Isolongifolene mitigates rotenone-induced dopamine depletion and motor deficits through anti-oxidative and anti-apoptotic effects in a rat model of Parkinson's disease

Balakrishnan, Rengasamy; Vijayraja, Dhanraj; Mohankumar, Thangavel; Manimaran, D; Ganesan, Palanivel; Choi, Dong‐Kug; Elangovan, Namasivayam

doi:10.1016/j.jchemneu.2020.101890

Cited by 27 publications

(19 citation statements)

References 51 publications

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“…Bcl-2 reduced apoptotic damage by diminishing the lipid peroxidation reaction that was normally triggered by cytotoxic agents such as ROS. 34 Taken together, our findings strongly suggested that ECG-Exo could inhibit Rot-triggered neurotoxicity mainly via decreasing mitophagy and cell apoptosis. These results confirmed that ECG-Exo could protect SHSY5Y cells against Rot-induced oxidative stress and apoptosis.…”

Section: Improved Protective Effects Of Ecg Exosomalsupporting

confidence: 54%

“…It was suggested that Bax enhanced apoptotic cell death by dimerizing Bcl-2 proteins, which increased Cyt-C release and subsequent activation of cleaved caspase-3, leading to apoptosis. Bcl-2 reduced apoptotic damage by diminishing the lipid peroxidation reaction that was normally triggered by cytotoxic agents such as ROS . Taken together, our findings strongly suggested that ECG-Exo could inhibit Rot-triggered neurotoxicity mainly via decreasing mitophagy and cell apoptosis.…”

Section: Resultsmentioning

confidence: 99%

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Enhanced Neuroprotective Effects of Epicatechin Gallate Encapsulated by Bovine Milk-Derived Exosomes against Parkinson’s Disease through Antiapoptosis and Antimitophagy

Luo

Sun

Huang

et al. 2021

J. Agric. Food Chem.

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Epicatechin gallate (ECG) is a main effective catechin widely existing in natural plants and food, with well-known health benefits. The present study first designed a new exosome-based delivery system for ECG and examined its neuroprotective effects on a rotenone (Rot)-induced Parkinson's disease (PD) model in vitro. Exosomes (Exo) were isolated from fresh bovine milk, and their average size was 85.15 ± 2.00 nm. ECG was encapsulated into Exo by a sonication method, and the loading efficiency of ECG-loaded exosomes (ECG-Exo) was 25.96 ± 0.45%. The neuroprotective effects of ECG-Exo were evaluated on Rot-induced SHSY5Y cells and compared with free ECG. Cell viability, cellular reactive oxygen species, apoptosis rate, and the expressions of caspase-3, Bax, Bcl-2, parkin, PINK1, and Atg5 were determined. Our results showed that Exo delivered ECG successfully into SHSY5Y cells and exhibited enhanced neuroprotective effects. ECG-Exo might inhibit SHSY5Y cell damage induced by Rot through antiapoptosis and antimitophagy.

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Section: Improved Protective Effects Of Ecg Exosomalsupporting

confidence: 54%

Section: Resultsmentioning

confidence: 99%

Enhanced Neuroprotective Effects of Epicatechin Gallate Encapsulated by Bovine Milk-Derived Exosomes against Parkinson’s Disease through Antiapoptosis and Antimitophagy

Luo

Sun

Huang

et al. 2021

J. Agric. Food Chem.

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“…Rotenone treatment evokes behavioral parkinsonism and about 75% depletion of striatal dopamine content in rodent [ 55 ]. Interestingly, we found reduced striatal A 2A AR availability in the rotenone model mice as compared to the control–aged group ( Table 5 ).…”

