Effects of sodium ferulate on amyloid-beta-induced MKK3/MKK6-p38 MAPK-Hsp27 signal pathway and apoptosis in rat hippocampus

Jin, Ying; Fan, Yuxin; Yan, Enzhi; Liu, Zhuo; Zong, Zhi‐Hong; Qi, Zhimin

doi:10.1111/j.1745-7254.2006.00414.x

Cited by 38 publications

(26 citation statements)

References 34 publications

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“…In addition, ferulic acid attenuates iron-induced oxidative damage and apoptosis in cultured neurons [14] and reduces the expression of inducible NOS and cyclooxygenase activity following exposure to lipopolysaccharides [15] . Our previous study showed that SF had protective effects from Aβ-induced neurotoxicity through the suppression of p38 mitogen-activated protein kinase and the upregulation of extracellular signal-regulated kinase (ERK) and Akt [16,17] . In the present study, we investigated the roles of the ERK pathway and phosphatidylinositol 3-kinase (PI3K) pathway in the neuroprotection by SF from glutamate toxicity.…”

Section: +mentioning

confidence: 99%

Neuroprotection by sodium ferulate against glutamate-induced apoptosis is mediated by ERK and PI3 kinase pathways

Jin

Yan

Fan

et al. 2007

Acta Pharmacologica Sinica

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Aim: To investigate whether sodium ferulate (SF) can protect cortical neurons from glutamate-induced neurotoxicity and the mechanisms responsible for this protection. Methods: Cultured cortical neurons were incubated with 50 µmol/L glutamate for either 30 min or 24 h, with or without pre-incubation with SF (100, 200, and 500 µmol/L, respectively). LY294002, wortmannin, PD98059, and U0126 were added respectively to the cells 1 h prior to SF treatment. After incubation with glutamate for 24 h, neuronal apoptosis was quantified by scoring the percentage of cells with apoptotic nuclear morphology after Hoechst 33258 staining. After incubation with glutamate for either 30 min or 24 h, cellular extracts were prepared for Western blotting of active caspase-3, poly (ADP-ribose) polymerase (PARP), µ-calpain, Bcl-2, phospho-Akt, phosphorylated ribosomal protein S6 protein kinase (p70S6K), phospho-mitogen-activated protein kinase kinase (MEK1/2) and phosphorylated extracellular signal-regulated kinase (ERK) 1/2. Results: SF reduced glutamate-evoked apoptotic morphology, active caspase-3 protein expression, and PARP cleavage and inhibited the glutamate-induced upregulation of the µ-calpain protein level. The inhibition of the phosphatidylinositol 3-kinase (PI3K) and the MEK/ERK1/2 pathways partly abrogated the protective effect of SF against glutamate-induced neuronal apoptosis. SF prevented the glutamateinduced decrease in the activity of the PI3K/Akt/p70S6K and the MEK/ERK1/2 pathways. Moreover, incubation of cortical neurons with SF for 30 min inhibited the reduction of the Bcl-2 expression induced by glutamate. Conclusion: The results indicate that PI3K/Akt/p70S6K and the MEK/ERK signaling pathways play important roles in the protective effect of SF against glutamate toxicity in cortical neurons.

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Section: +mentioning

confidence: 99%

Neuroprotection by sodium ferulate against glutamate-induced apoptosis is mediated by ERK and PI3 kinase pathways

Jin

Yan

Fan

et al. 2007

Acta Pharmacologica Sinica

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“…Also, sodium ferulate inhibited a b-amyloid-(1-40)-induced increase in phosphorylated-p38 mitogen-activated protein kinase (MKK3/MKK6), partly prevented a decrease in phosphorylated MAPKAPK2 and Hsp27 expression, and inhibited the activation of caspase cascades (caspase-3, caspase-7 and caspase-3 activities) (67). Sodium ferulate restored the arrangement and the number of hippocampal CA1 pyramidal neurons in the hippocampus of young adult rats subjected to b-amyloid-(1-40) (67) as well as the arrangement of hippocampal CA1 pyramidal neurons in the hippocampus of aged rats (68).…”

Section: Phenolic Acids As Efficient Ache and Bche Inhibitorsmentioning

confidence: 99%

Phenolic acids from malt are efficient acetylcholinesterase and butyrylcholinesterase inhibitors

