The Research Of Oxidative Stress Assosiated With Hyperglycemia Inhibitory Effect Of Astrocyte Activation After Cerebral Ischemia

Objective Observation and study of diabetes / hyperglycemia ischemic brain injury and under conditions of oxidative stress that high glucose inhibits the activation and proliferation of astrocytes mechanism after cerebral ischemia, in STZ-induced hyperglycemia focal cerebral ischemia-reperfusion SD rats as an animal model of oxidative stress factor(i NOS) involved in diabetes / hyperglycemia inhibition of cerebral ischemic injury astrocyte activation, thus providing a new target for diabetes / hyperglycemia prevention and treatment of stroke patients and ideas.Method STZ-induced hyperglycemia in focal cerebral ischemia and reperfusion SD rat as animal model, histopathological changes were observed normoglycemic group and hyperglycemia group by surgical operation make brain tissue ischemia and reperfusion by HE staining.Western blot expression, PCR transcriptional level and immunohistochemical staining techniques to detect i NOS factors and the relationship between astrocytes injury.Result 1.HE staining: In normoglycemic surgery group 1d after reperfusion were visibled when the nerve cell disorder, partial necrosis of nerve ischemic necrosis of the central area of a triangle or diamond yuan solid shrunk. 3d after reperfusion necrosis of neurons has been significantly dissolved, some foamy, at the edge infarction associated astrocyte proliferation. 7d after reperfusion necrosis absorbed by the number of neurons become less, some lightly stained nuclei structure is unclear, the number of its neighboring glial cells increased significantly. 14 d after reperfusion of ischemic necrosis basically been repaired properly, increased glial cell aggregation groups, glial nodules. 28 d ischemia reperfusion necrosis with no significant change in the recovery time 14 d. Hyperglycemia surgery group with normoglycemic perfusion group morphological changes similar circumstances in different time periods after 30 min ischemia, but brain edema, swelling of neuronal necrosis pyknosis dissolve all the more serious degree of normal glucose group, reducing the number of glial cells. 2.i NOS immunohistochemistry, Western blot, PCR Results: In normoglycemic surgery group 1d after reperfusion surgical group when the number of i NOS-positive cells increased, reaching a peak reperfusion 3d, 7d after fall down to the stable stage 14 d, the hyperglycemia group each isoform expression group with normal glucose group trend, but at the same time is higher than normal blood sugar group. 3. i NOS and GFAP immunohistochemical staining Results: In normal blood reperfusion 1d surgical group when the number of double-labeled positive cells increased reperfusion peaked at 7d, 14 d after declining to a stable phase, hyperglycemia group isoforms expression group trend with normal glucose group, but at the same time it is higher than normal blood sugar group.Conclusion 1. Hyperglycemia can aggravate cerebral ischemia and reperfusion injury, increased cerebral edema and neuronal degeneration; 2. Ischemia-reperfusion injury can cause astrocyte activation, hyperglycemia inhibit the activation; 3. Hyperglycemia significantly increased ischemia-reperfusion injury can cause i NOS expression in astrocytes, may be involved in high blood sugar inhibits the activation of astrocytes after cerebral ischemia, which involved high blood sugar aggravate cerebral ischemic injury.