IndraLab
Statements
reach
"Consistent with the finding that OTULIN overexpression was shown to delay NF-kappaB activation of TNF, whereas its knockdown was reported to increase the output of NF-kappaB signaling [XREF_BIBR, XREF_BIBR, XREF_BIBR], we found that OTULIN overexpression strongly depressed NF-kappaB activity and reduced the release of TNF-alpha, IL-1beta, and IL-6, which are the primary pro inflammatory cytokines that aggravate brain injury."
reach
"OTULIN overexpression significantly suppressed the production of TNF-alpha, IL-1beta, and IL-6 in PM and N9 cells via inhibiting the nuclear translocation of NF-kappaB p65 but had no effect on the pro inflammatory cytokines secreted by un activated microglia, which directly indicates that OTULIN suppressed microglia mediated neuroinflammation by inhibiting the NF-kappaB pathway and attenuated the release of inflammatory mediators under the in vitro ischemic condition."