Inhibition of the microglial voltage-gated proton channel 1 channel ameliorates diabetes-associated cognitive dysfunction by regulating axon demyelination

Figure 2 The voltage-gated proton channel 1 gene knockout improves the abnormal secretion of interleukin-1β and tumor necrosis factor-α in the corpus callosum of diabetic mice. A-F: The levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-α in the control group at P2; G-L: The levels of IL-1β and TNF-α in microglial cells were significantly elevated in the diabetic group; M-R: This response was effectively reversed by voltage-gated proton channel 1 gene knockout treatment; S-X: There was no significant difference in the IL-1β and TNF-α levels in the voltage-gated proton channel 1 gene knockout group compared with the control group. The scale bar = 50 μm. ^dP < 0.05. Iba-1: Ionized calcium-binding adaptor molecule 1; IL: Interleukin; TNF: Tumor necrosis factor; DB: Diabetic group; Hv1: The voltage-gated proton channel 1.