Kolaviron ameliorates behavioural deficit and injury to striatal dopaminergic terminals via modulation of oxidative burden, DJ-1 depletion and CD45R+ cells infiltration in MPTP-model of Parkinson’s disease

Farombi, Ebenezer O.; Awogbindin, Ifeoluwa O.; Owoeye, Olatunde; Abah, Victoria O; Izomoh, Edirin Rosemary; Ezekiel, I.

doi:10.1007/s11011-020-00578-3

Cited by 7 publications

(4 citation statements)

References 52 publications

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“…In line with our findings, it has been shown that KV can alleviate busulfan-induced brain damage via partial suppression of oxidative stress load, apoptosis, and neuroinflammation [ 62 ]. Furthermore, it has been shown that kolaviron can suppress 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced striatal load of oxidative stress, degeneration of dopaminergic neurons besides its down-regulation of caspase 3 in a model of Parkinson's disease [ 63 ]. However, there is no report on the effect of kolaviron on caspase 1 and this still warrants further research studies.…”

Section: Discussionmentioning

confidence: 99%

Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment

Nazari-Serenjeh,

Baluchnejadmojarad,

Hatami-Morassa

et al. 2024

Heliyon

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Section: Discussionmentioning

confidence: 99%

Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment

Nazari-Serenjeh,

Baluchnejadmojarad,

Hatami-Morassa

et al. 2024

Heliyon

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“…Administration of rotenone for 48 h leads to 'parkinsonism' a syndrome characterized by different neurological and neurobehavioral deficits which correlate with Parkinsonian symptoms (Prasad and Hung 2020). KV has been reported to be a promising antioxidant that could be useful in the management of Parkinson's disease (Farombi et al, 2019;Farombi et al, 2020) and clinical evidence of phase II trial of coenzyme Q10 (ubiquinone) against PD has shown that administration of coenzyme Q10, which is an antioxidant, slows the progressive loss of functional deficit seen in PD (Shults et al, 2020) but there is no research in the comparative evaluation between KV and coenzyme Q10 to know if one of the antioxidants could perform better than the other in preclinical studies.…”

Section: Discussionmentioning

confidence: 99%

“…Coenzyme Q10 (Ubiquinone), an electron acceptor for complexes I and II, has been reported to possess neuroprotective effects in multiple in vitro and animal models of neuronal toxicity (Jie, 2014). KV has been reported to be useful in the management of Parkinson's disease and its related behavioral abnormalities Farombi et al, 2020), but there is no study that defines the comparative evaluation and advantage of KV and coenzyme Q10 in rotenone-induced PD. The aim of this research was to assess the comparative pharmacological potential of kolaviron and coenzyme Q10 in rotenoneinduced neurotoxicity in rats' discrete brain regions.…”

Section: Introductionmentioning

confidence: 99%

Comparative influence of kolaviron and coenzyme Q10 on complex I activity, glutamate clearance, 3,4-dihydroxyphenethylamine metabolism, and redox stress in rotenone-induced neurotoxicity

Akinmoladun¹,

Saliu

Abilogun

et al. 2022

NJPS

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3,4-dihydroxyphenethylamine (dopamine) depletion, inhibition of complex I activity, oxidative stress, and glutamate excitotoxicity are cardinal biochemical features of neurotoxicity induced by systemic unilateral infusion of rotenone. Kolaviron (KV), a biflavonoid from Garcinia kola seeds, has been proven to have pharmacological effects against neurotoxicity. Coenzyme Q10 plays an essential role in mitochondrial oxidative phosphorylation and as an antioxidant. This study examined the comparative influence of kolaviron and coenzyme Q10 on complex I activity, dopamine metabolism, glutamate clearance, and redox stress in rotenone-induced neurotoxicity in the cortex, hippocampus, and striatum of the brain of rats. Adult Male Wistar rats were pretreated with 200 mg/kg KV or 100 mg/kg coenzyme Q10 for 7 days followed by administration of a progressive six doses of 1.5 mg/kg rotenone within the next 48 h after which the animals were euthanized and the brain excised. On the cortical, hippocampal, and striatal regions of the brain, complex I activity, dopamine metabolism, oxidative stress markers, as well as glutamate metabolism were carried out and analyzed. In all brain regions examined, KV and coenzyme Q10 pretreatment modulated complex I activity, ameliorated redox imbalance, and enhanced dopamine metabolism via increasing the activity of tyrosine hydroxylase and decreasing monoamine oxidase activity. KV facilitated glutamate clearance through augmentation of glutamate dehydrogenase and glutamine synthetase activities. The activity of KV was comparable to that of the mitochondrial membrane antioxidant compound, coenzyme Q10, this indicates that KV is a promising therapeutic agent in the treatment of Parkinson’s disease and its activity compares well with coenzyme Q10

