Figure 6Figure 6
Deficiency of HDAC3 in microglia suppresses the cGAS-STING-mediated autoimmune response . ( A and B ) Adult primary microglial cells were isolated from HDAC3 cKO (n = 6) and WT (n = 6) mice, and the mRNA levels of HDAC3 (A) and cGAS (B) were analyzed by real-time PCR. ( C ) The neurological deficits of HDAC3 cKO (n = 7) and WT (n = 15) mice subjected to tMCAO were assessed 24 h post-reperfusion. ( D and E ) Brain tissue isolated from WT (n = 14) and HDAC3 cKO (n = 7) mice 24 h post-reperfusion was stained with triphenyl tetrazolium chloride, and infarct volume was determined using ImageJ (D) and infarct volume was determined using Image J (E). ( F ) RNA was extracted from the ischemic penumbra cortex and contra cortex of HDAC3 cKO (n = 12) and WT (n = 14) mice subjected to tMCAO 6 h post-reperfusion, and the mRNA level of IL-6 was quantified by real-time PCR. ( G ) Serum was isolated from HDAC3 cKO (n = 13) and WT (n = 21) mice subjected to tMCAO 6 h post-reperfusion, and the level