高强度间歇训练
医学
肾功能
肾毒性
肌酐
间歇训练
内科学
偏心训练
单核细胞
内分泌学
肾
肿瘤坏死因子α
古怪的
量子力学
物理
作者
Allyne Baía Leite,Hernando Nascimento Lima,Chris Flores,Caroline Assunção Oliveira,Larissa Esterfanne Cavalcante Cunha,Jonas Luz Neves,Thiago Macêdo Lopes Correia,Fabrício Freire de Melo,Márcio Vasconcelos Oliveira,Amélia Cristina Mendes de Magalhães,Telma de Jesus Soares,Liliany Souza de Brito Amaral
出处
期刊:Life Sciences
[Elsevier]
日期:2020-12-10
卷期号:266: 118880-118880
被引量:21
标识
DOI:10.1016/j.lfs.2020.118880
摘要
Cisplatin (CP) is an antineoplastic widely used in the treatment of various solid tumors, however, its clinical application is limited by nephrotoxicity. Here, we compared the impact of preconditioning with high-intensity interval training (HIIT) with continuous training of low (LIT) and moderate (MIT) intensity on innate immunity markers in female rats with CP-induced acute kidney injury. The rats were divided into five groups (n = 7): saline control and sedentary (C + S); CP and sedentary (CP + S); CP and LIT (CP + LIT); CP and MIT (CP + MIT) and CP and HIIT (CP + HIIT). The training intensity was determined by a maximum running test. At the end of training, the rats received a single dose of CP (5 mg/kg), and 7 days later they were euthanized. We evaluated renal function parameters (serum creatinine, glomerular filtration rate and proteinuria), renal structure, macrophage tissue infiltration, immunolocalization of nuclear transcription factor kappa B (NF-κB), renal levels of tumor necrosis factor-alpha (TNF-α), interleukin 1β (IL-1β), and interleukin 6 (IL-6), and gene expression of monocyte chemoattractant protein-1 (MCP-1), toll-like receptor 4 (TLR4), and NF-κB in renal tissue. Although both MIT and HIIT attenuated the degree of renal injury, only the HIIT prevented changes in renal function. The three training protocols mitigated the increase in expression of all inflammatory markers, however, this effect was more pronounced in HIIT. All training protocols promoted renoprotective actions, but HIIT was more effective in mitigating CP-induced acute kidney injury, in part by modulation of important markers of the innate immune response.
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