The Nerve Protective Effect Of Neuregulin-1β And The Mechanism Research On Focal Cerebral Ischemia/Repefrusion Injury Rats

Objective:To observe the neurological score, cerebral infarction volume,the brain water content, CK and LDH activity in serum, SOD and MDAlevels of cerebral tissue and expression of receptor tyrosine protein kinaseB (TrkB) and the influence of Neuregulin-1β on brain tissure of ratsfollowing focal ischemia/reperfusion.Method:The rat middle cerebral artery occlusion models with filament offocal cerebral ischemia/reperfusion were established. SD male rats weredivided randomly into sham group，cerebral ischemia-reperfusion modelgroup and the NRG-1β group. The NRG-1β group was further dividedinto three sub-groups which were dealt with the low，middle and highdose of NRG-1β. The neurological scores, cerebral infarction volume andthe brain water content were detected after2h ischemia followed by24hreperfusion. CK and LDH activity in serum，SOD and MDA levels ofcerebral tissue were also measured. Moreover, the expression of TrkBmRNA were evaluated by RT-PCRResults: Compared with the model group，the neurological scores, braininfarct volume（P<0.05,P<0.01,P<0.001） and the brain water content（P<0.05,P<0.01）decreased; inhibit LDH（P<0.05,P<0.01） and CK （P<0.05,P<0.01） release, improve SOD（P<0.05,P<0.05,P<0.01）activity and reduce MDA （P<0.05,P<0.05,P<0.01）content. In addition,the expression of TrkB mRNA significantly increased in three doses ofNRG-1β groups（P<0.05,P<0.01,P<0.001）.Conclusion:1.NRG-1β can reduce brain infarction volume and brainwater content, can relieve damage of the brain cells and relieve cerebraledema，its effect has connection with its connection.2.NRG-1β canreduce the contents of LDH and CK in serum, have the effect that reducebrain damage，its effect has connection with its connection.3.NRG-1βcanincrease SOD content in brain tissue, and decrease MDA content, haveincreased scavenging oxygen free radicals, reducing the role of oxidativestress.4. NRG-1β can increase TrkB mRNA expression, TrkB increasemRNA expression mediated the NRG-1β protection of ischemiareperfusion injury in rats, but the one concrete through signaltransduction pathways need further in-depth study. NRG-1β on focalcerebral ischemia-reperfusion injury in rats with protection, itsmechanism may be related to increase the expression of tyrosine kinasereceptor B (TrkB).