Figure 5

Alterations in Neuronal reaction after spinal cord ischemia reperfusion (I/R) injury. (A) Effects on spinal immunoreactivity to neuronal marker NeuN in laminae IX of ventral gray matter after I/R injury. Scale bars are 200 μm. (B) Representative immunohistochemical localization of neurons (NeuN; green) and cleaved caspase3 (red) in laminae IX of spinal cord at 12 h and 36 h after I/R injury. Arrows delineate co-localization. Scale bars are 100 μm. (C) Quantification of the NeuN-positive neurons in laminae IX of ventral gray matter is presented as average of three independent experiments. (D) Histogram of the values for co-localized cells (cells with yellow signals) as the percent of the total NeuN-positive cells in laminae IX of ventral horn. Immunohistochemistry showed I/R led to the decrease in neuronal number of both spinal ventral horns and increase percentage of NeuN-cleaved caspase3-positive cells, suggesting the loss of neurons partly as a result of apoptosis. Pretreated with minocycline, TAK-242, PDTC were showed had neuroprotective effects as the decreases in number of neuronal apoptosis, intrathecal injection with LPS abrogated above effects. All data are presented as mean ± SEM (n = 8 per group). **P < .01 compared to Sham group; ^##P < .05 compared to I/R group.