The Neuroprotective Effects of Cinnamic Aldehyde in an MPTP Mouse Model of Parkinson’s Disease

Bae, Woom-Yee; Choi, Jae-Sun; Jeong, Joo‐Won

doi:10.3390/ijms19020551

Cited by 39 publications

(22 citation statements)

References 40 publications

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“…TCA is a major active component of cinnamon that was shown to have antioxidant, cholesterol-lowering, antineoplastic, antibacterial, and antifungal properties. The potential therapeutic effects of TCA were also studied in several disease models of neurodegeneration, including 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease [ 9 ] and 6-hydroxydopamine-induced dopaminergic injury models [ 10 ]. However, no studies examined whether TCA, a single compound derived from cinnamon, might be an effective therapeutic in AD.…”

Section: Introductionmentioning

confidence: 99%

Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice

Kim

Jeon

et al. 2020

IJMS

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Abnormal amyloid-β (Aβ) accumulation is the most significant feature of Alzheimer’s disease (AD). Among the several secretases involved in the generation of Aβ, β-secretase (BACE1) is the first rate-limiting enzyme in Aβ production that can be utilized to prevent the development of Aβ-related pathologies. Cinnamon extract, used in traditional medicine, was shown to inhibit the aggregation of tau protein and Aβ aggregation. However, the effect of trans-cinnamaldehyde (TCA), the main component of cinnamon, on Aβ deposition is unknown. Five-month-old 5XFAD mice were treated with TCA for eight weeks. Seven-month-old 5XFAD mice were evaluated for cognitive and spatial memory function. Brain samples collected at the conclusion of the treatment were assessed by immunofluorescence and biochemical analyses. Additional in vivo experiments were conducted to elucidate the mechanisms underlying the effect of TCA in the role of Aβ deposition. TCA treatment led to improvements in cognitive impairment and reduced Aβ deposition in the brains of 5XFAD mice. Interestingly, the levels of BACE1 were decreased, whereas the mRNA and protein levels of three well-known regulators of BACE1, silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor γ (PPARγ) coactivator 1α (PGC1α), and PPARγ, were increased in TCA-treated 5XFAD mice. TCA led to an improvement in AD pathology by reducing BACE1 levels through the activation of the SIRT1-PGC1α-PPARγ pathway, suggesting that TCA might be a useful therapeutic approach in AD.

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Section: Introductionmentioning

confidence: 99%

Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice

Kim

Jeon

et al. 2020

IJMS

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“…Chung, J. et al showed that cinnamic aldehyde could induce autophagy in macrophages. Another study demonstrated that cinnamic aldehyde exerts a neuroprotective effect in a Parkinson's disease model through autophagy inhibition 143 .…”

Section: Resultsmentioning

confidence: 99%

A systems pharmacology approach to identify the autophagy-inducing effects of Traditional Persian medicinal plants

Mosaddeghi

Eslami

Farahmandnejad

et al. 2021

Sci Rep

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Aging is correlated with several complex diseases, including type 2 diabetes, neurodegeneration diseases, and cancer. Identifying the nature of this correlation and treatment of age-related diseases has been a major subject of both modern and traditional medicine. Traditional Persian Medicine (TPM) embodies many prescriptions for the treatment of ARDs. Given that autophagy plays a critical role in antiaging processes, the present study aimed to examine whether the documented effect of plants used in TPM might be relevant to the induction of autophagy? To this end, the TPM-based medicinal herbs used in the treatment of the ARDs were identified from modern and traditional references. The known phytochemicals of these plants were then examined against literature for evidence of having autophagy inducing effects. As a result, several plants were identified to have multiple active ingredients, which indeed regulate the autophagy or its upstream pathways. In addition, gene set enrichment analysis of the identified targets confirmed the collective contribution of the identified targets in autophagy regulating processes. Also, the protein–protein interaction (PPI) network of the targets was reconstructed. Network centrality analysis of the PPI network identified mTOR as the key network hub. Given the well-documented role of mTOR in inhibiting autophagy, our results hence support the hypothesis that the antiaging mechanism of TPM-based medicines might involve autophagy induction. Chemoinformatics study of the phytochemicals using docking and molecular dynamics simulation identified, among other compounds, the cyclo-trijuglone of Juglans regia L. as a potential ATP-competitive inhibitor of mTOR. Our results hence, provide a basis for the study of TPM-based prescriptions using modern tools in the quest for developing synergistic therapies for ARDs.

