2019
DOI: 10.1016/j.pathophys.2019.07.005
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Camphor elicits up-regulation of hepatic and pulmonary pro-inflammatory cytokines and chemokines via activation of NF-kB in rats

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Cited by 23 publications
(8 citation statements)
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“…In our previous study, we reported that administration of methyl cellosolve significantly increase the renal levels of inflammatory cytokines after 7, 14 and 21 days of administration in rats [ 46 ]. Also administration of camphor was reported to increase the hepatic expressions of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and two chemokines called regulated upon activation normal T cell expressed and secreted (RANTES), and monocyte chemo-attractant protein 1 (MCP-1) in a dose dependent manner in rats [ 47 ].…”
Section: Discussionmentioning
confidence: 99%
“…In our previous study, we reported that administration of methyl cellosolve significantly increase the renal levels of inflammatory cytokines after 7, 14 and 21 days of administration in rats [ 46 ]. Also administration of camphor was reported to increase the hepatic expressions of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) and two chemokines called regulated upon activation normal T cell expressed and secreted (RANTES), and monocyte chemo-attractant protein 1 (MCP-1) in a dose dependent manner in rats [ 47 ].…”
Section: Discussionmentioning
confidence: 99%
“…Thus, we examined the effect of Sal-miR-58 on nuclear factor kB (NF-kB) p65 and p50, which play an essential role in the inflammatory response through regulation of genes encoding inflammatory cytokines (interleukin 1b [IL-1b], tumor necrosis factor a [TNF-a], IL-6). 21,22 The results showed that the expression levels of NF-kB p65 and p50 in the aortas of Ang IIinfused ApoE À/À mice were significantly higher than those in control mice, while Sal-miR-58 treatment significantly reduced the expression of NF-kB p65 and p50 ( Figure 1H). Consistently, compared with Ang II-infused ApoE À/À mice, the serum levels of inflammatory factors IL-1b, IL-6, and TNF-a also declined significantly after Sal-miR-58 administration to Ang II-infused ApoE À/À mice, as detected by ELISA ( Figure 1I).…”
Section: Synthetic Sal-mir-58 Induces Vsmc Autophagy and Inhibits Thementioning
confidence: 97%
“…During hyperglycemia-mediated oxidative stress, high levels of ROS lead to endothelial dysfunctions by damaging DNA, proteins, lipids, and by deregulating NO production and the redox sensitive transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2), which regulates the expression of genes encoding redox enzymes [ 10 , 17 , 18 , 19 , 20 , 21 ]. Furthermore, high glucose-induced oxidative stress activates the nuclear translocation of the nuclear factor kappa B (NFκB) transcriptional factor that induces the production of pro-inflammatory cytokines, such as interleukin-6 (IL-6) [ 22 ]. Conversely, hyperglycemia-caused redox changes may inhibit AMP-activated protein kinase (AMPK) signaling pathway, which exerts anti-inflammatory effects and acts as a key regulator of the endothelial function through induction of eNOS activity and NO vasodilator production [ 23 , 24 ].…”
Section: Introductionmentioning
confidence: 99%