Med, vol. 1, no. 7, pp. 806–820.
28-Yamada P., Amorim F., Moseley P., Schneider S., 2008. Heat shock protein 72 response to exercise in humans. Sports Med, vol. 38, no. 9, pp. 715-733.
29-Zhu J., Quyyumi A.A., WU H., sako G.C., et al., 2003. Increased serum levels of heat shock protein 70 are associated with low risk of coronary artery disease. Arterioscler Thromb Vasc Biols, vol. 23, no. 6, pp. 1055-9.
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