| The pathological mechanism of ischemic stroke and secondary cerebral ischemic damage is cerebral ischemia-reperfusion injury. Blood flowing in ischemic brain tissue restore supply, but fail to restore brain’s function even further aggravate damage. The physiological and pathological mechanism of Cerebral ischemia-reperfusion injury is very complex, it is the result of a number of mechanisms participating in joint. Inflammation takes a vital role for it is one of the pathological mechanism of cerebral ischemia-reperfusion injury. After cerebral ischemia leukocyte, microglia, astrocytes and other inflammatory cells under in a variety of inflammatory stimuli gather to the ischemic brain tissue, and release mediators of inflammation including the cytokines, inflammation-related enzymes, and then infiltrate to endothelial cell under the guidance of adhesion molecules, finally promote brain ischemic injury. Ischemic preconditioning is given in advance of a sublethal ischemic, hereafter can make body produce tolerance or adaptability to long time’s and fatal ischemia. Currently, there are a variety of pretreatment methods which can induce cerebral ischemic tolerance, as one of many methods, hyperbaric oxygen preconditioning has been shown in many documents to induce ischemic tolerance, reduce ischemia hypoxic injury, with showing good neuroprotection. But specific neuroprotective mechanism of hyperbaric oxygen preconditioning is not fully understood. Research in this area which effects of hyperbaric oxygen preconditioning on inflammation after cerebral ischemia-reperfusion injury is still relatively less. And the role of most inflammatory mediators in mechanism of hyperbaric oxygen inducing cerebral ischemic tolerance also remains being studied. Rats’middle cerebral artery occlusion (MCAO) model is used in this study, the effects of hyperbaric oxygen preconditioning on neurological deficit scores of MCAO rat, crecbral infarct area of MCAO rat, pathology of MCAO rat’s brain, inflammatory mediators in rats’ischemic brain tissue such as NF-kB, iNOS, COX-2, IL-13 and TNF-a is watched. The neuroprotective mechanism of hyperbaric oxygen preconditioning is initial explored from the aspect of the inflammatory reactions.Part I The effects of hyperbar ic oxygen preconditioning on rats after cerebral ischemia-reperfusion injuryObjective:To study whether hyperbaric oxygen preconditioning on rats after cerebral ischemia-reperfusion injury is of protective effectMethods:36 SD rats were randomly divided into sham group, model group and HBO group (n= 12). Model group and HBO group was induced by MCAO. HBO group were given five consecutive days (2ATA, 1h, once a day) hyperbaric oxygen preconditioning in advance, and after last pretreatment 3h were induced MCAO. At 24h after cerebral ischemia-reperfusion injury,all rats were given neurological deficit scores, sacrificed to detect cerebral infarct area used TTC staining and observe pathological section of brain tissue.Results:Rats’neurological deficit scores in HBO group significantly improved compared with model group (2.700000±0.632456 vs.3.425000±0.636396; P <0.05), cerebral infarct size was significantly reduced compared with model group (0.335±0.062 vs.0.434±0.049; P<0.05), the degree of brain pathology damage significantly mitigatedConclusion:Rats’MCAO focal cerebral ischemia-reperfusion injury model can well simulate human cerebral ischemic disease; there are protective effects of hyperbaric oxygen preconditioning on rats after cerebral ischemia-reperfusion injury.Part Ⅱ The effect of hyperbaric oxygen preconditioning on rats’inflammation after cerebral ischemia and reperfusion injuryObjective:To study the effect of hyperbaric oxygen preconditioning on rats’ inflammatory response after cerebral ischemia and reperfusion injuryMethods:Rats were taken hyperbaric oxygen preconditioning and established MCAO model according to the first part. At 24h after cerebral ischemia and reperfusion, rats’s ischemic brain tissue were taken, maked tissue homogenates, detected mRNA expression of NF-kB (P65), iNOS and COX-2 with Real time PCR, detected the protein expression of NF-kB (P65), iNOS and COX-2 useing Western-blotting, measured levels of IL-1 β and TNF-α by enzyme-linked immunosorbent assay (ELISA).Results:The mRNA relative expression and the protein expression of NF-kB, iNOS and COX-2 in ischemic brain tissue of Rats in HBO group were significantly lower than the model group (P<0.05), the content of IL-1β and TNF-α in ischemic brain tissue of Rats in HBO group compared with the model group, was significantly lower (P<0.05)Conelusion:Hyperbaric oxygen preconditioning may inhibit NF-kB activation, make downstream target gene expression of inflammatory mediators declined, and then inhibit inflammation after rats’cerebral ischemia, finally play a neuroprotective effect. |
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