Effects of Exercise Rehabilitation on Cardiac Fibrosis and Function in Rats with Myocardial Infarction

Changyong WU; Rui WANG; Suli BAO; Ruijie LI; Huang SUN; Yujia YE; Fei XU; Yunzhu PENG

doi:10.12259/j.issn.2095-610X.S20231004

Volume 44 Issue 10

Oct. 2023

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Changyong WU, Rui WANG, Suli BAO, Ruijie LI, Huang SUN, Yujia YE, Fei XU, Yunzhu PENG. Effects of Exercise Rehabilitation on Cardiac Fibrosis and Function in Rats with Myocardial Infarction[J]. Journal of Kunming Medical University, 2023, 44(10): 26-32. doi: 10.12259/j.issn.2095-610X.S20231004

Citation:

Changyong WU, Rui WANG, Suli BAO, Ruijie LI, Huang SUN, Yujia YE, Fei XU, Yunzhu PENG. Effects of Exercise Rehabilitation on Cardiac Fibrosis and Function in Rats with Myocardial Infarction[J]. Journal of Kunming Medical University, 2023, 44(10): 26-32. doi: 10.12259/j.issn.2095-610X.S20231004

Citation:

Changyong WU, Rui WANG, Suli BAO, Ruijie LI, Huang SUN, Yujia YE, Fei XU, Yunzhu PENG. Effects of Exercise Rehabilitation on Cardiac Fibrosis and Function in Rats with Myocardial Infarction[J]. Journal of Kunming Medical University, 2023, 44(10): 26-32. doi: 10.12259/j.issn.2095-610X.S20231004

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Effects of Exercise Rehabilitation on Cardiac Fibrosis and Function in Rats with Myocardial Infarction

doi: 10.12259/j.issn.2095-610X.S20231004

Dept. of Cardiology，The 1st Affiliated Hospital of Kunming Medical University， Kunming Yunnan 650032，China

Received Date: 2023-05-04
Available Online: 2023-09-11
Publish Date: 2023-10-25

Abstract

Abstract

Objective To explore the effect of exercise rehabilitation on cardiac fibrosis and function in rats with myocardial infarction. Methods Twenty-four male SD rats were randomly divided into four groups: MI-E group, MI-Sed group, Sham-E group and Sham-Sed group, with five to seven rats in each group. A myocardial infarction model was prepared using ligation of the left anterior descending coronary artery （LAD）, while the sham surgery group underwent needle insertion without ligation. One week after surgery, exercise training was initiated, including one week of adaptive exercise and four weeks of formal exercise. The non-exercise group did not participate in any exercise training throughout the study. After completion of the exercise regimen, echocardiography, HE staining, Masson staining, Tenel staining, and transmission electron microscopy were performed for evaluation. Results Compared with sham group, left ventricular wall thinning and systolic function were decreased in MI groups, especially in MI-Sed group （P < 0.05）, while LVESD, LVEF and FS were improved in MI-E group compared with MI-Sed group （P < 0.05）; there was no significant difference between Sham-E group and Sham-Sed group （P > 0.05）. Compared with the sham group, HE staining showed that cardiomyocyte exhibited different degrees of lysis with inflammatory cell infiltration and fibroblast proliferation in the MI group while the damage was milder in the MI-E group. Masson staining showed that cardiomyocyte was disorganized and myocardial fibrosis was significantly increased in the MI group compared with the sham group, while collagen volume fraction （CVF%） was decreased in the MI-E group compared with the MI-Sed group and the Sham-E group compared with the Sham-Sed group （P < 0.05）. Tunel staining showed that compared with the Sham group, the MI group had increased myocardial cell apoptosis, while the MI-E group had a lower myocardial cell apoptosis index compared to the MI-Sed group, Sham-E group, and Sham-Sed group （P < 0.05）. Transmission electron microscopy showed that compared with the Sham group, the MI group had severe damage to myocardial cells and mitochondria, as well as loose and disordered muscle fibers, while the MI-E group had milder myocardial cell injury, more intact mitochondrial structure, and more formation of autophagosomes. Conclusion Exercise rehabilitation can reduce cardiomyocyte damage and apoptosis, reduce myocardial infarct area, improve myocardial fibrosis and cardiac function in MI rats. Exercise can moderately induce autophagy level to play a cardioprotective role.
- Myocardial infarction,
- Exercise rehabilitation,
- Autophagy,
- Myocardial fibrosis

