A novel synthetic compound PHID (8-Phenyl-6a, 7, 8, 9, 9a, 10-hexahydro-6H-isoindolo [5, 6-g] quinoxaline-7, 9-dione) protects SH-SY5Y cells against MPP+-induced cytotoxicity through inhibition of reactive oxygen species generation and JNK signaling

Kim, In Su; Koppula, Sushruta; Kim, Byung‐Wook; Song, Min Dong; Jung, Ju Yeon; Lee, Gwang; Lee, Hee Soon; Choi, Dong‐Kug

doi:10.1016/j.ejphar.2010.09.063

Cited by 9 publications

(3 citation statements)

References 61 publications

(68 reference statements)

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“…Activation of the MAPK cascade may result in the activation of ERK1/2, p38, and JNK kinases (Martel‐Gallegos et al, ). According to our results, MPP + activated all MAPK pathways in neuronal SH‐SY5Y cells, consistent with the results from previous studies (Hashimoto, Yu, Koizumi, Ouchi, & Okabe, ; Kim et al, ; Ryan, McNicholas, & Taylor, ; Tsang & Chung, ). Thus, we examined whether P2Y6R was associated with the ERK, p38, and JNK signaling pathways.…”

Section: Discussionsupporting

confidence: 93%

Purinergic receptor P2Y6 contributes to 1‐methyl‐4‐phenylpyridinium‐induced oxidative stress and cell death in neuronal SH‐SY5Y cells

Qian

Yang

2017

J of Neuroscience Research

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Oxidative stress and neural degeneration have been shown to be involved in the pathogenesis of Parkinson's disease (PD). The P2Y6 purinergic receptor (P2Y6R) has been shown to participate in the activation of microglia and the production of pro-inflammatory factors induced by lipopolysaccharide to cause neuronal loss. However, the function of P2Y6R during oxidative stress in neurons is unclear. In the present study, 1-methyl-4-phenylpyridinium (MPP ) treatment increased the level of UDP/P2Y6R on neuronal SH-SY5Y cells. Importantly, pharmacological inhibition of P2Y6R or knockdown of P2Y6R using a siRNA exerted an increased protective effect by preventing MPP -induced increases in the levels of reactive oxygen species (ROS), superoxide anion, inducible nitric oxide synthase (iNOS), and malondialdehyde (MDA) and down-regulation of superoxide dismutase 1 (SOD1) expression. UDP, an agonist of P2Y6R, enhanced the effects of MPP , which was also inhibited by apyrase or MRS2578. Additionally, P2Y6R knockdown also significantly reversed both the loss of cell viability and the increase in the levels of phosphorylated extracellular signal-regulated protein kinase (p-ERK1/2) and p38 (p-p38) caused by MPP stimulation. However, the inhibition of the ERK1/2 and p38 kinase signaling pathways had no effect on P2Y6R expression. Taken together, these results support the hypothesis that P2Y6R expressed on neuronal SH-SY5Y cell is associated with the progression of oxidative stress and cell death induced by MPP , suggesting that P2Y6R may play an important role in the pathogenesis of PD.

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Section: Discussionsupporting

confidence: 93%

Purinergic receptor P2Y6 contributes to 1‐methyl‐4‐phenylpyridinium‐induced oxidative stress and cell death in neuronal SH‐SY5Y cells

Qian

Yang

2017

J of Neuroscience Research

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“…3,36,[40][41][42][43] Extensive animal model studies have been conducted about the sustained protective role of different synthetic and natural bioactive compounds against dopaminergic neuron loss in PD. [44][45][46][47][48][49] Based on limitations for using synthetic compounds, [50][51][52] natural phytobioactive compounds play an important role in preventing PD. 38,48 Phytobioactive compounds from various medicinal plants show neuroprotective effects in various animal models.…”

Section: Phytobioactive Compounds and Pdmentioning

confidence: 99%

Recent trends in the development of nanophytobioactive compounds and delivery systems for their possible role in reducing oxidative stress in Parkinson’s disease models

