Ferulic acid prevents cerebral ischemic injury‐induced reduction of hippocalcin expression

Koh, Phil-Ok

doi:10.1002/syn.21649

Cited by 25 publications

(12 citation statements)

References 26 publications

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“…Studies of the neuroprotection have been performed in both HT22 cells and middle cerebral artery occlusion (MCAO)-induced injury [ 20 , 21 ]. However memory deficits are also frequently noted after stroke.…”

Section: Introductionmentioning

confidence: 99%

Neuroprotection and spatial memory enhancement of four herbal mixture extract in HT22 hippocampal cells and a mouse model of focal cerebral ischemia

Ahn

Kim

et al. 2015

BMC Complement Altern Med

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BackgroundFour traditional Korean medicinal herbs which act in retarding the aging process, Polygonum multiflorum Thunb., Rehmannia glutinosa (Gaertn) Libosch., Polygala tenuifolia Willd., and Acorus gramineus Soland., were prepared by systematic investigation of Dongeuibogam (Treasured Mirror of Eastern Medicine), published in the early 17th century in Korea. This study was performed to evaluate beneficial effects of four herbal mixture extract (PMC-12) on hippocampal neuron and spatial memory.MethodsHigh performance liquid chromatography (HPLC) analysis was performed for standardization of PMC-12. Cell viability, lactate dehydrogenase, flow cytometry, reactive oxygen species (ROS), and Western blot assays were performed in HT22 hippocampal cells and immunohistochemistry and behavioral tests were performed in a mouse model of focal cerebral ischemia in order to observe alterations of hippocampal cell survival and subsequent memory function.ResultsIn the HPLC analysis, PMC-12 was standardized to contain 3.09 % 2,3,5,4′-tetrahydroxystilbene-2-O-β-D-glucoside, 0.35 % 3′,6-disinapoyl sucrose, and 0.79 % catalpol. In HT22 cells, pretreatment with PMC-12 resulted in significantly reduced glutamate-induced apoptotic cell death. Pretreatment with PMC-12 also resulted in suppression of ROS accumulation in connection with cellular Ca2+ level after exposure to glutamate. Expression levels of phosphorylated p38 mitogen-activated protein kinases (MAPK) and dephosphorylated phosphatidylinositol-3 kinase (PI3K) by glutamate exposure were recovered by pretreatment with either PMC-12 or anti-oxidant N-acetyl-L-cysteine (NAC). Expression levels of mature brain-derived neurotrophic factor (BDNF) and phosphorylated cAMP response element binding protein (CREB) were significantly enhanced by treatment with either PMC-12 or NAC. Combination treatment with PMC-12, NAC, and intracellular Ca2+ inhibitor BAPTA showed similar expression levels. In a mouse model of focal cerebral ischemia, we observed higher expression of mature BDNF and phosphorylation of CREB in the hippocampus and further confirmed improved spatial memory by treatment with PMC-12.ConclusionsOur results suggest that PMC-12 mainly exerted protective effects on hippocampal neurons through suppression of Ca2+-related ROS accumulation and regulation of signaling pathways of p38 MAPK and PI3K associated with mature BDNF expression and CREB phosphorylation and subsequently enhanced spatial memory.

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Section: Introductionmentioning

confidence: 99%

Neuroprotection and spatial memory enhancement of four herbal mixture extract in HT22 hippocampal cells and a mouse model of focal cerebral ischemia

Ahn

Kim

et al. 2015

BMC Complement Altern Med

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“…Recently, FA has been shown to prevent DA neurons from MPTP-induced toxicity, inhibits Alzheimer-like pathology, and cerebral ischemia, suggesting that this compound has beneficial effect on neurons and it can cross the blood–brain barrier to provide such effects to the brain. 15 , 18 , 21 , 22 …”

Section: Discussionmentioning

confidence: 99%

“… 12 – 21 The neuroprotective effect of FA has been reported in many experimental studies including brain injury, spinal ischemia, and Alzheimer-like pathology. 15 , 16 , 18 …”

Section: Introductionmentioning

confidence: 99%

Neuroprotective potential of ferulic acid in the rotenone model of Parkinson’s disease

Ojha

Javed

Azimullah

et al. 2015

DDDT

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Parkinson’s disease (PD) is a chronic, progressive, and the second most common form of neurodegenerative disorders. In order to explore novel agents for the treatment of PD, in the current study, we have evaluated the neuroprotective efficacy of ferulic acid (FA) using rotenone (ROT)-induced rat model of PD. ROT was administered 2.5 mg/kg body weight to male Wistar rats for 4 weeks to induce the PD. Since PD is progressive and chronic in nature, the paradigm for evaluating FA was based on chronic administration for 4 weeks at the dose of 50 mg/kg, 30 minutes prior to ROT administration. ROT administration caused significant reduction in endogenous antioxidants such as superoxide dismutase, catalase, and glutathione. ROT challenge-induced lipid peroxidation evidenced by increased malondialdehyde following perturbation of antioxidant defense. Apart from oxidative stress, ROT also activated proinflammatory cytokines and enhanced inflammatory mediators such as cyclooxygenase-2 and inducible nitric oxide synthase. The immunofluorescence analysis revealed a significant increase in the number of activated microglia and astrocytes accompanied by a significant loss of dopamine (DA) neurons in the substantia nigra pars compacta area upon ROT injection. However, treatment with FA rescued DA neurons in substantia nigra pars compacta area and nerve terminals in the striatum from the ROT insult. FA treatment also restored antioxidant enzymes, prevented depletion of glutathione, and inhibited lipid peroxidation. Following treatment with FA, the inflammatory mediators such as cyclooxygenase-2 and inducible nitric oxide synthase and proinflammatory cytokines were also reduced. Further, the results were supported by a remarkable reduction of Iba-1 and GFAP hyperactivity clearly suggests attenuation of microglial and astrocytic activation. Results of our study suggest that FA has promising neuroprotective effect against degenerative changes in PD, and the protective effects are mediated through its antioxidant and anti-inflammatory properties.