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“…Mice were administered four doses of 20 mg/kg body weight of MPTP (i.p) on the 8 th day at 2 h interval as previously described. [20] Before this, the mice were treated with corn oil-DMSO solution orally for a week.…”

Section: Group 3 (Mptp)mentioning

confidence: 99%

Neuroprotection of Kolaviron by Regulation of Nuclear Factor Erythroid 2-related Factor 2 in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Mice Model of Parkinson Disease

Awogbindin

Onasanwo

Ezekiel

et al. 2021

AJBPS

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Objectives: Parkinson’s disease (PD) is the most prevalent movement disorder. Available therapies are palliative with no effect on disease progression. We have previously demonstrated that kolaviron (KV), a natural anti-inflammatory and antioxidant agent, suppressed behavioral defect, redo-inflammation, and nigrostriatal pathology in rotenone PD model. The present study investigates the neuroprotective effect of KV focusing on DJ-1/nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. Material and Methods: All-trans retinoic acid (ATRA, 10 mg/kg/day) was used to inhibit Nrf2. PD was established with four doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (20 mg/kg) at 2 h interval. MPTP mice were pre-treated with either KV (200 mg/kg/day), ATRA or both for 7 days before MPTP. Mice were evaluated for locomotor defects and indices of oxidative stress, neuroinflammation and neurotransmission as well as pathological tyrosine hydroxylase expression PD were evaluated in the striatum. Results: ATRA alone in mice did not exhibit neurobehavioral defect but caused striatal toxicity, mild nigrostriatal pathology, significant nitrosative stress, and Nrf2 cascade inhibition. KV+ATRA mice were slow in movement with frequent short-lived interruptions and oxidative striatal pathology. ATRA aggravated MPTP-associated locomotor incompetence and could not prevent nigrostriatal toxicity with evident vacuolated striosome and pyknotic/degenerating dopaminergic neurons. MPTP induced acute locomotor, exploratory, and motor incompetence, which was prevented by KV treatment. In addition, KV treatment restored MPTP-mediated depletion of endogenous antioxidant, striatal nitrosative stress, and oxidative damage with elevated DJ-1 level, potentiated Nrf2/NAD(P)H; quinone oxidoreductase-1 cytoprotective capacity, reduced Kelch-like ECH-associated protein 1 expression, and limited striatal pathology. However, ATRA treatment attenuated all the protective effects of KV on MPTP-challenged mice. Meanwhile, other ATRA-combinations elicited significant DJ-1 and Nrf2 induction but are associated striatal toxicity/pathology. Conclusion: This suggests that KV may be conferring protection through a yet-undetermined DJ-1 downstream cytoprotective effect dependent on the KV-mediated attenuation of oxidative environment.

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Kolaviron ameliorates behavioural deficit and injury to striatal dopaminergic terminals via modulation of oxidative burden, DJ-1 depletion and CD45R+ cells infiltration in MPTP-model of Parkinson’s disease

Cited by 7 publications

References 52 publications

Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment

Kolaviron neuroprotective effect against okadaic acid-provoked cognitive impairment

Comparative influence of kolaviron and coenzyme Q10 on complex I activity, glutamate clearance, 3,4-dihydroxyphenethylamine metabolism, and redox stress in rotenone-induced neurotoxicity

Neuroprotection of Kolaviron by Regulation of Nuclear Factor Erythroid 2-related Factor 2 in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Mice Model of Parkinson Disease

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