| Objective: To discuss the expression of MCP-1,NSE and whether treated with celecoxib can relieve the injury of local cerebral ischemia-reperfusion in hyperlipidemia rats and possible mechanism.Method: 70 healthy male Wistar rats were randomly divided into 4 groups, sham-operated group (n=10), ischemia-reperfusion group (control group n=20), hyperlipidemia group (n=20), celecoxib group (n=20). Each group (B,C,D) was divided into 3 subgroups according to reperfusion 12h(n=5), 24h(n=10),48h(n=5) after ischemia for 1 hours. Respectively with high fat feed or ordinary feed eight weeks, first established hyperlipidemia rats, adopt rat tail blood, use spectrophotometer determination of each rat serum lipid levels. On this basis , using Longa-Zea's line boatel strategies for Wistar rats right measuring middle cerebral artery ischemia-reperfusion model (sham-operated group only exposed right common carotid artery don't do ischemia-reperfusion). D group rats regained consciousness and then were given celecoxib (25mg/kg/12h) line gavage treatment, the other 3 groups were given the same point in time equal volume of normal saline. Reference Zea-Longa's 5-point rating standard neurological function; back of the head of each group were decapitated at 2% triphenyl tetrazolium chloride (TTC) staining to determine ischemic site, with infarction volume image analysis system ; line HE staining pathological brain tissue; immunohistochemical observation MCP-1, NSE expression. Using statistical analysis software into SPSS18.0. Compared respectively:Neurological impairment score, cerebral infarction volume, cerebral pathomorphology, and the expression of MCP-1, NSE at the same reperfusion time between sham-operated group and control group, hyperlipidemia group and control group, celecoxib group and hyperlipidemia group.Results:1. Determinated rats'lipid levels:The of average weight of 70 rats is (110±10) g, the high-fat diet group and the ordinary diet group compared (P > 0.05); After 8 weeks, the high-fat diet group and ordinary diet group compared (P<0.05).The level of TC,LDL in serum were compared between the high-fat diet group and the ordinary diet group (P > 0.05); After 8 weeks, the high-fat diet group and ordinary diet group compared (P<0.05).2. The neurological impairment score: In control group was higher than that in the sham-operated group at every subgroup and(P<0.05); hyperlipidemia group was higher than that in the control group at every subgroup (P<0.05); Zea-Longa evaluation have no difference between the hyperlipidemia group and the celecoxib group except in the group of 12h, 24h reperfusion following 1h cerebral ischemia(P>0.05), but have difference between the hyperlipidemia group and the celecoxib group except in the group of 48h reperfusion following 1h cerebral ischemia(P<0.05).3. The infarction volume: Sham-operated group have no infarction area; in infarction volume appear at 1h cerebral ischemia and increased in 24h after reperfusion in the control group, the hyperlipidemia group and the celecoxib group. The infarction volume showed difference between the hyperlipidemia group and the control group (P<0.05); the infarction volume showed difference between the hyperlipidemia group and the celecoxib group (P<0.05).4. The morphological changes of cerebral tissue stained by HE: Sham-operated group had no infarction areas and evident pathological change. In control group and the hyperlipidemia group: the number of neurons at ischemic area decreased,nerve cells shrank and degenerated, apparent edema be tweet tissues and vacuolization. In celecoxib group: the number of neuron which appeared degeneration and necrosis decreased, vacuolization and inter-tissue edema became relieved compared with control group.5. Immunohistochemical result:The expression of in MCP-1: sham-operated group have a few MCP-1 cells; the control group compared with sham-operated group, the number of MCP-1 cells was increased significantly (P<0.05); compare with control group, the number of MCP-1 cells in the hyperlipidemia group was increased (P<0.05); compare with hyperlipidemia group, the number of MCP-1 cells at 48h in the celecoxib group was reduced (P<0.05).The expression of in NSE: sham-operated group have NSE cells; the control group compared with sham-operated group, the number of NSE cells was increased (P<0.05); compare with control group, the number of NSE cells in the hyperlipidemia group was increased (P<0.05); compare with hyperlipidemia group, the number of NSE cells at 48h in the celecoxib group was reduced (P<0.05).Conclusion:1. Hyperlipidemia may be take part in the process of cerebral ischemia-reperfusion and increased ischemia-reperfusion injury.2. MCP-1 may be take part in the process of cerebral ischemia-reperfusion and increased ischemia-reperfusion injury.3. Celecoxib has a neuroprotective effect. The neuroprotective mechanism of celecoxib may be related to reducing the expression of MCP-1. |
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