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. Author manuscript; available in PMC: 2019 Jun 1.
Published in final edited form as: J Neuroimmune Pharmacol. 2018 Feb 28;13(2):237–253. doi: 10.1007/s11481-018-9780-y

Fig. 7.

Fig. 7

Meth treatment potentiated LPS induced neurotoxicity and blocked by inflammasome inhibitors. Neuronal apoptosis was analyzed by combined TUNEL/DAPI staining, and quantification of apoptotic neurons was performed by normalization of TUNEL-positive cells to a total number of DAPI-positive cells. The apoptosis induced by incubation with supernatants of cultured microglia treated with indicated concentrations of Meth. The increased apoptotic neurons were visualized by green TUNEL-positive signals that were notably observed in LPS + Meth treatment group (A). The percentage of apoptotic neurons were counted and statistically analyzed. The quantified results were exhibited in the bar graph of panel A. The blockage effect of inflammasome inhibitors on Meth-induced neuronal apoptosis were examined and quantified in panel B. After priming with LPS for first 6 h, the inhibitors were applied 1 h before additional Meth treatment. The collected supernatant was transferred to cultured neuron and TUNEL-staining were performed. * p < .05, ** p < .01, *** p < .001 vs Ctrl. # p < .05, ## p < .01, ### p < .001 vs LPS. && p < .01, &&& p < .001 vs LPS + Meth 50 μM. Scale bar, 100 μm.