Section: Discussionmentioning

confidence: 99%

Quantitation of the A2A Adenosine Receptor Density in the Striatum of Mice and Pigs with [18F]FLUDA by Positron Emission Tomography

et al. 2022

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The cerebral expression of the A2A adenosine receptor (A2AAR) is altered in neurodegenerative diseases such as Parkinson’s (PD) and Huntington’s (HD) diseases, making these receptors an attractive diagnostic and therapeutic target. We aimed to further investigate the pharmacokinetic properties in the brain of our recently developed A2AAR–specific antagonist radiotracer [18F]FLUDA. For this purpose, we retrospectively analysed dynamic PET studies of healthy mice and rotenone–treated mice, and conducted dynamic PET studies with healthy pigs. We performed analysis of mouse brain time–activity curves to calculate the mean residence time (MRT) by non–compartmental analysis, and the binding potential (BPND) of [18F]FLUDA using the simplified reference tissue model (SRTM). For the pig studies, we performed a Logan graphical analysis to calculate the radiotracer distribution volume (VT) at baseline and under blocking conditions with tozadenant. The MRT of [18F]FLUDA in the striatum of mice was decreased by 30% after treatment with the A2AAR antagonist istradefylline. Mouse results showed the highest BPND (3.9 to 5.9) in the striatum. SRTM analysis showed a 20% lower A2AAR availability in the rotenone–treated mice compared to the control–aged group. Tozadenant treatment significantly decreased the VT (14.6 vs. 8.5 mL · g−1) and BPND values (1.3 vs. 0.3) in pig striatum. This study confirms the target specificity and a high BPND of [18F]FLUDA in the striatum. We conclude that [18F]FLUDA is a suitable tool for the non–invasive quantitation of altered A2AAR expression in neurodegenerative diseases such as PD and HD, by PET.

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“…Parkinson disease is pathologically characterized by Lewy bodies that result from the aggregation of α-synuclein, which is localized presynaptically particularly in the nerve terminals (Sorrentino & Giasson, 2020). Additionally, pathogenic processes in Parkinson Apoptosis has been implicated as the mechanism of dopaminergic neuronal loss in Parkinson disease, as illustrated by the identification of apoptotic cells and DNA fragmentation in the substantia nigra of Parkinson diseased patients in post-mortem and in vitro and in vivo studies (Balakrishnan et al, 2021;Erekat, 2018a;Ma et al, 2018;Teng et al, 2020). In addition to that, overexpression of active caspase-8, -9, and -3, as well as increased levels of pro-apoptotic proteins, such as BAX, and reduced anti-apoptotic Bcl-2 levels in the dopaminergic neurons of Parkinson disease in post-mortem and in vitro studies confirmed the role of apoptosis in the pathogenesis of Parkinson disease (Balakrishnan et al, 2021;Bose & Beal, 2016;Dong et al, 2020;Ma et al, 2018;Moujalled et al, 2021).…”

Section: Apoptosis In Parkinson Diseasementioning

confidence: 99%

Apoptosis and its therapeutic implications in neurodegenerative diseases

Erekat

2021

Clinical Anatomy

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Neurodegenerative disorders are characterized by progressive loss of particular populations of neurons. Apoptosis has been implicated in the pathogenesis of neurodegenerative diseases, including Parkinson disease, Alzheimer disease, Huntington disease, and amyotrophic lateral sclerosis. In this review, we focus on the existing notions relevant to comprehending the apoptotic death process, including the morphological features, mediators and regulators of cellular apoptosis. We also highlight the evidence of neuronal apoptotic death in Parkinson disease, Alzheimer disease, Huntington disease, and amyotrophic lateral sclerosis. Additionally, we present evidence of potential therapeutic agents that could modify the apoptotic pathway in the aforementioned neurodegenerative diseases and delay disease progression. Finally, we review the clinical trials that were conducted to evaluate the use of anti-apoptotic drugs in the treatment of the aforementioned neurodegenerative diseases, in order to highlight the essential need for early detection and intervention of neurodegenerative diseases in humans.

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Isolongifolene mitigates rotenone-induced dopamine depletion and motor deficits through anti-oxidative and anti-apoptotic effects in a rat model of Parkinson's disease

Cited by 27 publications

References 51 publications

Enhanced Neuroprotective Effects of Epicatechin Gallate Encapsulated by Bovine Milk-Derived Exosomes against Parkinson’s Disease through Antiapoptosis and Antimitophagy

Enhanced Neuroprotective Effects of Epicatechin Gallate Encapsulated by Bovine Milk-Derived Exosomes against Parkinson’s Disease through Antiapoptosis and Antimitophagy

Quantitation of the A2A Adenosine Receptor Density in the Striatum of Mice and Pigs with [18F]FLUDA by Positron Emission Tomography

Apoptosis and its therapeutic implications in neurodegenerative diseases

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