The Protective Effect Of Interleukin-10 On MCAO Rats And Its Possible Mechanism

Aim To study the change of IL-10 in focal ischemia tissue of brain and serum in MCAO of rats. To study the protective effect of IL-10 on the injury by focal cerebral ischemia in MCAO of rats and the mechanism of the effect of IL-10.Methods The middle cerebral artery(MCA) was occluded for different time with modified Zea Longa's MCAO model.The level of IL-10 in focal ischemia tissue of brain and blood serum was measured with double-antibody sandwich ELISA. Then was administered IL-10(0.5μg or 1μg) centrally into lateral ventricle 0.5h or 3h, the controls was administered saline. After 3h the rats were administered with IL-101μg centrally into lateral ventricle, the controls were administered with 5μl saline.Results The content of IL-10 in focal ischemia tissue fell to the lowest degree at 6 hours, then it increased compaired with the control.The concentration of IL-10 in serum fell to the lowest degree at 3 hours after ischemia and then it increased slowly compaired with the control. Compared with the saline group, the infarct volume marked and the quantity of neuron necrosis decreased, and the infarct volume of 1μg group is smaller than that of 0.5μg group, and the infarct volume of 0.5h group is smaller than that of 3h group. Compared with the saline group, the extravasation of leukocyte is significantly reduced in 0.5h group,and the extravasation of leukocyte in 1μg group is smaller than that of 0.5μg group.While compared with the saline group the 3h group show no difference. Compare with the sham control the content of NO ,MDA , the iNOS, cNOS and tNOS activity were in high level, the activity of SOD decreases in the focal brain and serum. After administered with IL-10, the content of NO ,MDA , and the iNOS activity in focal brain decrease, the activity of SOD increase. The activity of cNOS and tNOS didn't show significant difference. Compare with the saline these in serum didn't show significant difference.Conclusions IL-10 plays a protective role in focal ischemia. It may act as a protective role by inhibiting apoptotic cascade and decreasing the chemotaxis and extravasation of leukocyte to ischemia area. The decrease of NO content and iNOS activity and the increase of SOD activity after ischemia may all contribute to the protective role.