Ferulic acid provides neuroprotection against oxidative stress-related apoptosis after cerebral ischemia/reperfusion injury by inhibiting ICAM-1 mRNA expression in rats

Cheng, Chin-Yi; Su, Shan-Yu; Tang, Nou Ying; Ho, Tin Yun; Chiang, Su‐Yin; Hsieh, Ching Liang

doi:10.1016/j.brainres.2008.02.090

Cited by 200 publications

(131 citation statements)

References 46 publications

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“…Previous studies indicated that the administration of FA at the beginning of cerebral ischemia time point possesses anti-oxidative and anti-apoptotic effects in MCAo model [14,41] . Our data further suggest that FA provides a potential therapeutic modality to extend the time window in ischemic stroke-induced apoptosis and is a promising drug worthy of further investigation.…”

Section: Discussionmentioning

confidence: 98%

“…Toxic NO-mediated oxidative/nitrative stress during cerebral I/R injury may contribute to the activation of the apoptotic cascade [11] . In vitro studies [5,12] have demonstrated that the NO-induced apoptotic signaling cascade involves mitogen-activated protein (MAP) kinase-mediated Bax translocation from the cytosol to the mitochondria and subsequent caspase-3 activation in cultured In previous studies, FA reduces cerebral ischemic injury by weakening the expression of PSD-95 in the ischemic area and provides neuroprotection against apoptosis partly via inhibiting intercellular adhesion molecule-1 (ICAM-1) mRNA expression in a transient middle cerebral artery occlusion (MCAo) model [13,14] . In addition, FA inhibits glutamate-induced apoptosis through modulation of the MAP kinase signaling pathway in cultured cortical neurons [15] .…”

Section: Introductionmentioning

confidence: 99%

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Ferulic acid inhibits nitric oxide-induced apoptosis by enhancing GABAB1 receptor expression in transient focal cerebral ischemia in rats

Cheng

Tang

et al. 2010

Acta Pharmacol Sin

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Aim: Ferulic acid (4-hydroxy-3-methoxycinnamic acid, FA) provides neuroprotection against apoptosis in a transient middle cerebral artery occlusion (MCAo) model. This study was to further investigate the anti-apoptotic effect of FA during reperfusion after cerebral ischemia. Methods: Rats were subjected to 90 min of cerebral ischemia followed by 3 or 24 h of reperfusion after which they were sacrificed. Results: Intravenous FA (100 mg/kg) administered immediately after middle cerebral artery occlusion (MCAo) or 2 h after reperfusion effectively abrogated the elevation of postsynaptic density-95 (PSD-95), neuronal nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS), nitrotyrosine, and cleaved caspase-3 levels as well as apoptosis in the ischemic cortex at 24 h of reperfusion. FA further inhibited Bax translocation, cytochrome c release, and p38 mitogen-activated protein (MAP) kinase phosphorylation. Moreover, FA enhanced the expression of gamma-aminobutyric acid type B receptor subunit 1 (GABA B1 ) in the ischemic cortex at 3 and 24 h of reperfusion. In addition, nitrotyrosine-positive cells colocalized with cleaved caspase-3-positive cells, and phospho-p38 MAP kinasepositive cells colocalized with nitrotyrosine-and Bax-positive cells, indicating a positive relationship among the expression of nitrotyrosine, phospho-p38 MAP kinase, Bax, and cleaved caspase-3. The mutually exclusive expression of GABA B1 and nitrotyrosine revealed that there is a negative correlation between GABA B1 and nitrotyrosine expression profiles. Additionally, pretreatment with saclofen, a GABA B receptor antagonist, abolished the neuroprotection of FA against nitric oxide (NO)-induced apoptosis. Conclusion: FA significantly enhances GABA B1 receptor expression at early reperfusion and thereby provides neuroprotection against p38 MAP kinase-mediated NO-induced apoptosis at 24 h of reperfusion.Keywords: ferulic acid; neuronal nitric oxide synthase; inducible nitric oxide synthase; Bax; p38 mitogen-activated protein kinase; nitric oxide-induced apoptosis

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Ferulic acid inhibits nitric oxide-induced apoptosis by enhancing GABAB1 receptor expression in transient focal cerebral ischemia in rats

Cheng

Tang

et al. 2010

Acta Pharmacol Sin

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“…Ferulic acid (FA) is a phytochemical commonly found in many herbs used in traditional Chinese medicine (5). FA exhibits a wide range of therapeutic effects against various diseases like cancer, diabetes, and cardiovascular and neurodegenerative diseases (6,7). A wide spectrum of benefits to human health has been attributed to this phenolic compound, at least in part, because of its strong antioxidant activity (8).…”

Section: Introductionmentioning

confidence: 99%

Ferulic acid induces heme oxygenase-1 <i>via</i> activation of ERK and Nrf2

Qian

Wang

et al. 2011

DD&T

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“…The neuroprotection of phenolic acids in the central nervous system of experimental animals has been observed in numerous experiments (e.g. CHENG et al, 2008). It has been previously noted that phenolic acids can interact with proteins, especially those rich in proline, via hydrophobic or hydrogen bonding (HASLAM & LILLEY, 1988).…”

mentioning

confidence: 99%

The effect of the addition of selected phenolic acids on the rheological properties of heated solutions of whey proteins

Szwajgier¹,

Gustaw²

2015

Acta Alimentaria

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This study measured the fl ow behaviour of whey protein isolate mixtures with cinnamic or ferulic acids. Samples were heated in a vacuum (80 C, -0.9 atm, 280 r.p.m., 0.5 h). The fl ow curves of all samples showed a nonNewtonian shear thinning fl ow and the viscoelastic properties were typical for weak gel systems. At pH 6.0, 6.7, and 8.0, the highest shear stress values were obtained with 20, 40, and 40 mg of cinnamic acid g -1 protein, respectively. At pH 6.0, the use of ferulic acid (20 mg g -1 protein) resulted in the elevation of shear stress values, but at pH 8.0, ferulic acid caused a decrease in shear stress values in comparison to cinnamic acid. The thixotropic area (A T ) was increased in mixtures containing 20-40 mg cinnamic acid g -1 protein (at pH 6.7) and 20 mg of cinnamic acid g -1 protein (at pH 6.0). Similarly, the addition of ferulic acid (40 and 20 mg g -1 protein at pH 6.7 and 6.0, respectively) caused a signifi cant increase in A T . At pH 8.0, no signifi cant differences in A T values were observed between samples. Such systems can be applied with reference to health promoting foods such as WPI-based desserts.

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Ferulic acid provides neuroprotection against oxidative stress-related apoptosis after cerebral ischemia/reperfusion injury by inhibiting ICAM-1 mRNA expression in rats

Cited by 200 publications

References 46 publications

Ferulic acid inhibits nitric oxide-induced apoptosis by enhancing GABAB1 receptor expression in transient focal cerebral ischemia in rats

Ferulic acid inhibits nitric oxide-induced apoptosis by enhancing GABAB1 receptor expression in transient focal cerebral ischemia in rats

Ferulic acid induces heme oxygenase-1 <i>via</i> activation of ERK and Nrf2

The effect of the addition of selected phenolic acids on the rheological properties of heated solutions of whey proteins

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