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“…Ferulic acid exerts a neuroprotective effect in cerebral ischemia through its anti-oxidant and anti-inflammation activity. 35,36) Its protective effect might come from the sustained NO supplying and the anti-oxidant activity of acetyl ferulic acid.…”

Section: )mentioning

confidence: 99%

Anti-hypoxia Activity of the Novel NO Donor Acetyl Ferulic Isosorbide Mononitrate in Acute High-Altitude Hypoxia Mice

Fan

Jiang

et al. 2015

Biological & Pharmaceutical Bulletin

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Nitric oxide (NO) may act as either a pro-oxidant or an antioxidant in biological systems. Previous work has found inhalation of NO improved survival in a high altitude rat model. NO donor isosorbide mononitrate derivants might have a protective effect against hypoxia. We synthesized a series of isosorbide mononitrate derivant compounds to test their anti-hypoxia activities. Normobaric hypoxia and hypobaric hypoxia models were used to study the protective role of NO donor in mice. The results showed isosorbide mononitrate derivants had protective effects in hypoxia mice. Among those compounds, acetyl ferulic isosorbide mononitrate (AFIM) was the most effective. It prolonged the survival time during the normobaric hypoxia test. It decreased malondialdehyde (MDA) and H 2 O 2 in hypobaric hypoxia mice. The antioxidase activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) remained in normal ranges in the AFIM group. As a sign of mitochondrial dysfunction, the activities of ATPase were down regulated in mice under hypobaric hypoxia conditions. AFIM also protected ATPase activities. The protective effects of AFIM might come from a sustained NO supply and the release of acetyl ferulic acid with anti-oxidant activity.Key words altitude; hypoxia; nitric oxide; acetyl ferulic isosorbide mononitrate More than 140 M persons lives at above 2500 m (the conventional definition of high altitude as that where arterial O 2 saturation (SaO 2 ) measurably begins to fall).1) Barometric pressure falls with increasing altitude and consequently there is a reduction in the partial pressure of oxygen resulting in a hypoxic challenge to any individual ascending to altitude. With the ever increasing number of people ascending to high altitudes, medicines to deal with potential problems are becoming increasingly relevant to non-specialists, including general practitioners.A spectrum of high altitude illnesses can occur when the hypoxic stress outstrips the subject's ability to acclimatize. Acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) strike people who travel too fast to high altitudes that lie beyond their current level of acclimatization. 2)AMS is a condition affecting otherwise healthy individuals on going rapidly to altitude. A spectrum of symptoms related to acute mountain sickness may develop at altitudes below 3000 m: commonly reported symptoms are nausea, vomiting, headache, dizziness, fatigue, and sleep disturbance. 3)Acute hypoxia induces pulmonary vascular permeability and contributes to forms of noncardiogenic pulmonary edema such as high altitude pulmonary edema and acute respiratory distress syndrome.4,5) AMS can sharply limit recreation and work at high altitude, especially in the first few days following arrival at a new, higher altitude, and if AMS worsens and HACE develops, the risk of fatality is significant. 6) Although slow ascent to altitude remained the most important measure to prevent acute mountain sickness, evidence from the literature on high altitude...

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Ferulic acid prevents cerebral ischemic injury‐induced reduction of hippocalcin expression

Cited by 25 publications

References 26 publications

Neuroprotection and spatial memory enhancement of four herbal mixture extract in HT22 hippocampal cells and a mouse model of focal cerebral ischemia

Neuroprotection and spatial memory enhancement of four herbal mixture extract in HT22 hippocampal cells and a mouse model of focal cerebral ischemia

Neuroprotective potential of ferulic acid in the rotenone model of Parkinson’s disease

Anti-hypoxia Activity of the Novel NO Donor Acetyl Ferulic Isosorbide Mononitrate in Acute High-Altitude Hypoxia Mice

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Ferulic acid prevents cerebral ischemic injury‐induced reduction of hippocalcin expression

Cited by 25 publications

References 26 publications

Neuroprotection and spatial memory enhancement of four herbal mixture extract in HT22 hippocampal cells and a mouse model of focal cerebral ischemia

Neuroprotection and spatial memory enhancement of four herbal mixture extract in HT22 hippocampal cells and a mouse model of focal cerebral ischemia

Neuroprotective potential of ferulic acid in the rotenone model of Parkinson&rsquo;s disease

Anti-hypoxia Activity of the Novel NO Donor Acetyl Ferulic Isosorbide Mononitrate in Acute High-Altitude Hypoxia Mice

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Neuroprotective potential of ferulic acid in the rotenone model of Parkinson’s disease