Inhibiting Effect Of Interleukin-10 On Neurocyte Apoptosis And Its Mechanisms In Cerebral Ischemia In Rats

Object To investigate the inhibiting effect of interleukin-10 on neurocyte apoptosis in focal cerebral ischemia in rats and its molecular mechanisms. To study the effects of rehabilitative training on the recovery of neurological functions and interleukin-10 concentration in the brains post focal cerebral ischemia in rats.Methods Adult male Sprague-Dawley rats' focal cerebral ischemia was induced by Zea- Longa's thread method, and IL-10 was administered intracerebroventricularly 1h post MCAO. TUNEL staining was used to detect in situ cell apoptosis, immunohistochemical staining and RT-PCR were used to detect the expression of apoptosis regulatory gene Bcl-2,Bax,Fas, FasL and Caspase-3 in peri-infarct. Rats in rehabilitation group were administered balancing, grasping, rotating and walking training everyday, the neurological functions were measured at 3d, 7d and 14d post MCAO before killing, and the concentration of interleukin-10 in rats' brains was determined by ELISA method.Results Apoptotic neurocytes (TUNEL positive neurocytes), Bcl-2, Bax, Fas, FasL and Caspase-3 positive neurocytes were predominantly seen in striatum and sub-frontal/parietal cortex at the border of infarct core ,which represent ischemic penumbra. Compare to sham group, Cerebral ischemia significantly induced neurocyte apoptosis, upregulated the expression of Bcl-2, Bax, Fas, FasL and Caspase-3, and decreased the ratio of Bcl-2/Bax (p<0.01). Compare to vehicle group , IL-10 treatment significantly inhibited neurocyte apoptosis, downregulated the expression of proapoptosis regulatory gene Bax, FasL and Caspase-3 (p<0.05 or p<0.01), upregulated anti-apoptotic gene Bcl-2 expression(p<0.05), and increased the ratio of Bcl-2/Bax (p<0.01), but showed no effect on Fas expression( p>0.05).