Research Paper Volume 13, Issue 4 pp 6182—6193

Dexmedetomidine reverses MTX-induced neurotoxicity and inflammation in hippocampal HT22 cell lines via NCOA4-mediated ferritinophagy

DEX alleviated cytotoxicity and hippocampal neuronal inflammatory injury induced by MTX. (A) The cell viability of HT22 cells in different groups were measured by CCK-8 assay. (B) The activity of LDH in the culture media were measured using LDH assay kit. (C) The levels of IL-1β and (D) TNF-α in the culture media were measured using ELISA. (E) The relative expression of NF-κB in HT22 cells were measured by western-blot. (F) The representative results of apoptotic cells in control, MTX (G), MTX+1ng/mL DEX (H), MTX+10ng/mL DEX (I), and MTX+50 ng/mL DEX (J) group were tested by flow cytometry. (K) Flow cytometry analysis of HT22 cells in different groups. n=3; #p

Figure 1. DEX alleviated cytotoxicity and hippocampal neuronal inflammatory injury induced by MTX. (A) The cell viability of HT22 cells in different groups were measured by CCK-8 assay. (B) The activity of LDH in the culture media were measured using LDH assay kit. (C) The levels of IL-1β and (D) TNF-α in the culture media were measured using ELISA. (E) The relative expression of NF-κB in HT22 cells were measured by western-blot. (F) The representative results of apoptotic cells in control, MTX (G), MTX+1ng/mL DEX (H), MTX+10ng/mL DEX (I), and MTX+50 ng/mL DEX (J) group were tested by flow cytometry. (K) Flow cytometry analysis of HT22 cells in different groups. n=3; #p<0.05, vs Control; *p<0.05, vs MTX group.