Microglial polarization:
Microglial polarization appears to play a significant part in the
pathogenic processes of neuroinflammation following subarachnoid
hemorrhage, according to increasing data (Gao et al., 2021). Microglia
responds quickly to a variety of brain injuries by modifying the shape
and polarization of their cytoplasmic structures. After a SAH,
neuroinflammation develops over time and plays a role in both EBI and
the long-term decline in cognitive function. As resident immune cells,
microglia coordinates neuroinflammation differently in neurological
disorders with varying degrees of polarization (Zheng, Lyu, Lam, Lam,
Poon & Wong, 2020). After SAH, activated microglia are thought to
polarize into two phenotypes: classic M1 (pro-inflammatory) and
alternative M2 (anti-inflammatory), depending on the stimulus (Li &
Barres, 2018). Lipopolysaccharide (LPS) and the pro-inflammatory
cytokine interferon-γ (IFN-γ) traditionally stimulate microglia to the
M1 phenotype through the release of pro-inflammatory cytokines such as
tumor necrosis factor-α and interleukin-6 and When microglia are
stimulated by IL-4 or IL-13, they adopt an alternative M2 phenotype and
express anti-inflammatory molecules such as transforming growth factor
beta and IL-10 (Zheng, Lyu, Lam, Lam, Poon & Wong, 2020). According to
(Liu et al., 2020), Hb-induced microglial pro-inflammatory polarization
was inhibited more effectively by the RvD1-ALX/FPR2 connection,
potentially by negatively modulating the signaling activities of
IRAK1/TRAF6/NF-κB or MAPKs. Similarly, (You et al., 2016) indicated
that, Rapamycin and AZD8055 may promote a selective modification of
microglia polarization to the M2 phenotype for SAH therapy by inhibiting
the mTOR pathway. RhMFG-E8 treatment reduces the microglial inflammatory
response, which is linked to the M2 microglial shift and may have direct
neuroprotective effects, and it may include the integrin 3/SOCS3/STAT3
signaling pathway (Gao et al., 2021). (Wei et al., 2017) study, showed
that Erythropoietin reduces EBI after SAH by regulating microglia
polarization through the EPOR/JAK2-STAT3 pathway. The above facts
suggest that, modulating M1 and M2 microglial polarization could be a
promising neuroprotective strategy. Further studies are needed to better
understand the application of microglial modulation in SAH.