Effects of exercise preconditioning on NLRP3 and mitochondrial fission in isoproterenol-induced myocardial infarcted rats

Ahmadi, Azam; Kashef, Majid; Rajabi, Hamid; Salehpour, Mojtaba

doi:10.1007/s00580-022-03397-3

Cited by 2 publications

(4 citation statements)

References 52 publications

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“…A HIIT session consisted of a 5-minute warm-up (10-15 m/min of running) and 10 intervals of 1-minute running with a 2-minute rest between each interval (intensity of intervals: first week: 85% v peak, second week: 90% v peak, third week: 95% v peak, and fourth week: 100% v peak), and a 5 minutes cool-down (10 m/min of running). The v-peak test was repeated 24 hours after the last session of the training period [ 30 , 31 ].…”

Section: Methodsmentioning

confidence: 99%

The Exercise Preconditioning Effect on Cardiac Tissue Injury following Induction of Myocardial Infarction in Male Rats

Heiat

Ahmadi

Shojaeifard

2023

BioMed Research International

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Background and Objective. Studies have shown that physical activity not only reduces cardiovascular risk factors but also improves cardiac protection against ischemia-reperfusion. One of the protective pathways of the heart against ischemia is mitochondrial function protection, and the role of exercise preconditioning in this mechanism is important. We investigated the exercise pretraining on mitochondrial biogenesis effect, angiogenesis, and cardiac tissue injury in male rats following stroke. Materials and Methods. Twenty-four male rats were divided into 4 groups including MI, Sham, HIIT, and HIIT+MI ( N = 6 ). HIIT and HIIT+MI which underwent high-intensity interval training (HIIT) for 4 weeks (5 days a week). The training protocol included 10 intervals of 1-minute running, with 2 minutes rest between each interval. The training intensity was different every week according to the peak treadmill running speed (v peak) percentage of each rat. Isoproterenol injection was used to induce myocardial infarction (MI). Expressions of creatine kinase-MB (CK-MB), PGC-1α troponin-I, mitochondrial transcription factor A (TFAM), vascular endothelial growth factor (VEGF), and microRNA 126 (miR-126) genes were measured. The variables were measured using biochemical and RT-PCR methods. The significance level ( P value≤0.05) was analyzed using ANOVA test. Results. The results showed that 4 weeks of HIIT training led to a significant increase in PGC-1α, TFAm, and VEGF levels in the MI, HIIT, and HIIT+MI groups compared to the sham group ( P = 0.001 ). HIIT exercises increased miR-126 in the different groups compared to the sham group; however, it was not significant. Conclusion. The results obtained showed that HIIT exercise exerts cardio-protective effects to reduce cardiac tissue injury and necrosis against MI. These effects increase mitochondrial biogenesis and angiogenesis by inducing the increased expression of VEGF, TFAM, PGC-1α, and miR-126 genes in the heart tissue. Therefore, HIIT training, as a preconditioning program, was able to protect the cardiac tissue against MI.

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Section: Methodsmentioning

confidence: 99%

The Exercise Preconditioning Effect on Cardiac Tissue Injury following Induction of Myocardial Infarction in Male Rats

Heiat

Ahmadi

Shojaeifard

2023

BioMed Research International

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“…In other words, exercise acts like ischemia preconditioning, which stimulates beneficial cellular responses. Azam Ahmadi et al, 2022 found HIIT can effectively decrease heart injury and NLRP3 expression in rats with MI. Interestingly, dynamin-related protein 1 (Drp1), an essential mitochondrial fission protein, can activate NLRP3 inflammasome through ROS generation after MI (Ahmadi et al, 2022;Jiang et al, 2022).…”

Section: Exercise Improves MI and Inhibits Nlrp3 Inflammasomementioning

confidence: 99%

“…Azam Ahmadi et al, 2022 found HIIT can effectively decrease heart injury and NLRP3 expression in rats with MI. Interestingly, dynamin-related protein 1 (Drp1), an essential mitochondrial fission protein, can activate NLRP3 inflammasome through ROS generation after MI (Ahmadi et al, 2022;Jiang et al, 2022). However, the Azam Ahmadi team's work demonstrates exercise preconditioning (EP) in a short period did not affect Drp1 (Ahmadi et al, 2022), while inhibiting NLRP3 expression.…”

Section: Exercise Improves MI and Inhibits Nlrp3 Inflammasomementioning

confidence: 99%

“…Interestingly, dynamin-related protein 1 (Drp1), an essential mitochondrial fission protein, can activate NLRP3 inflammasome through ROS generation after MI (Ahmadi et al, 2022;Jiang et al, 2022). However, the Azam Ahmadi team's work demonstrates exercise preconditioning (EP) in a short period did not affect Drp1 (Ahmadi et al, 2022), while inhibiting NLRP3 expression. This finding indicates that EP in a short period is required to inhibit NLRP3 inflammasome independently of Drp1; the reduction of NLRP3 can occur through other mechanisms (Jiang et al, 2022).…”

Section: Exercise Improves MI and Inhibits Nlrp3 Inflammasomementioning

confidence: 99%

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NLRP3 inflammasome and pyroptosis in cardiovascular diseases and exercise intervention

Ding,

Song,

Yang

et al. 2024

Front. Pharmacol.

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NOD-like receptor protein 3 (NLRP3) inflammasome is an intracellular sensing protein complex that possesses NACHT, leucine-rich repeat, and pyrin domain, playing a crucial role in innate immunity. Activation of the NLRP3 inflammasome leads to the production of pro-inflammatory cellular contents, such as interleukin (IL)-1β and IL-18, and induction of inflammatory cell death known as pyroptosis, thereby amplifying or sustaining inflammation. While a balanced inflammatory response is beneficial for resolving damage and promoting tissue healing, excessive activation of the NLRP3 inflammasome and pyroptosis can have harmful effects. The involvement of the NLRP3 inflammasome has been observed in various cardiovascular diseases (CVD). Indeed, the NLRP3 inflammasome and its associated pyroptosis are closely linked to key cardiovascular risk factors including hyperlipidemia, diabetes, hypertension, obesity, and hyperhomocysteinemia. Exercise compared with medicine is a highly effective measure for both preventing and treating CVD. Interestingly, emerging evidence suggests that exercise improves CVD and inhibits the activity of NLRP3 inflammasome and pyroptosis. In this review, the activation mechanisms of the NLRP3 inflammasome and its pathogenic role in CVD are critically discussed. Importantly, the purpose is to emphasize the crucial role of exercise in managing CVD by suppressing NLRP3 inflammasome activity and proposes it as the foundation for developing novel treatment strategies.

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Effects of exercise preconditioning on NLRP3 and mitochondrial fission in isoproterenol-induced myocardial infarcted rats

Cited by 2 publications

References 52 publications

The Exercise Preconditioning Effect on Cardiac Tissue Injury following Induction of Myocardial Infarction in Male Rats

The Exercise Preconditioning Effect on Cardiac Tissue Injury following Induction of Myocardial Infarction in Male Rats

NLRP3 inflammasome and pyroptosis in cardiovascular diseases and exercise intervention

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