Szwajgier

Borowiec

2012

J. Inst. Brew.

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Anticholinesterase activities of mashes produced using wheat ('Wheat Pale') or barley malts ('Pilsner', 'Pale Ale', 'Munich Light', 'Carahell' or 'Carared') were studied by spectrophotometric method. The highest inhibition of acetylcholinesterase and butyrylcholinesterase was observed at 52 C and/or 64 C, followed by a decrease or stabilization of the activity at 72 C. Changes in the total phenolics content in the test mashes were correlated with changes in the acetylcholinesterase and/or butyrylcholinesterase activities. Phenolic acids were singled out from phenolic compounds for more detailed studies owing to their simplicity and structural similarity to well-known cholinesterase inhibitors. The main phenolic acids in the test malts were ferulic, gallic, p-coumaric and vanillic acids followed by chlorogenic, caffeic, syringic, p-OH-benzoic, sinapic and protocatechuic acids. The anticholinesterase activities of the phenolic acids were studied using model standard solutions at concentrations similar to the maximal content of these compounds in the test mashes. Among the phenolic acids, p-coumaric acid had the largest share in the anticholinesterase activity, even though it was present in the test mashes at a significantly lower concentration (~0.38 mM L À1 ) than ferulic acid (~1.00 mM L À1 ). Sinapic acid and p-OH-benzoic acid (0.03 and 0.01 mM L À1 , respectively) were equally efficient inhibitors as ferulic acid at~1.00 mM L À1 . This preliminary study should be extended to other phenolic compounds from malt (wort) in the near future.

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“…Sodium ferulate is shown to prevent amyloid beta-induced mitogen-activated protein kinase kinase (MKK) 3/MKK6-p38 MAPK activity in rat hippocampus (Jin et al 2006), showing the suppression of the age-related Jun N-terminal kinase (JNK) pathway and upregulation of mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK)1/2 pathway in aged rat hippocampus (Jin et al 2008). In human umbilical vein endothelial cells (HUVECs), ferulate blocked the JNK pathway, but did not change the ERK (Ma et al 2010a).…”

Section: Introductionmentioning

confidence: 99%

Attenuation of age-related changes in FOXO3a activity and the PI3K/Akt pathway by short-term feeding of ferulate

Choi

Kim

Lee

et al. 2011

AGE

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Ferulate (4-hydroxy-3-methoxycinnamic acid) is a well-known phenolic compound that scavenges free radicals and exerts anti-inflammatory effects. Forkhead box O3a (FOXO3a), a transcription factor that plays important roles in aging processes, decreases with age and is negatively regulated through phosphorylation by phosphatidylinositol 3-kinase (PI3K)/Akt signaling. The present study investigated the efficacy of short-term ferulate feeding on age-related changes in PI3K/Akt/FOXO3a and upstream insulin signaling pathways in aged rats. In addition, changes in manganese superoxide dismutase (MnSOD) and catalase expression were examined because of their dependence on PI3K/Akt/FOXO3a activity. Short-term feeding experiments were done with a diet containing ferulate that was given to aged rats at doses of 3 or 6 mg kg −1 day −1 for 10 days.Results showed that FOXO3a activity was increased in the ferulate-fed old group compared with the control old group. Also, ferulate suppressed the PI3K/Akt signaling pathway that is responsible for FOXO3a inhibition in aged rats. Plasma insulin levels and the upstream insulin signaling pathway were also modulated by ferulate correspondingly with PI3K/ Akt/FOXO3a activity. The age-related decrease in two major antioxidant enzymes, MnSOD and catalase, was blunted by ferulate, which was accompanied by FOXO3a transcriptional activity. The significance of the present study is the finding that short-term feeding of ferulate effectively modulates age-related renal FOXO3a, PI3K/Akt and insulin signaling pathways, and MnSOD and catalase expression, all of which may be beneficial for attenuating the aging process.

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Effects of sodium ferulate on amyloid-beta-induced MKK3/MKK6-p38 MAPK-Hsp27 signal pathway and apoptosis in rat hippocampus

Cited by 38 publications

References 34 publications

Neuroprotection by sodium ferulate against glutamate-induced apoptosis is mediated by ERK and PI3 kinase pathways

Neuroprotection by sodium ferulate against glutamate-induced apoptosis is mediated by ERK and PI3 kinase pathways

Phenolic acids from malt are efficient acetylcholinesterase and butyrylcholinesterase inhibitors

Attenuation of age-related changes in FOXO3a activity and the PI3K/Akt pathway by short-term feeding of ferulate

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