Fig 2: Knockdown of GPNMB activated the NF-?B signalling pathways but inhibited the AKT signalling pathways. The expression of GPNMB, p-AKT, AKT, p-P65, and P65 in HK-2 cells was detected by western blot analysis. ***p < 0.001 vs. LPS, ****p < 0.001 vs. LPS, ####p < 0.0001 vs. LPS+Mel, n = 3.

Fig 3: Knockdown of GPNMB reversed the anti-inflammatory and antiapoptotic effect of Mel in HK-2 cells treated with LPS. (a–c) The expression of inflammatory cytokines (IL-1ß, IL-6, and TNF-a) was detected by ELISA kits. (d) The apoptosis rate of HK-2 cells was detected by TUNEL staining (green). Magnification: 200x. *p < 0.01 vs. LPS, **p < 0.01 vs. LPS, ***p < 0.001 vs. LPS, ###p < 0.001 vs. LPS+Mel, and ####p < 0.0001 vs. LPS+Mel, n = 3.

Fig 4: Mel induced the expression of GPNMB and mediated the AKT and NF-?B signalling pathways in HK-2 cells treated with LPS. (a) The expression of GPNMB in HK-2 cells was detected by western blot analysis. (b) The expression of p-AKT, AKT, p-P65, and P65 in HK-2 cells was detected by western blot analysis. **p < 0.01 vs. control, ****p < 0.0001 vs. control, ###p < 0.001 vs. LPS, and ####p < 0.0001 vs. LPS, n = 3.

Fig 5: Differentially expressed genes when comparing the autopsy (control), focal cortical dysplasia (FCD) ILAE type IIa (FCD IIa) and FCD ILAE type IIb (FCD IIb) groups. (A–D) Expression of HMGCS1, HMGCR, SQLE, and MTRNR2L12, respectively, in the gray matter. (E) Expression of GPNMB in the white matter. Please refer to the text for details on fold change for each gene and the corresponding statistical significance (adjusted p-value).