AI Summary & Key Takeaways
AI InsightThe possible protective effect of increased hepcidin in the trained groups can be explained by the antiinflammatory effects of IL-6 and long-term training.
📌 3 Key Takeaways
Abstract
Background/aim: Exercise benefits the cardiovascular system, but strenuous exercise can cause cardiac damage and induce cytokine production, particularly that of interleukin-6 (IL-6). Hepcidin, which is primarily regulated by IL-6, increases after exercise. Hepcidin is a possible protective factor against the adverse effects of strenuous exercise such as oxidative stress. The aim of the study is to reveal that training increases hepcidin and attenuates increased levels of IL-6 in the hearts of exhaustively exercised rats by comparing the IL-6 and hepcidin mRNA expression levels in trained and untrained groups. Materials and methods: Thirty male Wistar albino rats were assigned to the following groups: sedentary controls (Con); untrained animals that acutely completed exhaustive exercise and were sacrificed immediately after exhaustion (UT-i) or 1 day after exhaustion (UT-1); and long-term trained animals that completed exhaustive exercise and were sacrificed immediately after exhaustion (T-i) or 1 day after exhaustion (T-1). mRNA levels were examined by reverse transcription PCR. Results: IL-6 levels significantly increased in the UT-i, T-i, and T-1 groups compared to the Con group (P = 0.000, P = 0.024, P = 0.001), with maximal IL-6 expression found in the UT-i group. Hepcidin levels significantly increased in the T-1 group (P = 0.000) compared to the control. Conclusion: Increased IL-6 levels in rats show that exhaustive exercise can cause cardiac inflammation. However, long-term training attenuated the severity of the inflammation. The possible protective effect of increased hepcidin in the trained groups can be explained by the antiinflammatory effects of IL-6 and long-term training.