Ferulic acid pretreatment mitigates MPTP-induced motor impairment and histopathological alterations in C57BL/6 mice

Sangeetha, N.; Chellappan, David Raj; Chinnaswamy, Prabu; Thulasingam, Senthilkumar

doi:10.3109/13880209.2014.993041

Cited by 47 publications

(34 citation statements)

References 38 publications

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“…[16]; dose-dependent amelioration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced loss of nigrostriatal dopaminergic neurons, the decrease of the Bax/Bcl2 ratio, reduction of pro-apoptotic protein Bax levels and increased expression of anti-apoptotic protein Bcl2 in PD C57BI/6 mice model (ferulic acid was given via injections for 7 days, at a dose of 20, 40 and 80 mg/kg) [17];…”

Section: Figurementioning

confidence: 99%

The Neuroprotective Effects of Phenolic Acids: Molecular Mechanism of Action

2017

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The neuroprotective role of phenolic acids from food has previously been reported by many authors. In this review, the role of phenolic acids in ameliorating depression, ischemia/reperfusion injury, neuroinflammation, apoptosis, glutamate-induced toxicity, epilepsy, imbalance after traumatic brain injury, hyperinsulinemia-induced memory impairment, hearing and vision disturbances, Parkinson’s disease, Huntington’s disease, anti-amyotrophic lateral sclerosis, Chagas disease and other less distributed diseases is discussed. This review covers the in vitro, ex vivo and in vivo studies concerning the prevention and treatment of neurological disorders (on the biochemical and gene expression levels) by phenolic acids.

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Section: Figurementioning

confidence: 99%

The Neuroprotective Effects of Phenolic Acids: Molecular Mechanism of Action

2017

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“…Importantly, very recent studies have shown that FA attenuated neuroinflammation and improved behavioral deficits against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. 21 , 22 MPTP is mainly used to develop PD model in mice and nonhuman primates. However, for unknown reasons, among rodents the rats are resistant, but mouse specifically C57BL/6 strain, is highly sensitive to MPTP.…”

Section: Introductionmentioning

confidence: 99%

“… 23 Previous studies show that intraperitoneally administered MPTP (25–30 mg/kg body weight) once daily for five consecutive days leads to the development of Parkinsonism in mice. 22 , 24 Administration of these doses of MPTP for very short duration is considered as an acute model of PD. Moreover, MPTP model shows nonprogressive mode of cell death, motor impairments, and lack of intracytoplasmic inclusion of α-synuclein.…”

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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“…Catalepsy test is a widely used noninvasive method designed to evaluate mouse limb strength . It has also been used to investigate the effects of neuromuscular disorders .…”

Section: Discussionmentioning

confidence: 99%

“…The production of catalepsy in animals by neuroleptic drugs is adduced to the inhibition of dopaminergic function and is antagonized by dopaminergic agonists . Both clinical and experimentally induced motor side effects and catalepsies have been shown to respond to dopamine receptor agonists . In contrast, the antagonists of D2 receptors or muscarinic receptor agonists exhibit opposite effects .…”

Section: Discussionmentioning

confidence: 99%

Amlodipine, an L‐type calcium channel blocker, protects against chlorpromazine‐induced neurobehavioural deficits in mice

Kale

Awodele

Ogundare

et al. 2017

Fundamemntal Clinical Pharma

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This study investigated the modulatory and chemopreventive benefit of amlodipine (AML), a dihydropyridine calcium channel antagonist, against neurobehavioural abnormalities (NAs) associated with chlorpromazine (CPZ) toxicity in mice. Adult mice were divided into five groups of six animals/group. Group 1 (control) was administered saline (10 mL/kg i.p.). Group 2 received CPZ (2 mg/kg i.p.). Groups 3 and 4 received bromocriptine (BMC, 2.5 mg/kg s.c.) and AML (1 mg/kg s.c.), respectively, while group 5 received their combination. Groups 3-5 later received CPZ 30 min after initial treatments. Animals were subjected to neurobehavioural tests and euthanized 18 h later. CPZ-induced NAs were characterized by significant increase (P < 0.001) in cataleptic behaviour and lowered (P < 0.05) spontaneous activity reaction time in mice. There were also significant (P < 0.001) increases in malondialdehyde levels and decreased locomotion plus learning and memory parameters (P < 0.05-0.001). AML pretreatment alone did not alleviate CPZ-induced motor deficits in the mice. While pretreatment with BMC alone attenuated CPZ-associated catalepsy, its combination with AML further protected mice against NAs. Furthermore, BMC pretreatment did not affect CPZ-induced increase in malondialdehyde level, but AML or BMC+AML significantly (P < 0.05) decreased malondialdehyde in the CPZ-treated rats. Reduced glutathione levels and activities of superoxide dismutase and catalase remained elevated in all treatment groups. In conclusion, data from this study suggest possible chemopreventive benefit of AML alone or in combination with BMC against CPZ-associated neurobehavioural deficits. The ameliorative effect of AML may be related to its antioxidant and/or calcium channel blocking property.

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Ferulic acid pretreatment mitigates MPTP-induced motor impairment and histopathological alterations in C57BL/6 mice

Abstract: This study provides elementary evidence for the neuroprotective action of FA against MPTP-induced PD in mice and warrants further studies.

Cited by 47 publications

References 38 publications

The Neuroprotective Effects of Phenolic Acids: Molecular Mechanism of Action

The Neuroprotective Effects of Phenolic Acids: Molecular Mechanism of Action

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

Amlodipine, an L‐type calcium channel blocker, protects against chlorpromazine‐induced neurobehavioural deficits in mice

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Ferulic acid pretreatment mitigates MPTP-induced motor impairment and histopathological alterations in C57BL/6 mice

Abstract: This study provides elementary evidence for the neuroprotective action of FA against MPTP-induced PD in mice and warrants further studies.

Cited by 47 publications

References 38 publications

The Neuroprotective Effects of Phenolic Acids: Molecular Mechanism of Action

The Neuroprotective Effects of Phenolic Acids: Molecular Mechanism of Action

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

Amlodipine, an L‐type calcium channel blocker, protects against chlorpromazine‐induced neurobehavioural deficits in mice

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