Moreover, protein and mRNA levels of DSS-induced proinflammatory cytokines in colon, including TNF-α, IL-1β, << IL-18 >>, IL-17A and IFN-γ, were markedly suppressed by [[ Fc11a-2 ]].


Moreover, protein and mRNA levels of DSS-induced proinflammatory cytokines in colon, including TNF-α, IL-1β, IL-18, << IL-17A >> and IFN-γ, were markedly suppressed by [[ Fc11a-2 ]].


Moreover, protein and mRNA levels of DSS-induced proinflammatory cytokines in colon, including TNF-α, IL-1β, IL-18, IL-17A and << IFN-γ >>, were markedly suppressed by [[ Fc11a-2 ]].


Furthermore, a decreased CD11c(+) macrophage infiltration in colons and inactivation of << caspase-1 >> in peritoneal macrophages were detected in [[ Fc11a ]]-2-treated mice.


The mechanism of action of << Fc11a-2 >> was related to the inhibition of the cleavage of [[ pro-caspase-1 ]], pro-IL-1β and pro-IL-18 which in turn suppressed the activation of NLRP3 inflammasome.


The mechanism of action of << Fc11a-2 >> was related to the inhibition of the cleavage of pro-caspase-1, [[ pro-IL-1β ]] and pro-IL-18 which in turn suppressed the activation of NLRP3 inflammasome.


The mechanism of action of << Fc11a-2 >> was related to the inhibition of the cleavage of pro-caspase-1, pro-IL-1β and [[ pro-IL-18 ]] which in turn suppressed the activation of NLRP3 inflammasome.


The mechanism of action of << Fc11a-2 >> was related to the inhibition of the cleavage of pro-caspase-1, pro-IL-1β and pro-IL-18 which in turn suppressed the activation of [[ NLRP3 ]] inflammasome.


Taken together, our results demonstrate the ability of << Fc11a-2 >> to inhibit [[ NLRP3 ]] inflammasome activation and its potential use in the treatment of inflammatory bowel diseases.


At PND35, the medial prefrontal cortex (mPFC) of rats given << MPH >> showed 55% greater immunoreactivity (-ir) for the catecholamine marker [[ tyrosine hydroxylase ]] (TH), 60% more Nissl-stained cells, and 40% less norepinephrine transporter (NET)-ir density.


At PND35, the medial prefrontal cortex (mPFC) of rats given << MPH >> showed 55% greater immunoreactivity (-ir) for the catecholamine marker tyrosine hydroxylase ([[ TH ]]), 60% more Nissl-stained cells, and 40% less norepinephrine transporter (NET)-ir density.


At PND35, the medial prefrontal cortex (mPFC) of rats given << MPH >> showed 55% greater immunoreactivity (-ir) for the catecholamine marker tyrosine hydroxylase (TH), 60% more Nissl-stained cells, and 40% less [[ norepinephrine transporter ]] (NET)-ir density.


At PND35, the medial prefrontal cortex (mPFC) of rats given << MPH >> showed 55% greater immunoreactivity (-ir) for the catecholamine marker tyrosine hydroxylase (TH), 60% more Nissl-stained cells, and 40% less norepinephrine transporter ([[ NET ]])-ir density.


In hippocampal dentate gyrus, << MPH >>-receiving rats showed a 51% decrease in NET-ir density and a 61% expanded distribution of the new-cell marker PSA-NCAM (polysialylated form of [[ neural cell adhesion molecule ]]).


In hippocampal dentate gyrus, << MPH >>-receiving rats showed a 51% decrease in NET-ir density and a 61% expanded distribution of the new-cell marker PSA-[[ NCAM ]] (polysialylated form of neural cell adhesion molecule).


In hippocampal dentate gyrus, << MPH >>-receiving rats showed a 51% decrease in [[ NET ]]-ir density and a 61% expanded distribution of the new-cell marker PSA-NCAM (polysialylated form of neural cell adhesion molecule).


In medial striatum, TH-ir decreased by 21%, and in hypothalamus << neuropeptide Y >>-ir increased by 10% in [[ MPH ]]-exposed rats.


In medial striatum, << TH >>-ir decreased by 21%, and in hypothalamus neuropeptide Y-ir increased by 10% in [[ MPH ]]-exposed rats.