Role of JNK signal pathway in brain injury after resuscitation in a rat model of asphyxia cardiac arrest

• DOI: 10.3760/cma.j.issn.0254-1416.2012.01.024
• Publication Date: 2012-01-20
• Authors: Long Chen; Gongjian Liu; Xiyan Chen; Yan Zhang; Qin Cheng; Mao-yin Zhang

Objective To evaluate the role of JNK signal pathway in brain injury after resuscitation a rat model asphyxia cardiac arrest.Methods Forty healthy male SD rats 'weighing 300-350 g were randomly divided into 4 groups ( n =10 each):sham operation group (group SH) ; arrest CA) SP600125-JNK inhibitor SP) and dimethyl sulfexide (DMSO) group.The anesthetized with intraperitoneal pentobarbital 45 mg/kg,tracheostomized mechanically ventilated.PETCO2 was maintained at 35-45 mm Hg.Femoral artery vein cannulated for BP monitoring fluid infusion.Cardiac induced by clamping tracheal tube until ECG activity disappeared MAP ＜ 10 Hg.Resuscitation started 3 min arrest.MAP ＞ 60 Hg HR 250 bpm considered to be signs successful resuscitation.SP600125 20 mg/kg DMSO 0.2 ml injected iv as soon chest compression SP respectively.The animals sacrificed 5 h their brains removed determination wet/dry (W/D) weight ratio microscopic examination hippocampus.Neuronal apoptosis detected TUNEL.Results Cardiac significantly increased W/D number apoptotic cells CA.SP600125 attenuated arrest-induced increase but did not.Conclusion is involved arrest.

Key words: JNK mitogen-activated protein kinases; Asphyxia; Heart arrest; Brain injuries