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References(16)

References

[1]	Virani S S,Alonso A,Benjamin E J,et al. Heart disease and stroke statistics-2020 update: A report from the American Heart Association[J]. Circulation,2020,141(9):e139-e596.
[2]	中国心血管健康与疾病报告编写组. 中国心血管健康与疾病报告2021概要[J]. 中国循环杂志,2022,37(6):553-578.
[3]	中国心血管疾病患者居家康复专家共识编写组. 中国心血管疾病患者居家康复专家共识[J]. 中国循环杂志,2022,37(2):108-121.
[4]	Thomas R J,Beatty A L,Beckie T M,et al. Home-based cardiac rehabilitation: A scientific statement from the American Association of Cardiovascular and Pulmonary Rehabilitation,the American Heart Association,and the American College of Cardiology[J]. Circulation,2019,140(1):e69-e89.
[5]	Li H,Qin S,Liang Q,et al. Exercise training enhances myocardial mitophagy and improves cardiac function via Irisin/FNDC5-PINK1/Parkin pathway in MI mice[J]. Biomedicines,2021,9(6):701. doi: 10.3390/biomedicines9060701
[6]	Dikic I and Elazar Z. Mechanism and medical implications of mammalian autophagy[J]. Nat Rev Mol Cell Biol,2018,19(6):349-364. doi: 10.1038/s41580-018-0003-4
[7]	Zacchigna S,Paldino A,Falcão-Pires I,et al. Towards standardization of echocardiography for the evaluation of left ventricular function in adult rodents: A position paper of the ESC working group on myocardial function[J]. Cardiovasc Res,2021,117(1):43-59. doi: 10.1093/cvr/cvaa110
[8]	Hong G,Rui G,Zhang D,et al. A smartphone-assisted pressure-measuring-based diagnosis system for acute myocardial infarction diagnosis[J]. Int J Nanomedicine,2019,14:2451-2464. doi: 10.2147/IJN.S197541
[9]	Lai C C,Tang C Y,Fu S K,et al. Effects of swimming training on myocardial protection in rats[J]. Biomed Rep,2022,16(3):19. doi: 10.3892/br.2022.1502
[10]	Xiao L,He H,Ma L,et al. Effects of miR-29a and miR-101a expression on myocardial interstitial collagen generation after aerobic exercise in myocardial-infarcted rats[J]. Arch Med Res,2017,48(1):27-34. doi: 10.1016/j.arcmed.2017.01.006
[11]	Liang Q,Cai M,Zhang J,et al. Role of muscle-specific histone methyltransferase (Smyd1) in exercise-induced cardioprotection against pathological remodeling after myocardial infarction[J]. Int J Mol Sci,2020,21(19):7010. doi: 10.3390/ijms21197010
[12]	Lee Y,Kang E B,Kwon I,et al. Cardiac kinetophagy coincides with activation of anabolic signaling[J]. Med Sci Sports Exerc,2016,48(2):219-226. doi: 10.1249/MSS.0000000000000774
[13]	Dai M,Hillmeister P. Exercise-mediated autophagy in cardiovascular diseases[J]. Acta Physiol (Oxf),2022,236(3):e13890. doi: 10.1111/apha.13890
[14]	Li J Y,Pan S S,Wang J Y,et al. Changes in autophagy levels in rat myocardium during exercise preconditioning-initiated cardioprotective effects[J]. Int Heart J,2019,60(2):419-428. doi: 10.1536/ihj.18-310
[15]	Cho J M,Park S K,Ghosh R,et al. Late-in-life treadmill training rejuvenates autophagy,protein aggregate clearance,and function in mouse hearts[J]. Aging Cell,2021,20(10):e13467. doi: 10.1111/acel.13467
[16]	Jiang L,Shen X,Dun Y,et al. Exercise combined with trimetazidine improves anti-fatal stress capacity through enhancing autophagy and heat shock protein 70 of myocardium in mice[J]. Int J Med Sci,2021,18(7):1680-1686. doi: 10.7150/ijms.53899

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