Research Paper Volume 12, Issue 21 pp 21161—21185

Tim-3 deteriorates neuroinflammatory and neurocyte apoptosis after subarachnoid hemorrhage through the Nrf2/HMGB1 signaling pathway in rats

Figure 4. AAV-Tim-3 treatment stimulated microglial activation and upregulated production of the inflammatory cytokines IL-1β, IL-17, IL-18, and TNF-α at 24 post-SAH. Representative images of Iba1- and CD68-positive cells in the sham, SAH, SAH+AAV-NC, and SAH+AAV-Tim-3 groups (A). AAV-Tim-3 treatment increased the expression of the pro-inflammatory cytokines, IL-1β (B), IL-17 (C), and IL-18 (D), TNF-α (E) (n = 6 in each group). Data are expressed as mean ± SD. *p < 0.05, ***p < 0.001. Iba1, ionized calcium binding adapter molecule 1; CD, cluster of differentiation.