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Objective: To investigate the role of the JNK pathway in the pathogenesis of acute carbon monoxide poisoning with delayed encephalopathy . Methods : 120 male SD rats were randomly divided into blank control group (BC group ) , acute carbon monoxide poisoning with delayed encephalopathy group (CO group ) and JNK inhibitor SP600125 (SP ) 3 group , n = 40 . Using a static inhalation exposure law the establishment of delayed encephalopathy rat model of acute carbon monoxide poisoning , 1,3,7,14,28 d after exposure selected five when the phase point , Morris water maze test detection average escape latency , for the first time crossing the platform , the number of crossing the platform of learning and memory ability indicators (14,28 d phase ) , immunohistochemistry staining p-JNK protein expression in the hippocampus (1,3 d phase ) , the Tunel apoptosis detection assay hippocampal pyramidal cell apoptosis (3,7,14,28 d phase ) HE staining rat cerebral cortex and hippocampus pathological changes . Results: acute CO poisoning in rat brain tissue edema of neurons , nuclear condensation and fragmentation , reduction in the number of neurons and other pathological changes . Three groups of rats in the Morris water maze test results average escape latency , the first time through the platform time group comparison : CO group gt ; SP group gt ; BC group (P lt; 0.01); while the number of crossing the platform , the second quadrant movement distance ( time ) / total movement distance ( time ) between the two groups : the CO groups lt ; SP group lt; BC group (P lt; 0.01). p-JNK expression in CO rats hippocampus significantly increased compared to the BC group ( P lt; 0.01 ) , the SP group than in the CO group expression significantly decreased ( P lt ; 0.01 ) , compared to the BC group significantly increased ( P lt; 0.01 ) ; from the first three days of the pyramidal cells in the hippocampus , CO group apoptosis increased most obvious increased 7 and 14 days , 28 days is still increased , the apoptotic index compared with the BC group was significantly higher ( P lt; 0.01 ) , while the SP apoptotic index significantly lower compared with the CO group (P lt; 0.01). Conclusion : JNK signaling pathway involved in the occurrence of delayed encephalopathy of acute carbon monoxide poisoning , to application specific inhibitor SP600125 blocking its transduction reduces apoptosis of neurons in the hippocampus , alleviate acute carbon monoxide poisoning damage on learning and memory ability .
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