تاثیر هشت هفته تمرین مقاومتی شدید و متوسط برMicroRNA های مرتبط با انتقال معکوس کلسترول در موش‌های سالمند نژاد ویستار

نوع مقاله : علمی - پژوهشی

نویسندگان

1 گروه علوم ورزشی، دانشکده ادبیات و علوم انسانی، دانشگاه شهرکرد، شهرکرد، ایران

2 گروه زیست شناسی، دانشکده علوم پایه، دانشگاه شهرکرد، شهرکرد، ایران

چکیده

هدف: سالمندی با اختلالات عمومی در متابولیسم چربی و عوامل التهابی همراه است که به آترواسکروز منجر میشود.
هدف از این مقاله، بررسی تاثیر دو نوع تمرین مقاومتی شدید و متوسط بر MicroRNA های مرتبط با انتقال معکوس
کلسترول در موش های سالمند است.
روش ها: سی سر موش صحرایی نر نژاد ویستار مسن ) 23 ماهه(، به صورت تصادفی براساس وزن موشها در شروع
پژوهش در دو گروه تمرینی و یک گروه کنترل، شامل گروه تمرین مقاومتی با شدت متوسط ) n=10 (، تمرین مقاومتی با
شدت بالا ) n=10 ( و گروه کنترل ) n=10 ( قرار گرفتند. تمرین مقاومتی، شامل 8 هفته تمرین مقاومتی نردبان با شدت
زیاد ) 80 % از MVCC ( و شدت متوسط ) 60 % از MVCC ( و 5 روز در هفته بود. بعد از دوره تمرین بیان miR-33a و
miR-144 و بیان پروتئین ABCA1 به روش RT–PCR اندازهگیری شد. تجزیه تحلیل آماری با استفاده از آزمون آنوا با
سطح معنی داری ) 05 / P≥0 ( انجام شد.
نتایج: نتایج نشان داد، میزان بیان miR-33a و miR-144 دو گروه مقاومتی شدید و مقاومتی متوسط به طور معنیداری،
کمتر از گروه کنترل بود و میزان بیان mRNA ژن ABCA1 گروه مقاومتی شدید، پس از هشت هفته تمرین افزایش
معنیداری داشت ) 05 / p>0 (. البته تفاوت میزان بیان miR-33a و miR-144 متعاقب تمرین مقاومتی شدید و متوسط
معنیدار نبود ) 05 / p<0 (. با این حال، در باره بیان mRNA ژن ABCA1 تفاوت معنی داری در دو گروه مقاومتی شدید و
متوسط مشاهده شد.
نتیجه گیری: به نظر می رسد، تمرین مقاومتی با شدت متوسط یا شدید می تواند با کاهش بیان miR-33a و miR-144
افزایش بیان mRNA ژن ABCA1 در بهبود وضعیت تصلب شرایین افراد سالمند مؤثر واقع شود.

کلیدواژه‌ها


عنوان مقاله [English]

The ٍeffect of Eight Weeks of Moderate and High Intensity Resistance Training on micro-RNAs Associated with Reverse Cholesterol Transport in Older Wistar rats

نویسندگان [English]

  • mehdi taheri gandomany 1
  • Mohammad Faramarzi 1
  • Ebrahim Banitalebi 1
  • Rohollah Hemmati 2
1 Department of Exercise Physiology, Shahrekord University, Shahrekord. Iran
2 Department of Biology, Faculty of Basic Sciences, Shahrekord University, Shahrekord, Iran
چکیده [English]


Purpose: Aging is associated with systemic dysfunctions in lipid metabolism and chronic inflammatory state which contribute to atherosclerotic. The purpose of this study was to investigate the effect of moderate and high intensity resistance training on micro-RNAs Associated with reverse cholesterol transport in Wistar elderly rats.
Methods: Thirty male Wistar rats (23 months old) were randomly, based on the weight of rats at the start of the study, divided into two experiment and one control group including moderate intensity resistance training (n = 10), high intensity resistance training (n = 10) and the control group (n = 10). Resistance training included 8 weeks of climbing a ladder with high intensity (80% MVCC) and moderate intensity (60% of MVCC) and 5 days a week. After completing training, expression of mir-33 and miR-144 and ABCA1 were measured RT-PCR technique. The statistical analysis was performed using ANOVA test with significance level of (P ≤0.05).
Results: There was significance decrease in expression of miR-33a and miR-144 and increase in expression of ABCA1 in both high and moderate resistance groups (P ≤0.05). Also, there was significant difference between the mRNA expression of ABCA1 levels in high and moderate resistance training (P>0.05). However, there was no significant difference expression of miR-33a and miR-144 level between groups.
Conclusion: It seems that moderate and high intensity resistance training can cause decrease the expression of miR-33a and miR-144 result to increase in mRNA expression of ABCA1.