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“…CA which is the major constituent of cinnamon oil exhibits a wide range of biological activities, including antipyretic, antitumoral, antibacterial, antidiabetic, anti-inflammatory, and antioxidant activities (Chew et al 2010;Kim et al 2006;Koh et al 1998;Lv et al 2017;Nour et al 2018;Sharma et al 2018;Shaughnessy et al 2001;Xue et al 2011;Zhu et al 2017). It also reportedly exerts neuroprotective effects against cerebral ischemia (Chen et al 2016;Zhao et al 2015), glutamate excitotoxicity (Lv et al 2017), and neurodegenerative diseases such as Alzheimer's and Parkinson's diseases (Bae et al 2018;George et al 2013), and it also has anti-neuroinflammatory effects on neuronal cell cultures (Bae et al 2018;Fu et al 2017;Ho et al 2013;Shi et al 2017;Yang et al 2016), as well as vasorelaxant effects on the isolated rat aorta (Alvarez-Collazo et al 2014;Xue et al 2011;Yanaga et al 2006), mesenteric artery (Veras et al 2013), mouse ear artery (Aubdool et al 2016), and porcine coronary artery (Raffai et al 2014), and in cerebral arteries (Earley et al 2009). Because of these neuroprotective and vasodilatory effects, we hypothesized that CA potentially exerts protective effects against SAH-induced EBI and vasospasm.…”

Section: Discussionmentioning

confidence: 99%

“…It reportedly exhibits various therapeutic properties (Xue et al 2011), including antitumoral, antipyretic, antimicrobial, antidiabetic, antimutagenic, antioxidant, and anti-inflammatory activities (Chew et al 2010;Kim et al 2006;Koh et al 1998;Lv et al 2017;Nour et al 2018;Sharma et al 2018;Shaughnessy et al 2001;Xue et al 2011). Numerous studies have shown that CA exhibits potent neuroprotective activity, inhibiting neuroinflammation, oxidative stress, and apoptosis (Bae et al 2018;Chen et al 2016;Fu et al 2017;Ho et al 2013;Lv et al 2017;Pyo et al 2013;Shi et al 2017;Yang et al 2016;Zhao et al 2015). Its vasodilator effects have also been widely studied and demonstrated in various vessels, such as the mouse ear artery (Aubdool et al 2016), rat aorta (Alvarez-Collazo et al 2014;Xue eet al 2011;Yanaga et al 2006), mesenteric artery (Veras et al 2013), and porcine coronary artery (Raffai et al 2014), as well as in cerebral arteries (Earley et al 2009).…”

Section: Introductionmentioning

confidence: 99%

The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits

et al. 2019

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The neuroprotective and vasodilatory effects of cinnamaldehyde have been widely studied and documented. On the basis of these findings, we hypothesized that cinnamaldehyde exhibits therapeutic effects on subarachnoid hemorrhage-induced early brain injury and cerebral vasospasm. Thirty-two adult male New Zealand white rabbits were randomly divided into four groups of eight rabbits: control, subarachnoid hemorrhage, subarachnoid hemorrhage + vehicle, and subarachnoid hemorrhage + cinnamaldehyde. An intraperitoneal dose of 50 mg/kg cinnamaldehyde was administered 5 min following an intracisternal blood injection, followed by three further daily injections at identical doses. The animals were sacrificed 72 h after subarachnoid hemorrhage was induced. The crosssectional areas and arterial wall thicknesses of the basilar artery were measured and hippocampal degeneration scores were evaluated. Treatment with cinnamaldehyde was effective in providing neuroprotection and attenuating cerebral vasospasm after subarachnoid hemorrhage in rabbits. It effectively increased the cross-sectional areas of the basilar artery and reduced the arterial wall thickness; in addition, hippocampal degeneration scores were lower in the cinnamaldehyde group. The findings of this study showed, for the first time to our knowledge, that cinnamaldehyde exhibits neuroprotective activity against subarachnoid hemorrhage-induced early brain injury and that it can prevent vasospasm. Potential mechanisms underlying the neuroprotection and vasodilation were discussed. Cinnamaldehyde could play a role in subarachnoid hemorrhage treatment.

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The Neuroprotective Effects of Cinnamic Aldehyde in an MPTP Mouse Model of Parkinson’s Disease

Cited by 39 publications

References 40 publications

Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice

Trans-Cinnamaldehyde Alleviates Amyloid-Beta Pathogenesis via the SIRT1-PGC1α-PPARγ Pathway in 5XFAD Transgenic Mice

A systems pharmacology approach to identify the autophagy-inducing effects of Traditional Persian medicinal plants

The effects of Cinnamaldehyde on early brain injury and cerebral vasospasm following experimental subarachnoid hemorrhage in rabbits

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