J Neuroimmunol 257:28 (2013)
Ma S, Zhong D, Chen H, Zheng Y, Sun Y, Luo J, Li H, Li G, Yin Y.
Ischemic cerebral infarction is a leading cause of death and disability, but the key inflammatory cytokines were not fully understood and no successful therapy has been established. We have used the methods of reverse transcriptase-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), western blot, and immunohistochemical staining to detect the dynamic changes of IL-23/IL-17 axis in brain infarction and BMSC treatment on the sixth day. BMSC transplantation could reduce the infarct size (P<0.05) and improve functional deficits (P<0.001) in brain infarction. The level of IL-23/IL-17 axis expression is higher (P<0.05) in pMCAO-operated group than that in sham operated group. BMSC treatment could reduce IL-23 expression (P<0.05) and attenuate IL-17 expression (P<0.01) both in serum and around infarct lesion. So we have drawn the conclusion that IL-23/IL-17 axis induces inflammation in the pathophysiological process of cerebral infarction. BMSC treatment plays therapeutic role by immunomodulating the expression of IL-23/IL-17 axis. These findings may help to understand the cytokines in cerebral infarction and open up a possible new way of immunological treatment.