کلیدواژه‌ها [English]

  • 33a
  • miR
  • 144
  • ABCA1
  • Atherosclerosis
1. Seres I, Paragh G, Deschene E, Fulop T, Khalil
A. Study of factors influencing the decreased
HDL associated PON1 activity with aging. Experimental
Gerontology. 2004;39(1):59-66.
2. Rotllan N, Price N, Pati P, Goedeke L, Fernandez-
Hernando C. microRNAs in lipoprotein
metabolism and cardiometabolic disorders.
Atherosclerosis. 2016;246:352-60.
3. Ono K, Horie T, Nishino T, Baba O, Kuwabara
Y, Kimura T. Micrornas and high-density lipoprotein
cholesterol metabolism. International
heart journal. 2015;56(4):365-71.
4. Ono K, Horie T, Nishino T, Baba O, Kuwabara
Y, Yokode M, et al. MicroRNA-33a/b in lipid
metabolism - novel "thrifty" models. Circ J.
2015;79(2):278-84.
5. Taghipoor Asramy A, Ghanbari-Niaki A,
Naghizadeh Qomi M, Bashi M, Mehdi M. The
effect of running with bee pollen on muscleABCA1 and APOA-1 mRNA expression in rats:
brief report. Tehran University Medical Journal
TUMS Publications. 2016;74(7):530-4.
6. Abente EJ, Subramanian M, Ramachandran
V, Najafi-Shoushtari SH. MicroRNAs in obesity-
associated disorders. Arch Biochem Biophys.
2016;589:108-19.
7. de Aguiar Vallim TQ, Tarling EJ, Kim T, Civelek
M, Baldán Á, Esau C, et al. MicroRNA-144
Regulates Hepatic ATP Binding Cassette Transporter
A1 and Plasma High-Density Lipoprotein
After Activation of the Nuclear Receptor
Farnesoid X ReceptorNovelty and Significance.
Circulation research. 2013;112(12):1602-12.
8. Filipowicz W, Bhattacharyya SN, Sonenberg
N. Mechanisms of post-transcriptional regulation
by microRNAs: are the answers in sight?
Nature Reviews Genetics. 2008;9(2):102-14.
9. Novák J, Bienertová-Vašků J, Kára T, Novák
M. MicroRNAs involved in the lipid metabolism
and their possible implications for atherosclerosis
development and treatment. Mediators
of inflammation. 2014;2014.
10. Rottiers V, Näär AM. MicroRNAs in metabolism
and metabolic disorders. Nature reviews
Molecular cell biology. 2012;13(4):239-50.
11. Horie T, Baba O, Kuwabara Y, Chujo Y,
Watanabe S, Kinoshita M, et al. MicroRNA-
33 deficiency reduces the progression
of atherosclerotic plaque in ApoE−/− mice.
Journal of the American Heart Association.
2012;1(6):e003376.
12. Rayner KJ, Sheedy FJ, Esau CC, Hussain FN,
Temel RE, Parathath S, et al. Antagonism of
miR-33 in mice promotes reverse cholesterol
transport and regression of atherosclerosis. J
Clin Invest. 2011;121(7):2921-31.
13. de Aguiar Vallim T, Tarling E, Kim T, Civelek
M, Baldan A, Esau C, et al. MicroRNA-144 regulates
hepatic ABCA1 and plasma HDL following
activation of the nuclear receptor FXR. Circulation
research. 2013:CIRCRESAHA. 112.300648.
14. Ramírez CM, Rotllan N, Vlassov AV,
Dávalos A, Li M, Goedeke L, et al. Control
of Cholesterol Metabolism and Plasma
High-Density Lipoprotein Levels by microRNA-
144Novelty and Significance. Circulation
research. 2013;112(12):1592-601.
15. Mann S, Beedie C, Jimenez A. Differential
effects of aerobic exercise, resistance training
and combined exercise modalities on cholesterol
and the lipid profile: review, synthesis
and recommendations. Sports Medicine.
2014;44(2):211-21.
16. Nybo L, Sundstrup E, Jakobsen MD, Mohr
M, Hornstrup T, Simonsen L, et al. High-intensity
training versus traditional exercise interventions
for promoting health. Medicine & Science
