Oxidative stress and Parkinson’s disease: mechanisms and perspectives of treatment

Katunina, E A; Titova, Nataliya; Малыхина, Е. А.; Gasanov, M. G.; Makarova, A A; Воронина, Т. А.; Nerobkova, L. N.; Sukhorukova, N. A.; Avakyan, G. N.

doi:10.17116/jnevro201511571141-145

Cited by 4 publications

(5 citation statements)

References 31 publications

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“…In addition, oxidative stress-induced apoptosis participates in the development of nervous system diseases, whereas intervention with antioxidants reduces the apoptosis via inhibiting the generation of ROS and thereby resulting in neuroprotective effects (19). Multiple studies have reported that ROS contributes to the apoptosis-associated mechanism of MPP + -mediated neurotoxicity (30).…”

Section: Discussionmentioning

confidence: 99%

Tectorigenin attenuates the MPP+‑induced SH‑SY5Y cell damage, indicating a potential beneficial role in Parkinson's disease by oxidative stress inhibition

et al. 2017

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Abstract.Tectorigenin is a plant isoflavonoid primarily derived from the flowers of Pueraria thomsonii Benth. Although various biological properties of tectorigenin have been reported, such as its antioxidant activity, the effects of tectorigenin on the cellular models of Parkinson's disease have not yet been elucidated. The aims of the current study were to investigate whether tectorigenin prevents neurotoxicity induced by MPP + (also known as 1-methyl-4-phenylpyridinium) in SH-SY5Y cells and to elucidate the underlying protective mechanism. Cell viability and lactate dehydrogenase release were measured. The morphological changes of apoptotic cells were observed by Hoechst 33258 staining. Caspase-3, superoxide dismutase, catalase and glutathione peroxidase activity was measured using commercially available ELISA kits. The expression of cytochrome c, Bax, Bcl-2 and NADPH oxidase were detected by western blot analysis. The results indicated that treatment with MPP + causes a significant decrease in the viability of cells and an increase in apoptosis, as evidenced by the upregulation of apoptotic cells, caspase-3 activity and cytochrome c expression. By contrast, these effects were all reversed by pretreatment with tectorigenin in SH-SY5Y cells. Tectorigenin also inhibited the MPP + -induced changes of Bax and Bcl-2 levels. In addition, pretreatment with tectorigenin mitigated the MPP + -caused increases in the levels of reactive oxygen species and NADPH oxidase protein in SH-SY5Y cells. Simultaneously, tectorigenin abolished the downregulation of antioxidant enzymes, including superoxide dismutase, catalase and glutathione peroxidase, that was induced by MPP + . In conclusion, the present study data indicate that the neuroprotective effect of tectorigenin against MPP + -induced cytotoxicity and apoptosis may be involved in attenuating oxidative stress and enhancing antioxidant defense.

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Section: Discussionmentioning

confidence: 99%

Tectorigenin attenuates the MPP+‑induced SH‑SY5Y cell damage, indicating a potential beneficial role in Parkinson's disease by oxidative stress inhibition

et al. 2017

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“…However, the activity of antioxidant systems decreases with age, contributing to the age-related decline in the resistance of dopaminergic nigrostriatal neurons to pro-Parkinsonian factors and the progressive increase in PD patients. The concept of oxidative stress in the pathochemical mechanisms of neuronal damage in PD defines an avenue for pathogenetic therapy with antioxidants [ 43 ]. The high content of paramagnetic centers in melanins enables them to deactivate radicals due to their high electron absorption capacity.…”

Section: Discussionmentioning

confidence: 99%

Regulatory effect of bacterial melanin on the isoforms of new superoxide-producing associates from rat tissues in rotenone-induced Parkinson’s disease

