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2015 ; 48
(3
): 172-7
Nephropedia Template TP
gab.com Text
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Twit Text #
English Wikipedia
Celastrol ameliorates cytokine toxicity and pro-inflammatory immune responses by
suppressing NF-?B activation in RINm5F beta cells
#MMPMID25059279
Ju SM
; Youn GS
; Cho YS
; Choi SY
; Park J
BMB Rep
2015[Mar]; 48
(3
): 172-7
PMID25059279
show ga
Upregulation of pro-inflammatory mediators contributes to ?-cell destruction and
enhanced infiltration of immune cells into pancreatic islets during development
of type 1 diabetes mellitus. In this study, we examined the regulatory effects
and the mechanisms of action of celastrol against cytotoxicity and
pro-inflammatory immune responses in the RINm5F rat pancreatic ?-cell line
stimulated with a combination of interleukin-1 beta, tumor necrosis factor-alpha,
and interferon-?. Celastrol significantly restored cytokine-induced cell death
and significantly inhibited cytokine-induced nitric oxide production. In
addition, the protective effect of celastrol was correlated with a reduction in
pro-inflammatory mediators, such as inducible nitric oxide synthase,
cyclooxygenase-2, and CC chemokine ligand 2. Furthermore, celastrol significantly
suppressed cytokine- induced signaling cascades leading to nuclear factor kappa B
(NF-?B) activation, including I?B-kinase (IKK) activation, I?B degradation, p65
phosphorylation, and p65 DNA binding activity. These results suggest that
celastrol may exert its cytoprotective activity by suppressing cytokine-induced
expression of pro-inflammatory mediators by inhibiting activation of NF-?B in
RINm5F cells.
|Animals
[MESH]
|Cell Line
[MESH]
|Chemokine CCL2/metabolism
[MESH]
|Cyclooxygenase 2/metabolism
[MESH]
|Cytokines/*toxicity
[MESH]
|Inflammation Mediators/*toxicity
[MESH]
|NF-kappa B/*metabolism
[MESH]
|Nitric Oxide Synthase Type II/antagonists & inhibitors
[MESH]