Inhaled molecular hydrogen attenuates intense acute exercise-induced hippocampal inflammation in sedentary rats

Autor(es)

Nogueira, Jonatas E. ^{[1, 2]} ; de Deus, Junia L. ^[3] ; Amorim, Mateus R. ^[3] ; Batalhao, Marcelo E. ^[4] ; Leao, Ricardo M. ^[5] ; Carnio, Evelin C. ^{[5, 4]} ; Branco, Luiz G. S. ^{[5, 2, 3]}

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Sch Phys Educ & Sports Ribeirao Preto, Ribeirao Preto, SP - Brazil

^[2] Univ Sao Paulo, Postgrad Program Rehabil & Funct Performance, Ribeirao Preto, SP - Brazil

^[3] Univ Sao Paulo, Dent Sch Ribeirao Preto, Dept Basic & Oral Biol, BR-14040904 Ribeirao Preto, SP - Brazil

^[4] Univ Sao Paulo, Sch Nursing Ribeirao Preto, Dept Gen & Specialized Nursing, Ribeirao Preto, SP - Brazil

^[5] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, Ribeirao Preto, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Neuroscience Letters; v. 715, JAN 10 2020.
• Citações Web of Science: 0

Resumo

Physical exercise-induced inflammation may be beneficial when exercise is regular but it may be harmful when exercise is intense and performed by unaccustomed individuals/rats. Molecular hydrogen (H-2) has recently emerged as a powerful anti-inflammatory, antioxidant and anti-apoptotic molecule in a number of pathological conditions, but little is known about its putative role under physiological conditions such as physical exercise. Therefore, we tested the hypothesis that H-2 decreases intense acute exercise-induced inflammation in the hippocampus, since it is a brain region particularly susceptible to inflammation. Moreover, we also assessed hippocampus oxidative status. Rats ran on a sealed treadmill inhaling either the H-2 (2% H-2, 21% O-2, balanced with N-2) or the control gas (0% H-2, 21% O-2, balanced with N-2) and hippocampal samples were collected immediately or 3 h after exercise. We measured hippocampal levels of cytokines {[}tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, IL-6 and IL-10] and oxidative markers {[}superoxide dismutase (SOD), thiobarbituric acid reactive species (TBARS) and nitrite/nitrate (NOx)]. Exercise increased TNF-alpha, IL-6 and IL-10 immediately after the session, whereas no change in IL-1 beta levels was observed. Conversely, exercise did not cause any change in SOD activity, TSARS and NOx levels. H-2 inhibited the exercise-induced surges in TNF-alpha and IL-6, and potentiated the IL-10 surge, immediately after the exercise. Moreover, no change in IL1-beta levels of rats inhaling H-2 was observed. Regarding the oxidative stress markers, H-2 failed to cause any change in SOD activity, TBARS and NOx levels. No significant change was observed in any of the assessed parameters 3 h after the exercise bout. These data are consistent with the notion that H-2 acts as a powerful anti-inflammatory agent not only down-modulating proinflammatory cytokines (TNF-alpha and IL-6) but also upregulating an anti-inflammatory cytokine (IL-10) production without affecting the local oxidative stress status. These data indicate that H-2 effectively decreases exercise-induced inflammation in the hippocampus, despite the fact that this region is particularly prone to inflammatory insults. (AU)

• Processo FAPESP: 16/17681-9 - Alterações fisiopatológicas durante a inflamação sistêmica
• Beneficiário: Luiz Guilherme de Siqueira Branco
• Modalidade de apoio: Auxílio à Pesquisa - Temático