Inflammatory bowel diseases (IBDs) are autoimmune disorders of the gut. It is increasingly
clear that voluntary exercise (VE) may exert protection against IBDs, but the exact
background mechanism needs to be elucidated. In the present study, we aimed to investigate
the possible role of NETosis and the antioxidant peroxiredoxin (Prdx) enzyme family
in VE-induced protection. Wistar Han rats were randomly divided into two groups: sedentary
(SED) and VE. After the 6-week voluntary wheel running, animals were treated with
2,4,6-trinitrobenzene sulphonic acid (TNBS) as a model of colitis. Here, we found
that VE significantly decreased inflammation and ulceration of the colon in the VE
TNBS group compared with SED TNBS. We also found that VE significantly decreased the
expression of protein arginine deiminase 4 (PAD4) and myeloperoxidase (MPO), and markedly
reduced citrullinated histone H3 (citH3) compared with SED TNBS. Furthermore, VE caused
a significant increase in the levels of Prdx6 in the control and TNBS groups. Taken
together, we found that a prior 6-week VE effectively reduces inflammation in TNBS-induced
colitis, and we suggest that the protective effect of VE may be mediated via the inhibition
of NETosis and upregulation of Prdx6 antioxidant.
