بررسي تأثير تمرين بازتواني قلبي بر بيان ژن ABCA 1 در سلول‌هاي PBMN مبتلايان به ايسكمي قلبي

آترواسكلروز مهمترين بيماري قلب و عروق و عامل اصلي مرگ و مير در دنيا است. ABCA1 مسئول اصلي تشكيل ذراتHDL بوده و به همين دليل احتمالاً در پيشگيري و جلوگيري از گسترش آترواسكلروزيس نقش دارد. هدف از مطالعه حاضر بررسي تأثير يك دوره تمرين ورزشي بازتواني قلبي بر بيان ژن ABCA1 سلول‌هاي PBMN مي‌باشد. مواد و روش‌ها: 23 نفر از بيماران مرد مبتلا به گرفتگي عروق قلبي انتخاب و به‌صورت تصادفي ساده به دو گروه كنترل و تجربي تقسيم شدند. گروه تجربي به مدت 8 هفته و هر هفته سه جلسه به مدت يك ساعت تمرينات مقاومتي سبك با شدت 40 تا 60 درصد يك تكرار بيشينه انجام دادند. قبل از شروع و بعد از پايان تمرينات ميزان m-RNA ABCA1 به روش RT-PCR اندازه‌گيري و اطلاعات به‌وسيله تحليل كوواريانس در سطح 05/0

Atherosclerotic heart disease is a major important cause of mortality in most countries. ABCA1 transporter is responsible for making and forming of HDL particles and therefore probably plays a crucial role in prevention of atherosclerosis. The purpose of this study was to assess the effect of rehabilitation training on ABCA1 gene expression of peripheral blood mononuclear cells (PBMN). Methods: Twenty three myocardial infractions patients were randomly selected and assigned into two groups; control (N=11) and experimental (N=12). Moderate resistance training was conducted by experimental group for 60 minutes at three sessions for eight weeks with 40-60% of one repetition maximum (1RM). Blood sample of subjects were collected before and after training. PBMN cells were separated and m-RNA purification was performed by real–time PCR. Data was analyzed by ANCOVA in SPSS software (significant leve equal 0.05). Results: Results showed that expression of PBMN ABCA1 m-RNA was significantly increased with moderate resistance training in myocardial infractions patient group. There was no significant differences in mean of HDL-C, LDL-C (P>0.05). Conclusion: As result that moderate resistance training increases the expression of ABCA1 gene on PBMN cells of MI patient, improves the function of reverse cholesterol transfer, and probably prevents repetition of Ischemic