Inhibition of TNF-α, IL-1β, and IL-6 productions and NF-κB activation in lipopolysaccharide-activated RAW 264.7 macrophages by catalposide, an iridoid glycoside isolated from Catalpa ovata G. Don (Bignoniaceae)

An, Shengjun; Pae, Hyun‐Ock; Oh, Gi‐Su; Choi, Byung-Min; Jeong, Seung-Il; Jang, Seon Il; Oh, Hyuncheol; Kwon, Tae-Oh; Song, Choong Eui; Chung, Hun‐Taeg

doi:10.1016/s1567-5769(02)00085-1

Cited by 88 publications

(38 citation statements)

References 18 publications

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“…NF-kB plays a critical role in the regulation of inflammation by activating transcription of proinflammatory genes, enzymes and cytokines, including COX-2, iNOS, TNFa, IL-1β, and IL-6 [13,14]. Under normal circumstances, NFkB p50/p65 binds to IkB, sequestering IkB in the cytoplasm in an inactive form.…”

Section: Effect Of Meta060 On the Nf-kb Signaling Pathwaymentioning

confidence: 99%

META060 inhibits multiple kinases in the NF-κB pathway and suppresses LPS – mediated inflammation in vitro and ex vivo

Desai¹,

Konda²,

Darland³

et al. 2009

Inflamm. Res.

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Section: Effect Of Meta060 On the Nf-kb Signaling Pathwaymentioning

confidence: 99%

META060 inhibits multiple kinases in the NF-κB pathway and suppresses LPS – mediated inflammation in vitro and ex vivo

Desai¹,

Konda²,

Darland³

et al. 2009

Inflamm. Res.

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“…The inflammation features production of a variety of inflammatory cytokines, such as interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor-α 64 (TNF-α) and C-reactive protein (CRP), and activation of the inflammatory cells like monocytes/macrophages [1][2][3][4]. Among the inflammatory cytokines, CRP shows the strongest association with increased risk of cardiovascular events.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II Induces the Expression of C-reactive Protein via MAPK-Dependent Signal Pathway in U937 Macrophages

Liu²,

Han³

et al. 2011

Cell Physiol Biochem

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Atherosclerosis is an inflammatory disease in the vessel wall. As an inflammatory molecule, C-reactive protein (CRP) participates in all stages of atherosclerotic process. Although angiotensin II (Ang II) can stimulate the vascular cells to produce CRP, it is unknown whether Ang II induces CRP expression in macrophages. The present study was to observe effect of Ang II on CRP production and the related signal pathway in U937 macrophages so as to provide more evidence for the proinflammatory action of Ang II. The results showed that Ang II significantly increased mRNA and protein expression of CRP in U937 macrophages in time- and concentration-dependent manners. AT₁ receptor blocker losartan blocked Ang II -induced CRP expression in mRNA and protein levels in U937 macrophages. Losartan and complex II inhibitor TIFA decreased Ang II -stimulated reactive oxygen species (ROS) generation, and antioxidant NAC completely abolished Ang II -induced CRP expression in U937 macrophages. The further study indicated that losartan, NAC, MEK1/2 inhibitor PD98059, p38MAPK inhibitor SB203580 obviously inhibited ERK1/2 and p38MAPK phosphorylation, and PD98059, SB203580 and NF-ĸB inhibitor PDTC reduced Ang II -induced mRNA and protein expression of CRP in U937 macrophages. These demonstrate that Ang II is capable of inducing CRP generation in macrophages via AT₁-ROS-ERK1/2/p38MAPK-NF-ĸB signal pathway, which contributes to better understanding of the proinflammatory and proatherosclerotic actions of Ang II.

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“…Aucubin exerts widely ranging biological effects that include reducing blood pressure, protecting the liver, anti-inflammatory and anti-microbial activities, analgesic effects, and antitumor activity [12,24] . Recently, aucubin was shown to attenuate apoptosis induced by H 2 …”

mentioning

confidence: 99%

Neuroprotection of aucubin in primary diabetic encephalopathy

Xue

Jin

et al. 2008

SCI CHINA SER C

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Hippocampal neuronal apoptosis accompanied by impairment of cognitive function occurs in primary diabetic encephalopathy. In this study, we investigated the neuroprotective mechanism of the iridoid glycoside, aucubin, using rats (n=8). Diabetes mellitus was induced in the rats by intraperitoneal (i.p.) injection of streptozotocin (60 mg/kg body weight). After 65 d, half of the DM rats were administered aucubin (5 mg/kg; i.p.) for 15 d, yielding treatment DM+A. A third group of rats received no streptozotocin or aucibin, and served as controls (CON). Encephalopathy was assessed using Y-maze behavioral testing. Rats were euthanized on Day 87, and hippocampi were excised for visual (light and transmission electron microscopic) and immunochemical (Western blot; immunohistochemical) assessments of the CA1 subfield for apoptosis and expression of regulatory proteins Bcl-2 and Bax. Treatment responses to all the parameters examined (body weight, plasma glucose, Y-maze error rates, pyramidal cell ultrastructure, proportions of apoptotic cells, levels of expression of Bcl-2 and Bax, and survivability of neuronal cells) were identical: there were highly significant differences between DM and CON groups (P<0.001), but the effects were significantly moderated (P<0.01) in DM+A compared with DM. These findings confirm the association of apoptosis with the encephalopathic effects of diabetes mellitus, and suggest a major role of the expression levels of Bcl-2 and Bax in the regulation of apoptotic cell death. All of the results suggest that aucubin could effectively inhibit apoptosis by modulating the expressions of Bcl-2 and Bax genes.

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Inhibition of TNF-α, IL-1β, and IL-6 productions and NF-κB activation in lipopolysaccharide-activated RAW 264.7 macrophages by catalposide, an iridoid glycoside isolated from Catalpa ovata G. Don (Bignoniaceae)

Cited by 88 publications

References 18 publications

META060 inhibits multiple kinases in the NF-κB pathway and suppresses LPS – mediated inflammation in vitro and ex vivo

META060 inhibits multiple kinases in the NF-κB pathway and suppresses LPS – mediated inflammation in vitro and ex vivo

Angiotensin II Induces the Expression of C-reactive Protein via MAPK-Dependent Signal Pathway in U937 Macrophages

Neuroprotection of aucubin in primary diabetic encephalopathy

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