Genes involved in inflammatory processes mediated by NFkB
and other signaling pathways were generally up-regulated at baseline in both SH and SHHF rats compared with WKY rats, along with several metabolic and pathological processes.
We have investigated the pl[kappa]B[alpha] level in cytosol and NFkB
(p65) level in nucleus to identify NF[kappa]B activation.
is a key regulator of genes involved in cell activation and proliferation (Grilli et al.
and phosphorylated c-Jun (p-c-Jun) nuclear binding activity.
In this respect it is interesting to note, that boswellic acids including 11-keto-[beta]-boswellic acid (KBA) and/or O-acetyl-l1-keto-[beta]-boswellic acid (AKBA) have been shown to inhibit leukotriene production in polymorph neutrophlles (PMN) with little effect on COX-2, and are inhibiting NFkB
as well as some proinflammatoiy cytokines in vitro (Cuaz-Perolin et al.
The identified networks showed enrichment for various canonical pathways, including NFkB
and IL-8 signaling.
Sera were evaluated in duplicate by commercially available ELISA kits for the following: bone-alkaline phosphatase (b-ALP; IDS Ltd., UK), collagen C-telopeptide (CTX, Nordic Bioscience Diagnostics, Nordic, Herlev, Denmark), osteoprotegerin (OPG, IDS Ltd.) and soluble receptor activator of NFKB
ligand (sRANKL; IDS Ltd.).
(70) Although antioxidant protection by tocotrienol is involved, mechanisms targeting inflammatory pathways such as NFkB
and STAT-3 produced during ionizing radiation may play a crucial role in improving clinical outcomes by enhancing radiosensitivity and decreasing side effects.
Cellular calcium levels can activate NFKB
producing immune activation.
Crocetin reduces TNBS-induced experimental colitis in mice by downregulation of NFkB
. Saudi J.
Transcriptional activity of IL-8 promoter and nuclear factor kappa B (NFkB
) in ZnO-treated BEAS-2B cells was measured using transient gene transfection of the luciferase reporter construct with or without p65 constructs.
Delta-tocotrienol most effectively induced cell death of prostate cancer cells, and activated programmed cell death while disrupting NFkB