NF-κB
When cells are exposed to damaging stimuli, the protein NF-κB is
immediately activated and has been linked to a wide range of
inflammatory illnesses. Inflammation and innate immunity are both
affected by this protein complex, which controls DNA transcription. The
NF-κB pathway is activated by TLRs, TNF receptors, and IL receptors
recognizing different PAMPS and DAMPS (Okada & Suzuki, 2017). Because
it regulates the development of a vasoconstrictor, NF-κB signaling and
its downstream cytokine products are crucial to the pathophysiology of
SAH. Using various drugs to inhibit NF-κB activity, several authors have
observed improved neurological scores, decreased neuronal death, reduced
BBB permeability, and lower inflammatory cytokines following SAH.
(Chang, Wu, Lin, Hwang & Kwan, 2012; Liu, Yang, Pan, Liu & Ma, 2016;
Zhang et al., 2015) , Future research on NF-κB is promising, and the
usefulness of employing this molecule as a therapeutic target in the
treatment of SAH in humans needs to be determined. In the study by Liu
et al. (Liu et al., 2016) Matrine was found to reduce EBI in rats
following subarachnoid hemorrhage by inhibiting NF-κB via PI3K/Akt and
inducing HO-1 via Keap1/Nrf2.