in Sports & Exercise. 2010;42(10):1951-8.
17. O'Donovan G, Owen A, Bird SR, Kearney
EM, Nevill AM, Jones DW, et al. Changes
in cardiorespiratory fitness and coronary
heart disease risk factors following 24 wk of
moderate-or high-intensity exercise of equal
energy cost. Journal of applied physiology.
2005;98(5):1619-25.
18. Vatani DS, Ahmadi S, Dehrashid KA, Gharibi
F. MINERVA MEDICA COPYRIGHT®. The Journal of sports medicine and physical fitness.
2011;51:695-700.
19. Fett C FW, Marchini J. Circuit weight training
vs jogging in metabolic risk factors of
overweight/obese women. . Arq Bras Cardiol
2009;93(5):519–25.
20. Rashid Lamir A, Dorody S, Ebrahimi Atri A.
The effect of a session of resistance and aerobic
exercise on the expression of ABCA1 gene
in trained girls. Journal of sport and Biological
Sciences. 2012;4(12):5-22.
21. Haji Hasani A, Ravasi A, kordy MR, Rashid
lLamir A. The Effect of Moderate Resistance
Training on Lymphocyte Cells ABCA1 Gene Expression,
HDL and LDL in male with Coronary
Artery Disease. Journal of sport and Biological
Sciences. 2018:[in press].
22. Ghanbari-Niaki A. Treadmill exercise training
enhances ATP-binding cassette protein-A1
(ABCA1) expression in male rats’ heart and
gastrocnemius muscles. Int J Endocrinol Metab.
2010;8(4):206-10.
23. Tofighi A, Rahmani F, Qarakhanlou BJ, Babaei
S. The effect of regular aerobic exercise
on reverse cholesterol transport A1 and apo
lipoprotein aI gene expression in inactive
women. Iranian Red Crescent Medical Journal.
2015;17(4).
24. Rayner KJ, Suarez Y, Davalos A, Parathath S,
Fitzgerald ML, Tamehiro N, et al. MiR-33 contributes
to the regulation of cholesterol homeostasis.
Science. 2010;328(5985):1570-3.
25. de Cassia Marqueti R, Almeida JA, Nakagaki
WR, Guzzoni V, Boghi F, Renner A, et al. Resistance
training minimizes the biomechanical
effects of aging in three different rat tendons.
J Biomech. 2017;53:29-35.
26. Krug AL, Macedo AG, Zago AS, Rush
JW, Santos CF, Amaral SL. High-intensity resistance
training attenuates dexamethasone-
induced muscle atrophy. Muscle Nerve.
2016;53(5):779-88.
27. Macedo AG, Krug AL, Herrera NA, Zago AS,
Rush JW, Amaral SL. Low-intensity resistance
training attenuates dexamethasone-induced
atrophy in the flexor hallucis longus muscle. J
Steroid Biochem Mol Biol. 2014;143:357-64.
28. Kim SH, Kim GJ, Umemura T, Lee SG, Cho
KJ. Aberrant expression of plasma microRNA-
33a in an atherosclerosis-risk group. Mol
Biol Rep. 2017;44(1):79-88.
29. Marquart TJ, Allen RM, Ory DS, Baldán Á.
miR-33 links SREBP-2 induction to repression of
sterol transporters. Proceedings of the National
Academy of Sciences. 2010;107(27):12228-
32.
30. Rotllan N, Ramirez CM, Aryal B, Esau CC,
Fernandez-Hernando C. Therapeutic silencing
of microRNA-33 inhibits the progression of atherosclerosis
in Ldlr-/- mice--brief report. Arterioscler
Thromb Vasc Biol. 2013;33(8):1973-7.
31. Ramirez CM, Rotllan N, Vlassov AV, Davalos
A, Li M, Goedeke L, et al. Control of cholesterol
metabolism and plasma high-density
lipoprotein levels by microRNA-144. Circ Res.
2013;112(12):1592-601.
32. Karunakaran D, Thrush AB, Nguyen MA,
Richards L, Geoffrion M, Singaravelu R, et al. Macrophage Mitochondrial Energy Status
Regulates Cholesterol Efflux and Is Enhanced
by Anti-miR33 in Atherosclerosis. Circ Res.
2015;117(3):266-78.