Danielyan,

Nebogova,

Simonyan

et al. 2023

BMC Neurosci

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According to recent research, selective neuronal vulnerability in Parkinson’s disease (PD) results from several phenotypic traits, including calcium-dependent, feed-forward control of mitochondrial respiration leading to elevated reactive oxygen species and cytosolic calcium concentration, an extensive axonal arbor, and a reactive neurotransmitter. Therefore, antioxidant therapy is a promising direction in the treatment of PD. In vitro studies have indicated the survival-promoting activity of bacterial melanin (BM) on midbrain dopaminergic neuron cultures. It has been established that BM has a number of protective and anti-inflammatory properties, so there is a high probability of a protective effect of BM in the early stages of PD. In this study, PD was induced through the unilateral intracerebral administration of rotenone followed by bacterial melanin. Tissues (brain, lungs, and small intestine) from the observed groups underwent isolation and purification to extract isoforms of new thermostable superoxide (О2−)-producing associates between NADPH-containing lipoprotein (NLP) and NADPH oxidase-Nox (NLP-Nox). The optical absorption spectral characteristics, specific amounts, stationary concentration of the produced О2−, and the content of NADPH in the observed associates were determined. The optical absorption spectra of the NLP-Nox isoforms in the visible and UV regions in the experimental groups did not differ from those of the control group. However, compared with the control group, the specific content of the total fractions of NLP-Nox isoforms associated with PD groups was higher, especially in the small intestine. These findings suggest that the described changes may represent a novel mechanism for rotenone-induced PD. Furthermore, bacterial melanin demonstrated antioxidant properties and regulated membrane formation in the brain, lung, and small intestine. This regulation occurred by inhibiting the release of new membrane-bound formations (NLP-Nox associates) from these membranes while simultaneously regulating the steady-state concentration of the formed О2−.

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“…Enhanced oxidative stress and neuroinflammation [5,6] are involved in the pathogenesis of PD. We then explored whether SIP can relieve PD during repressing oxidative stress and inflammatory response.…”

Section: Discussionmentioning

confidence: 99%

“…The main pathological features of PD are the deposition of Lewy bodies and loss of dopaminergic neurons in substantia nigra pars compacta (SNc) [2–4]. Enhanced oxidative stress and inflammatory responses [5,6], protein misfolding and aggregation [7], and dysfunction of the ubiquitin-proteasome system [8] are involved in the pathogenesis of PD, but the exact mechanism leading to degeneration of dopaminergic neurons remains unclear. Current drugs for the treatment of PD are mainly based on improving dopamine concentration in the brain or activating dopamine receptors to improve the motor symptoms of PD [9].…”

Section: Introductionmentioning

confidence: 99%

The Neuroprotective Effect of Steroid Receptor Coactivator-Interacting Protein (SIP) in Astrocyte Model of 1-Methyl-4-Phenylpyridinium (MPP⁺)-Induced Parkinson’s Disease

2019

Med Sci Monit

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Background The purpose of this study was to investigate the role and mechanism of steroid receptor coactivator-interacting protein (SIP) in an astrocyte model of 1-methyl-4-phenylpyridinium (MPP + )-induced Parkinson’s disease. Material/Methods To perform our study, a Parkinson’s disease cell model was established by treating the rat glioblastoma cell line C6 with MPP + . SIP was overexpressed in C6 cells using SIP-plasmid. Cell viability and apoptosis were analyzed using MTT assay and flow cytometer respectively. Tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels were detected using enzyme linked immunosorbent assay and quantitative reverse transcription PCR. Besides, lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) production, and superoxide dismutase (SOD) enzyme activity were determined in the present study. For protein and mRNA detection, western blot assay, and qRT-PCR were performed respectively. Results SIP was decreased in MPP + -induced C6 cells. SIP overexpression relieved MPP + -induced cytotoxicity of C6 cells, displayed as increased cell viability and reduced cell apoptosis and reduced LDH release. Besides, SIP inhibited MPP + -induced inflammatory response and oxidative stress, evidenced by decreased levels of inflammatory factors (TNF-α and IL-1β), reduced ROS generation and enhanced SOD activity. Moreover, MPP + -induced nuclear factor-κB activation was inhibited by SIP overexpression. Conclusions SIP was downregulated in Parkinson’s disease and it played a protective role in the development Parkinson’s disease, thus may be a promising target for Parkinson’s disease treatment.

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Oxidative stress and Parkinson’s disease: mechanisms and perspectives of treatment

Cited by 4 publications

References 31 publications

Tectorigenin attenuates the MPP+‑induced SH‑SY5Y cell damage, indicating a potential beneficial role in Parkinson's disease by oxidative stress inhibition

Tectorigenin attenuates the MPP+‑induced SH‑SY5Y cell damage, indicating a potential beneficial role in Parkinson's disease by oxidative stress inhibition

Regulatory effect of bacterial melanin on the isoforms of new superoxide-producing associates from rat tissues in rotenone-induced Parkinson’s disease

The Neuroprotective Effect of Steroid Receptor Coactivator-Interacting Protein (SIP) in Astrocyte Model of 1-Methyl-4-Phenylpyridinium (MPP⁺)-Induced Parkinson’s Disease

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