Mizokami, T.; Shimada, M.; Suzuki, K. Neutrophil Depletion Attenuates Acute Renal Injury after Exhaustive Exercise in Mice. Experimental Physiology 2024, doi:10.1113/ep091362.
Mizokami, T.; Shimada, M.; Suzuki, K. Neutrophil Depletion Attenuates Acute Renal Injury after Exhaustive Exercise in Mice. Experimental Physiology 2024, doi:10.1113/ep091362.
Mizokami, T.; Shimada, M.; Suzuki, K. Neutrophil Depletion Attenuates Acute Renal Injury after Exhaustive Exercise in Mice. Experimental Physiology 2024, doi:10.1113/ep091362.
Mizokami, T.; Shimada, M.; Suzuki, K. Neutrophil Depletion Attenuates Acute Renal Injury after Exhaustive Exercise in Mice. Experimental Physiology 2024, doi:10.1113/ep091362.
Abstract
Prolonged exercise induces acute renal injury; however, the precise mechanism remains unclear. We investigated the effects of neutrophil depletion in male C57BL/6J mice. Male C57BL/6J mice were divided into four groups: sedentary with control antibody, sedentary with antineutrophil antibody, exhaustive exercise with control antibody, and exhaustive exercise with antineutrophil antibody. Antineutrophil (1A8) or control antibody was administered intraperitoneally to the mice prior to their running on a treadmill. Renal histology was assessed 24 h after exhaustive exercise, and the concentration of kidney injury molecule (KIM)-1 was measured using enzyme-linked immunosorbent assay. The expression levels of inflammatory cytokines were measured using quantitative reverse transcriptase-polymerase chain reaction. Furthermore, nicotinamide adenine dinucleotide phosphate oxidase activity and hydrogen peroxide concentration in the kidneys were measured. The pathologic changes were manifested as congested and swollen glomeruli, tubular dilatation, and nuclear infiltration after exhaustive exercise. These changes were suppressed by the administration of the 1A8 antibodies. KIM-1 concentration increased after exhaustive exercise but were reduced by the 1A8 antibodies. Treatment with the 1A8 antibody also decreased exhaustive exercise-induced inflammation and reactive oxygen species levels in the kidney. These results suggest that neutrophils contribute to exercise-induced acute renal injury by regulating inflammation and reactive oxygen species levels.
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