Inhibitors of Nitric Oxide Synthesis and TNF-α Expression from Magnolia obovata in Activated Macrophages

Son, Haeng Ja; Lee, Hwa Jin; Yun‐Choi, Hye Sook; Ryu, Jae‐Ha

doi:10.1055/s-2000-8592

Cited by 79 publications

(56 citation statements)

References 11 publications

(14 reference statements)

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“…The suppression of invasion (32) and angiogenesis (33) reported previously agrees with the results reported here. The inflammatory cytokines TNF and interleukin-8, both known to promote angiogenesis, have also been shown to be down-regulated by honokiol (4,5). The down-regulation of nitric oxide synthesis by honokiol reported previously (4) also likely occurs through the suppression of NF-nB activation as reported here.…”

Section: Discussionsupporting

confidence: 53%

“…Extensive research has shown that honokiol inhibits skin tumor promotion (3), inhibits nitric oxide synthesis and tumor necrosis factor (TNF) expression (4,5), inhibits invasion (6), down-regulates antiapoptotic protein Bcl-x L (7), inhibits angiogenesis and tumor growth in vivo (8), induces caspasedependent apoptosis in B-cell chronic lymphocytic leukemia cells through down-regulation of the antiapoptotic protein Mcl-1 (9), and overcomes drug resistance in multiple myeloma (10). Exactly how honokiol mediates all these effects is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

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Honokiol Potentiates Apoptosis, Suppresses Osteoclastogenesis, and Inhibits Invasion through Modulation of Nuclear Factor-κB Activation Pathway

Ahn

Sethi

Shishodia

et al. 2006

Molecular Cancer Research

125

112

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Recent reports have indicated that honokiol can induce apoptosis, suppress tumor growth, and inhibit angiogenesis. In this report, we found that honokiol potentiated the apoptosis induced by tumor necrosis factor (TNF) and chemotherapeutic agents, suppressed TNF-induced tumor cell invasion, and inhibited RANKL-induced osteoclastogenesis, all of which are known to require nuclear factor-KB (NF-KB) activation. Honokiol suppressed NF-KB activation induced by a variety of inflammatory stimuli, and this suppression was not cell type specific. Further studies showed that honokiol blocked TNF-induced phosphorylation, ubiquitination, and degradation of IKBA through the inhibition of activation of IKBA kinase and of Akt. This led to suppression of the phosphorylation and nuclear translocation of p65 and NF-KB-dependent reporter gene expression. Magnolol, a honokiol isomer, was equally active. The expression of NF-KB-regulated gene products involved in antiapoptosis (IAP1, IAP2, Bcl-x L , Bcl-2, cFLIP, TRAF1, and survivin), proliferation (cyclin D1, cyclooxygenase-2, and c-myc), invasion (matrix metalloproteinase-9 and intercellular adhesion molecule-1), and angiogenesis (vascular endothelial growth factor) were also down-regulated by honokiol. Honokiol also down-regulated NF-KB activation in in vivo mouse dorsal skin model. Thus, overall, our results indicate that NF-KB and NF-KB-regulated gene expression inhibited by honokiol enhances apoptosis and suppresses osteoclastogenesis and invasion. (Mol Cancer Res 2006;4(9):621 -33)

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Section: Discussionsupporting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Honokiol Potentiates Apoptosis, Suppresses Osteoclastogenesis, and Inhibits Invasion through Modulation of Nuclear Factor-κB Activation Pathway

Ahn

Sethi

Shishodia

et al. 2006

Molecular Cancer Research

125

112

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“…Honokiol also exhibits a number of pharmacological actions, including anti-oxidative, anti-microbial, anxiolytic, anti-neoplastic and anti-platelet effects. Several reports also suggest anti-inflammatory and anti-fibrotic roles of honokiol in studies on neutrophils and hepatic fibrosis (Son et al, 2000;Liou et al, 2003;Park et al, 2005). Our recent work also demonstrated that honokiol attenuated experimental anti-Thy1 nephritis and suppressed endothelial cell apoptosis induced by high glucose concentrations, by inhibiting oxidative stress (Chiang et al, 2006;Sheu et al, 2008).…”

Section: Introductionmentioning

confidence: 67%

Honokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro‐inflammatory factors in vivo and in vitro

Chiang

Sheu

Lin

et al. 2011

British J Pharmacology

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BACKGROUND AND PURPOSE Renal fibrosis acts as the common pathway leading to the development of end-stage renal disease. The present study investigated, in vivo and in vitro, the anti-fibrotic and anti-inflammatory effects, particularly on the epithelial to mesenchymal transition of renal tubular cells, exerted by honokiol, a phytochemical used in traditional medicine, and mechanisms underlying these effects. EXPERIMENTAL APPROACH Anti-fibrotic effects in vivo were assayed in a rat model of renal fibrosis [the unilateral ureteral obstruction (UUO) model]. A rat tubular epithelial cell line (NRK-52E) was stimulated by transforming growth factor-beta 1 (TGF-beta 1) and treated with honokiol to explore possible mechanisms of these anti-fibrotic effects. Gene or protein expression was analysed by Northern or Western blotting. Transcriptional regulation was investigated using luciferase activity driven by a connective tissue growth factor (CTGF) promoter. KEY RESULTS Honokiol slowed development of renal fibrosis both in vivo and in vitro. Honokiol treatment attenuated tubulointerstitial fibrosis and expression of pro-fibrotic factors in the UUO model. Honokiol also decreased expression of the mRNA for the chemokine CCL2 and for the intracellular adhesion molecule-1, as well as accumulation of type I (alpha 1) collagen and fibronectin in UUO kidneys. Phosphorylation of Smad-2/3 induced by TGF-beta 1 and CTGF luciferase activity in renal tubular cells were also inhibited by honokiol. CONCLUSIONS AND IMPLICATIONS Honokiol suppressed expression of pro-fibrotic and pro-inflammatory factors and of extracellular matrix proteins. Honokiol may become a therapeutic agent to prevent renal fibrosis

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“…3B, right panel) that was similar to its inhibitory effect on TNF-α production. It has been reported that honokiol blocks iNOS expression at the transcriptional level (9,13). Interestingly, honokiol inhibition appears to be lower in the toll like receptor 2 (TLR2)-mediated signaling pathway.…”

Section: Resultsmentioning

confidence: 99%

Inhibitors of Nitric Oxide Synthesis and TNF-α Expression from Magnolia obovata in Activated Macrophages

Cited by 79 publications

References 11 publications

Honokiol Potentiates Apoptosis, Suppresses Osteoclastogenesis, and Inhibits Invasion through Modulation of Nuclear Factor-κB Activation Pathway

Honokiol Potentiates Apoptosis, Suppresses Osteoclastogenesis, and Inhibits Invasion through Modulation of Nuclear Factor-κB Activation Pathway

Honokiol ameliorates renal fibrosis by inhibiting extracellular matrix and pro‐inflammatory factors in vivo and in vitro

Inhibitory effects of honokiol on LPS and PMA-induced cellular responses of macrophages and monocytes

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