Honokiol protects rat brain from focal cerebral ischemia–reperfusion injury by inhibiting neutrophil infiltration and reactive oxygen species production

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

doi:10.1016/j.brainres.2003.08.026

Cited by 142 publications

(108 citation statements)

References 35 publications

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“…The infarct volume induced by CI/R injury in this study (around 20% of the right brain hemisphere) was comparable with that of our previous reports [20,27]. Taxifolin (0.1-1.0 lg/kg) dosedependently ameliorated CI/R-induced brain infarction by 40-65% (Figure 1 upper panel, one-way ANOVA, p<0.05).…”

Section: Protective Effect Of Taxifolin Against Ci/r-induced Cerebralsupporting

confidence: 91%

“…We previously reported that enhancement of MPO activity in CI/R-injured brain closely paralleled cerebral MDA formation in infarct tissue in a time-dependent manner [27]. In this study, CI/R induced-leukocyte infiltration, as measured by MPO activity in the cerebral infarct area, peaked at 24 h, which was comparable to the result of our previous report [27].…”

Section: Effects Of Taxifolin On Ci/r-induced Cox-2 and Inos Expressisupporting

confidence: 90%

“…In this study, CI/Rinduced cerebral lipid peroxidation, as assayed by MDA formation, occurred in a time-dependent manner that peaked at 24 h as in our previous report [27]. Taxifolin dose-dependently prevented CI/R-induced MDA formation (Figure 1 lower panel, one-way ANOVA, p<0.05, n=10 for each group).…”

Section: Protective Effects Of Taxifolin Against Ci/r-induced Oxidatisupporting

confidence: 84%

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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: Protective Effect Of Taxifolin Against Ci/r-induced Cerebralsupporting

confidence: 91%

Section: Effects Of Taxifolin On Ci/r-induced Cox-2 and Inos Expressisupporting

confidence: 90%

Section: Protective Effects Of Taxifolin Against Ci/r-induced Oxidatisupporting

confidence: 84%

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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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“…13 In addition, several groups have shown that mice deficient in the gp91 subunit of NOX2 have smaller infarcts than do wild-type mice, [27][28][29] and that outcomes from experimental cerebral ischemiareperfusion are improved with early administration of the pharmacological NOX inhibitors apocynin 29 -33 and honokiol. 34,35 These results identify NOX as a promising target for therapeutic intervention, but it is possible that the efficacy of these treatment strategies may be due largely or in part to inhibition of NOX in cell types other than microglia. 25 There are as yet no published studies addressing the efficacy of NOX inhibitors administered at delayed time points after ischemia, in a manner selectively targeting the inflammatory response.…”

Section: Superoxide Productionmentioning

confidence: 99%

Microglial Activation in Stroke: Therapeutic Targets

2010

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Summary:Microglial activation is an early response to brain ischemia and many other stressors. Microglia continuously monitor and respond to changes in brain homeostasis and to specific signaling molecules expressed or released by neighboring cells. These signaling molecules, including ATP, glutamate, cytokines, prostaglandins, zinc, reactive oxygen species, and HSP60, may induce microglial proliferation and migration to the sites of injury. They also induce a nonspecific innate immune response that may exacerbate acute ischemic injury. This innate immune response includes release of reactive oxygen species, cytokines, and proteases. Microglial activation requires hours to days to fully develop, and thus presents a target for therapeutic intervention with a much longer window of opportunity than acute neuroprotection. Effective agents are now available for blocking both microglial receptor activation and the microglia effector responses that drive the inflammatory response after stroke. Effective agents are also available for targeting the signal transduction mechanisms linking these events. However, the innate immune response can have beneficial as well deleterious effects on outcome after stoke, and a challenge will be to find ways to selectively suppress the deleterious effects of microglial activation after stroke without compromising neurovascular repair and remodeling.

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“…1A) (1,2). HNK has long been known to have antithrombosis, antibacterial and anxiolytic effects (3)(4)(5)(6). However, its antitumor activities have only recently been described.…”

Section: Introductionmentioning

confidence: 99%

Honokiol, a natural biphenyl, inhibits in vitro and in vivo growth of breast cancer through induction of apoptosis and cell cycle arrest

Wolf¹,

O’Kelly

Wakimoto

et al. 2007

Int J Oncol

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Abstract. Honokiol (HNK), a naturally occurring biphenyl, possesses potent antineoplastic and antiangiogenic properties. We investigated the in vitro and in vivo activity of HNK against breast cancer. HNK exhibited potent anti-proliferative activity against breast cancer cell lines and enhanced the activity of other drugs used for the treatment of breast cancer. In vivo, HNK was highly effective against breast cancer in nude mice. We identified two different effects of HNK on breast cancer cells: cell cycle inhibition, observed at lower doses of HNK, and induction of apoptosis, observed at higher doses of the compound. Our data suggest that HNK is a systemically available, non-toxic inhibitor of breast cancer growth and should be examined for clinical applications.

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Honokiol protects rat brain from focal cerebral ischemia–reperfusion injury by inhibiting neutrophil infiltration and reactive oxygen species production

Cited by 142 publications

References 35 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

Microglial Activation in Stroke: Therapeutic Targets

Honokiol, a natural biphenyl, inhibits in vitro and in vivo growth of breast cancer through induction of apoptosis and cell cycle arrest

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