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. 2022 Jun 6;18(1):141–149. doi: 10.4103/1673-5374.344829

Figure 5.

Figure 5

Effect of maraviroc on the expression of the NLRP3 inflammasome after traumatic brain injury.

(A–G) Representative western blot bands and quantitative data of NLRP3 (B), ASC (C), cleaved caspase-1 p20 (D), IL-1β (E), IL-18 (F), and cleaved GSDMD (G) in the pericontusional cerebral cortex 3 days post-TBI. Maraviroc treatment alleviated the TBI-induced activation of NLRP3 inflammasome components and substrates at 3 days postinjury compared with the TBI + vehicle group (P = 0.0082 for B, P < 0.05 for C–G). (H–I) Representative immunofluorescence staining micrographs for caspase-1 p20 (green) in the perilesional cortex at 3 days post-TBI. The black boxes in the hematoxylin and eosin-stained illustration show the perilesional cortex. Scale bars: 100 µm. Maraviroc treatment significantly decreased the number of caspase-1 p20-positive cells compared with the TBI + vehicle group (P = 0.0027). One-way analysis of variance followed by Tukey’s post hoc test was used. Data are shown as the mean ± SD (n = 5/group). All experiments were repeated at least three times. ASC: Apoptosis-associated speck-like protein containing a CARD; DAPI: 4′,6-diamidino-2-phenylindole; GSDMD: gasdermin-D; IL: interleukin; NLRP3: NACHT, LRR, and PYD domains-containing protein 3; TBI: traumatic brain injury.