The anti-inflammatory effect of honokiol on neutrophils: mechanisms in the inhibition of reactive oxygen species production

Liou, Kuo Tong; Shen, Yuh Chiang; Chen, Chieh Fu; Tsao, Cheng Ming; Tsai, Shen Kou

doi:10.1016/s0014-2999(03)02121-6

Cited by 158 publications

(107 citation statements)

References 36 publications

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“…The present study together with our previous results [38] confirmed that CI/R-induced infarction developed along with leukocyte infiltration into the infarct area that also paralleled cerebral lipid peroxidation in the infarct area, indicating that oxidative stress elicited by leukocytes did contribute to the infarction. Taxifolin dose-dependently prevented CI/R-induced leukocyte accumulation (Table 1) and effectively decreased the ROS produced by leukocytes (Table 2), and ROS and NO produced by microglial cells (Table 3), revealing that the anti-oxidative effect is responsible for taxifolin's protective effects, and taxifolin could exert its protective effects by modulating inflammatory cells including microglial cells and leukocytes.…”

Section: Discussionsupporting

confidence: 90%

Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation

Wang¹,

et al. 2005

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SummaryInfarction in adult rat brain was induced by middle cerebral arterial occlusion (MCAO) followed by reperfusion to examine whether taxifolin could reduce cerebral ischemic reperfusion (CI/R) injury. Taxifolin administration (0.1 and 1.0 lg/kg, i.v.) 60 min after MCAO ameliorated infarction (by 42%±7% and 62%±6%, respectively), which was accompanied by a dramatic reduction in malondialdehyde and nitrotyrosine adduct formation, two markers for oxidative tissue damage. Overproduction of reactive oxygen species (ROS) and nitric oxide (NO) via oxidative enzymes (e.g., COX-2 and iNOS) was responsible for this oxidative damage. Taxifolin inhibited leukocyte infiltration, and COX-2 and iNOS expressions in CI/R-injured brain. Taxifolin also prevented Mac-1 and ICAM-1 expression, two key counter-receptors involved in firm adhesion/transmigration of leukocytes to the endothelium, which partially accounted for the limited leukocyte infiltration. ROS, generated by leukocytes and microglial cells, activated nuclear factor-kappa B (NF-jB) that in turn signaled up-regulation of inflammatory proteins. NF-jB activity in CI/R was enhanced 2.5-fold over that of sham group and was inhibited by taxifolin. Production of both ROS and NO by leukocytes and microglial cells was significantly antagonized by taxifolin. These data suggest that amelioration of CI/R injury by taxifolin may be attributed to its antioxidative effect, which in turn modulates NF-jB activation that mediates CI/R injury.

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Section: Discussionsupporting

confidence: 90%

Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation

Wang¹,

et al. 2005

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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: Introductionsupporting

confidence: 61%

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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“…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%

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

126

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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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The anti-inflammatory effect of honokiol on neutrophils: mechanisms in the inhibition of reactive oxygen species production

Cited by 158 publications

References 36 publications

Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation

Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation

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

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

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