Fig. 1

Succinylation level was increased in aging or activated MGs acompanied by metabolic reprogramming. (A) Schematic experimental workflow for the identification of succinylation level, MG activated status, neuroinflammation level in the aging mice. (B) Succinylation level and neuroinflammation level of the aging mice.(young: n = 3 and aging n = 6); (a) Succinylation level between the young and aging mice confirmed by WB; (b) Proinflammatory cytokine Tnf-α transcription level evaluated by qPCR. C. MG activation states in the cortex (×20) and inset (×40) confirmed by IHC. Bar = 500 μm(×20) and 100 μm(×40). D. Succinylation level and aging-related genes in the long-term culture PriMG aging model; (a) Schematic of the long-term culture model; (b) Aging-related genes detected by qPCR; (c) Succinylation level between 3-day and 21-day cultured PriMG confirmed by WB. E. Succinylation level and aging-related genes in the VP16 induced MG aging model; (a) Aging-related genes detected by qPCR; (b) Succinylation level between CTL and VP16 treated groups confirmed by WB. F. Succinylation level in the mitochondrial lysate of hippocampus between CTL and LPS treated mice in the ip. treatment model. G. Succinylation level and SCoA concentration in the LPS treated PriMG and BV2 cells; (a) Succinylation level between CTL and LPS treated PriMGs confirmed by WB; (b) Succinylation level between CTL and LPS treated BV2 cells confirmed by WB; (c) The concentration of SCoA in cellular total lysate detected by colorimetric method. H. Schematic of the metabolic profile detected by Seahorse XF96 analyzer. I. The glycolytic rate changes following LPS treatment detected by the glycolytic rate assays. J. The ATP production rate changes following LPS treatment detected by the real-time ATP production rate assays. K. The levels of ATP and LA in cellular total lysate detected by ELISA. n = 3/group, * P < 0.05, ** P < 0.01, *** P < 0.005, **** P < 0.001