This study was undertaken to determine whether ischaemia/reperfusion (I/R)-induced
brain injury and
dextran sulfate sodium (DSS)-induced
colitis in mice are related. A cerebral I/R model of mice was established by blocking the bilateral common carotid arteries; 3% DSS in
drinking water was administered to mice for 7 days to induce
colitis; mice with cerebral I/R and
colitis were administered DSS for 7 days from the third day onwards after acute cerebral I/R. Brain damage and intestinal
inflammation were also tested. The results revealed that cerebral I/R induced brain damage and a marked increase in
glial fibrillary acidic protein (GFAP) expression and upregulation of Rho-associated coiled coil-forming
protein kinase (RhoA/ROCK) pathway in mouse hippocampal tissues. However, in the colon tissues of mice with
colitis, we found a reduction in GFAP. In addition, the expression of endogenous
hydrogen sulphide (H2S) synthase reduced in mice brain tissues with cerebral I/R injury, as well. as in mouse colon tissues with
colitis. Interestingly, the cerebral I/R-induced pathological changes in mouse brain tissues were aggravated by
colitis,
colitis mediated colon
inflammation, and pathological changes in intestinal tissues had deteriorated when the mice suffered cerebral I/R 2 days before DSS administration. However,
brain injury and colon
inflammation in mice suffering from both cerebral I/R and
colitis were ameliorated by
NaHS, an exogenous H2S donor. Furthermore, we found that
NaHS promoted the transformation of astrocytes from "A1" to "A2" type. These findings reveal that cerebral I/R injury and
colitis are related, the mechanism is correlated with endogenous H2S deficiency.