Protective effect of vinpocetine against neurotoxicity of manganese in adult male rats

Nadeem, Rania I.; Ahmed, Hebatalla I.; El-Sayeh, Bahia M.

doi:10.1007/s00210-018-1498-0

Cited by 33 publications

(15 citation statements)

References 96 publications

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“…Our findings also agree with earlier findings on the ability of plant alkaloid extracts to ameliorate Mn-induced impairment in the locomotor performance and survival rate of D. melanogaster [14, 38]. Furthermore, it has also been reported that plant alkaloid extract ameliorated Mn-induced neurotoxicity in rats [39, 40].…”

Section: Resultssupporting

confidence: 93%

Effect of Alkaloid Extract from African Jointfir (Gnetum africanum) Leaves on Manganese‐Induced Toxicity in Drosophila melanogaster

Oboh

Ogunsuyi

Awonyemi

et al. 2018

Oxidative Medicine and Cellular Longevity

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Metal-induced toxicity in fruit fly (Drosophila melanogaster) is one of the established models for studying neurotoxicity and neurodegenerative diseases. Phytochemicals, especially alkaloids, have been reported to exhibit neuroprotection. Here, we assessed the protective effect of alkaloid extract from African Jointfir (Gnetum africanum) leaf on manganese- (Mn-) induced toxicity in wild type fruit fly. Flies were exposed to 10 mM Mn, the alkaloid extract and cotreatment of Mn plus extract, respectively. The survival rate and locomotor performance of the flies were assessed 5 days posttreatment, at which point the flies were homogenized and assayed for acetylcholinesterase (AChE) activity, nitric oxide (NO), and reactive oxygen species (ROS) levels. Results showed that the extract significantly reverted Mn-induced reduction in the survival rate and locomotor performance of the flies. Furthermore, the extract counteracted the Mn-induced elevation in AChE activity, NO, and ROS levels. The alkaloid extract of the African Jointfir leaf may hence be a source of useful phytochemicals for the development of novel therapies for the management of neurodegeneration.

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Section: Resultssupporting

confidence: 93%

Effect of Alkaloid Extract from African Jointfir (Gnetum africanum) Leaves on Manganese‐Induced Toxicity in Drosophila melanogaster

Oboh

Ogunsuyi

Awonyemi

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…The antiapoptotic effect of vinpocetine against renal IRI may be due to direct inhibition of activated caspase-3 or indirectly due to its antioxidant and anti-inflammatory effects. [68,69]…”

Section: Discussionmentioning

confidence: 99%

Renoprotective effect of vinpocetine against ischemia/reperfusion injury: Modulation of NADPH oxidase/Nrf2, IKKβ/NF‐κB p65, and cleaved caspase‐3 expressions

Azouz

Hersi

Ali

et al. 2022

J Biochem & Molecular Tox

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Ischemia/reperfusion injury (IRI) during kidney transplantation is a serious clinical problem with a high mortality rate and a lack of therapy. Therefore, there is a need to improve the ability of the kidney to tolerate IRI during transplantation. This study aimed to investigate the possible protective effect of vinpocetine; a derivative of vincamine alkaloid; against renal IRI in rats with the elucidation of the involved mechanisms. Vinpocetine (25 mg/kg; i.p.) was administered for 10 successive days before the induction of ischemia by bilateral clamping of both renal pedicles for 45 min followed by 24 h of reperfusion. Blood and renal tissue samples were then collected for biochemical, molecular, and histopathological investigations. Vinpocetine significantly reduced serum creatinine and blood urea nitrogen levels in rats subjected to IRI. It also reduced mRNA expression of NADPH oxidase and renal content of malondialdehyde, while enhanced Nrf2 protein expression and renal content of reduced glutathione. The suppression of the provoked inflammatory response was evident by the downregulation of IKKβ and NF‐κB p65 protein expressions, as well as their downstream inflammatory markers; tumor necrosis factor‐α, interleukin‐6, and myeloperoxidase. In addition, vinpocetine reduced protein expression of the apoptotic executioner cleaved caspase‐3. These nephroprotective effects were confirmed by the improvement in histopathological features. Collectively, the protective effect of vinpocetine against IRI could be attributed to modulation of NADPH oxidase/Nrf2, IKKβ/NF‐κB p65, and cleaved caspase‐3 expressions. Thus, vinpocetine could improve oxidant/antioxidant balance, suppress triggered inflammatory response, and promote renal cell survival after IRI.

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“…Vinpocetine, a synthetic derivative of the vinca alkaloid vincamine, attenuated Mn-induced oxidative stress and apoptosis in rats ( Nadeem et al, 2018 ) and NE-4C cells ( Bora et al, 2016 ). D-ribose-L-cysteine, a cysteine analog exhibiting antioxidant properties, attenuated Mn-induced oxidative stress and toxicity by enhancing CAT and SOD activity in rats ( Akingbade et al, 2022 ).…”

Section: Neurotherapeutics and Their Potential Underlying Mechanisms ...mentioning

confidence: 99%

Mechanisms of manganese-induced neurotoxicity and the pursuit of neurotherapeutic strategies

et al. 2022

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Chronic exposure to elevated levels of manganese via occupational or environmental settings causes a neurological disorder known as manganism, resembling the symptoms of Parkinson’s disease, such as motor deficits and cognitive impairment. Numerous studies have been conducted to characterize manganese’s neurotoxicity mechanisms in search of effective therapeutics, including natural and synthetic compounds to treat manganese toxicity. Several potential molecular targets of manganese toxicity at the epigenetic and transcriptional levels have been identified recently, which may contribute to develop more precise and effective gene therapies. This review updates findings on manganese-induced neurotoxicity mechanisms on intracellular insults such as oxidative stress, inflammation, excitotoxicity, and mitophagy, as well as transcriptional dysregulations involving Yin Yang 1, RE1-silencing transcription factor, transcription factor EB, and nuclear factor erythroid 2-related factor 2 that could be targets of manganese neurotoxicity therapies. This review also features intracellular proteins such as PTEN-inducible kinase 1, parkin, sirtuins, leucine-rich repeat kinase 2, and α-synuclein, which are associated with manganese-induced dysregulation of autophagy/mitophagy. In addition, newer therapeutic approaches to treat manganese’s neurotoxicity including natural and synthetic compounds modulating excitotoxicity, autophagy, and mitophagy, were reviewed. Taken together, in-depth mechanistic knowledge accompanied by advances in gene and drug delivery strategies will make significant progress in the development of reliable therapeutic interventions against manganese-induced neurotoxicity.

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Protective effect of vinpocetine against neurotoxicity of manganese in adult male rats

Cited by 33 publications

References 96 publications

Effect of Alkaloid Extract from African Jointfir (Gnetum africanum) Leaves on Manganese‐Induced Toxicity in Drosophila melanogaster

Effect of Alkaloid Extract from African Jointfir (Gnetum africanum) Leaves on Manganese‐Induced Toxicity in Drosophila melanogaster

Renoprotective effect of vinpocetine against ischemia/reperfusion injury: Modulation of NADPH oxidase/Nrf2, IKKβ/NF‐κB p65, and cleaved caspase‐3 expressions

Mechanisms of manganese-induced neurotoxicity and the pursuit of neurotherapeutic strategies

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