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- W2051234144 abstract "activation as showed by inducible nitric oxide synthase expression and production of inflammatory mediators such as NO, TNF-α, and IL-1β. However, DMPO blocked these inflammatory responses. LPS-induced TNF-α and NO are known to induce ER stress and apoptosis. ER stress was shown by activation of PERK and induction of CHOP, which is known to be involved in apoptosis. Notably, DMPO downregulated LPSinduced ER stress. Furthermore, LPS decreased anti-apoptotic protein 14-3-3 expression, but increased caspase-3 activation. As expected, DMPO restored 14-3-3 expression but, unexpectedly, has a synergistic effect on caspase-3 activation by LPS. Even though upregulating the apoptotic marker caspase-3, DMPO protected cells from LPS-induced DNA damage as showed by inhibiting phosphorylation of histone H2A, acetylation of histone H2B, and phosphorylation of DNA damage sensor p53 and checkpoint Chk1. In order to understand the mechanistic basis of DMPO for the above-mentioned effects, we determined the phosphorylation of Akt, mitogen-activated protein kinases (MAPKs), and IκB-α that are linked to NF-κB activation. DMPO inhibited phosphorylation of Akt, MAPKs (ERK, JNK/SAPK and p38), and IκB-α, which led to inhibition of NF-κB activation. Taken together, DMPO prevented macrophage activation, ER-stress and DNA damage triggered by LPS throughout the blocking of Akt and MAPKs signaling pathways. The analysis of DMPO effects on signaling and gene expression in “inflamed” cells would help us develop new therapeutic applications of this old nitrone spin trap. Supported by NIEHS 5R00ES015415." @default.
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- W2051234144 date "2010-01-01" @default.
- W2051234144 modified "2023-10-16" @default.
- W2051234144 title "Smoking Cessation Effect of Tea Component Theanine Through Inhibition of Nicotine Acetylcholine Receptor" @default.
- W2051234144 doi "https://doi.org/10.1016/j.freeradbiomed.2010.10.593" @default.
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