The Study On The Effect Of JNK Signaling Pathway In The Pathogeneses Of Delayed Encephalopathy After Acute Carbon Monoxide Poisoning

Objective: To study the effect of c-Jun N-terminal kinase (JNK) signaling pathway in the pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning.Methods: One hundred and twenty male SD rats were randomly divided into three groups: blank control group(BC group),delayed encephalopathy after acute carbon monoxide poisoning group (CO group) and the JNK inhibitor SP600125 group (SP group),forty rats in each group. The rat model was induced by static inhaled exposure method. The time points of 1st ,3rd,7th,14th and 28th day after acute carbon monoxide poisoning was set for measuring the changes. Morris water maze test was used to measure the learning ability and memory such as the average escaped latency, time of the first pass through platform, number of pass through platform(14d,28d). The expression of p-JNK in hippocampal area was measured by immunohistochemistry(1d,3d). The apoptosis of pyramidal neurons at hippocampal gyrus area was measured by in situ apoptosis detection (3d,7d,14d and 28d).The pathological change at substantia corticalis and hippocampal gyrus of rats brain was observed by H-E.Results: Neuronal cells edema, nuclear pyknosis, nuclear fragmentation, number of neurons reducing and other pathological changes were showen in rats brain after acute carbon monoxide poisoning. In Morris water maze test, the average escaped latency and time of the first pass through platform were shown that CO group > SP group >BC group(P<0.01), but number of pass through platform and movement distance(time) in the second quadrant/total movement distance(time) were shown that CO group < SP group