Ganesan¹,

Ko²,

Kim³

et al. 2015

IJN

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102

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Oxidative stress plays a very critical role in neurodegenerative diseases, such as Parkinson’s disease (PD), which is the second most common neurodegenerative disease among elderly people worldwide. Increasing evidence has suggested that phytobioactive compounds show enhanced benefits in cell and animal models of PD. Curcumin, resveratrol, ginsenosides, quercetin, and catechin are phyto-derived bioactive compounds with important roles in the prevention and treatment of PD. However, in vivo studies suggest that their concentrations are very low to cross blood–brain barrier thereby it limits bioavailability, stability, and dissolution at target sites in the brain. To overcome these problems, nanophytomedicine with the controlled size of 1–100 nm is used to maximize efficiency in the treatment of PD. Nanosizing of phytobioactive compounds enhances the permeability into the brain with maximized efficiency and stability. Several nanodelivery techniques, including solid lipid nanoparticles, nanostructured lipid carriers, nanoliposomes, and nanoniosomes can be used for controlled delivery of nanobioactive compounds to brain. Nanocompounds, such as ginsenosides (19.9 nm) synthesized using a nanoemulsion technique, showed enhanced bioavailability in the rat brain. Here, we discuss the most recent trends and applications in PD, including 1) the role of phytobioactive compounds in reducing oxidative stress and their bioavailability; 2) the role of nanotechnology in reducing oxidative stress during PD; 3) nanodelivery systems; and 4) various nanophytobioactive compounds and their role in PD.

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“…PC12 cells have obvious synapses formation, and are capable of producing nerve-related proteins following stimulation by nerve growth factor (NGF) ( 10 ). Certain small synthetic molecules have been reported to exhibit neuroprotective activities against neurotoxin-induced toxicity in SH-SY5Y and PC12 cells via mitochondrial pathways ( 11 , 12 ).…”

Section: Introductionmentioning

confidence: 99%

Investigation of the neuroprotective effects of a novel synthetic compound via the mitochondrial pathway

Wang

Zhang

et al. 2017

Molecular Medicine Reports

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The present study aimed to investigate the neuroprotective effect of a novel synthetic compound (5zou) on differentiated PC12 cells against 6-hydroxydopamine (6-OHDA) and L-glutamic acid (L-Glu) neurotoxin-induced cell injury and the potential mechanisms involved. 5zou is a 2, 2-disubstituted 1,2-dihydropyridine. PC12 cells were treated with 6-OHDA and L-Glu to establish neurotoxic cell models. MTT assay, DCFH-DA staining, Fluo-4-AM staining, JC-1 staining and western blotting were used to determine the changes in cell viability, intracellular reactive oxygen species concentration, Ca2+ influx, mitochondrial membrane potential and the protein expressions of B-cell lymphoma-2 (Bcl-2) and B-cell lymphoma-extra large (Bcl-xL). Morphological analysis demonstrated the effect of 5zous on neuritogenesis and differentiation in PC12 cells. The results suggested that 5zou rescued the cell viability, intracellular ROS level, Ca2+ influx, mitochondrial membrane potential, and expression of Bcl-2 and Bcl-xL, which were altered by 6-OHDA and L-Glu. The study confirmed that 5zou has neuroprotective effects on neurotoxin-induced differentiated PC12 cells injury, potentially via the mitochondrial apoptosis pathway.

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A novel synthetic compound PHID (8-Phenyl-6a, 7, 8, 9, 9a, 10-hexahydro-6H-isoindolo [5, 6-g] quinoxaline-7, 9-dione) protects SH-SY5Y cells against MPP+-induced cytotoxicity through inhibition of reactive oxygen species generation and JNK signaling

Cited by 9 publications

References 61 publications

Purinergic receptor P2Y6 contributes to 1‐methyl‐4‐phenylpyridinium‐induced oxidative stress and cell death in neuronal SH‐SY5Y cells

Purinergic receptor P2Y6 contributes to 1‐methyl‐4‐phenylpyridinium‐induced oxidative stress and cell death in neuronal SH‐SY5Y cells

Recent trends in the development of nanophytobioactive compounds and delivery systems for their possible role in reducing oxidative stress in Parkinson’s disease models

Investigation of the neuroprotective effects of a novel synthetic compound via the mitochondrial pathway

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A novel synthetic compound PHID (8-Phenyl-6a, 7, 8, 9, 9a, 10-hexahydro-6H-isoindolo [5, 6-g] quinoxaline-7, 9-dione) protects SH-SY5Y cells against MPP+-induced cytotoxicity through inhibition of reactive oxygen species generation and JNK signaling

Cited by 9 publications

References 61 publications

Purinergic receptor P2Y6 contributes to 1‐methyl‐4‐phenylpyridinium‐induced oxidative stress and cell death in neuronal SH‐SY5Y cells

Purinergic receptor P2Y6 contributes to 1‐methyl‐4‐phenylpyridinium‐induced oxidative stress and cell death in neuronal SH‐SY5Y cells

Recent trends in the development of nanophytobioactive compounds and delivery systems for their possible role in reducing oxidative stress in Parkinson&rsquo;s disease models

Investigation of the neuroprotective effects of a novel synthetic compound via the mitochondrial pathway

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Product

Resources

About

Recent trends in the development of nanophytobioactive compounds and delivery systems for their possible role in reducing oxidative stress in Parkinson’s disease models