Investigating the role of Sirt1-modulated oxidative stress in relation to benign paroxysmal positional vertigo and Parkinson's disease

Tsai, Kun Ling; Cheng, Yuan-Yang; Leu, Hsin Bang; Lee, Yi Yen; Chen, Tzeng Ji; Liu, Ding Hao; Kao, Chung Lan

doi:10.1016/j.neurobiolaging.2015.05.012

Cited by 34 publications

(28 citation statements)

References 53 publications

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“…A limitation of this study was that there were no results for markers after the repositioning maneuver or follow-up period [20] . Recently, Tsai et al [21] found that the serum levels of the oxidative stress marker malondialdehyde were higher in the BPPV group before the repositioning maneuver. The levels of the antioxidant enzyme superoxide dismutase were higher in the post-maneuver group, suggesting the possible role of oxidative stress in BPPV.…”

Section: Discussionmentioning

confidence: 98%

The Role of Oxidative Stress and Inflammatory Mediators in Benign Paroxysmal Positional Vertigo

Gucluturk

Unal²,

İsmi³

et al. 2016

Int Adv Otol

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OBJECTIVE:Benign paroxysmal positional vertigo (BPPV) is the most common peripheral cause of vertigo. It can be defined as transient vertigo induced by rapid changes in head position associated with a characteristic paroxysmal positional nystagmus. The aim of this study was to search for the possible role of oxidative stress and inflammatory mediators in the pathogenesis of BPPV. MATERIALS and METHODS:Total antioxidant status as well as paraoxonase, tumor necrosis factor alpha, interleukin (IL) 6, and IL-1β levels were evaluated in peripheral venous serum samples of 30 BPPV and 30 control patients. RESULTS:Total antioxidant status levels were lower in the BPPV group than in the control group (p=0.008). After Epley's repositioning maneuver in the vertigo group, there was a statistically significant decline in IL-1β levels at the first and third month visits (p=0.014 for first month and p=0.013 for third month). CONCLUSION:Our findings suggested that IL-1β and oxidative stress contributed to the pathogenesis of BPPV.

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Section: Discussionmentioning

confidence: 98%

The Role of Oxidative Stress and Inflammatory Mediators in Benign Paroxysmal Positional Vertigo

Gucluturk

Unal²,

İsmi³

et al. 2016

Int Adv Otol

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“…SIRT1 is implicated in stress-responsive signaling pathways, cardiovascular disease, diabetes, and neurodegenerative disorders, and has recently become a target for drug development (Pallas et al, 2008;Baur et al, 2012;Hernandez-Jimenez et al, 2013). Recently, the neuroprotective properties of SIRT1 have also been described in PD depending on anti-apoptotic and anti-oxidant features (Tsai et al, 2015;Zou et al, 2016). In present study, we found that MPP þ treatment obviously decreased the SIRT1 activity, SIRT1 mRNA and protein levels in SH-SY5Y cells, which is also consistent with the research done by Dong et al (2016), Tao et al (2016), and Zou et al (2016).…”

Section: Discussionmentioning

confidence: 99%

SIRT1 mediates salidroside‐elicited protective effects against MPP⁺‐induced apoptosis and oxidative stress in SH‐SY5Y cells: involvement in suppressing MAPK pathways

Wang

Sun

Wang

et al. 2017

Cell Biology International

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Parkinson's disease (PD) is a progressive neurodegenerative disease, leading to tremor, rigidity, bradykinesia, and gait impairment. Salidroside has been reported to exhibit antioxidative and neuroprotective properties in PD. However, the underlying neuroprotective mechanisms effects of salidroside are poorly understood. Recently, a growing body of evidences suggest that silent information regulator 1 (SIRT1) plays important roles in the pathophysiology of PD. Hence, the present study investigated the roles of SIRT1 in neuroprotective effect of salidroside against N-methyl-4-phenylpyridinium (MPP þ )-induced SH-SY5Y cell injury. Our findings revealed that salidroside attenuates MPP þ -induced neurotoxicity as evidenced by the increase in cell viability, and the decreases in the caspase-3 activity and apoptosis ratio. Simultaneously, salidroside pretreatment remarkably increased SIRT1 activity, SIRT1 mRNA and protein levels in MPP þ -treated SH-SY5Y cell. However, sirtinol, a SIRT1 activation inhibitor, significantly blocked the inhibitory effects of salidroside on MPP þ -induced cytotoxicity and apoptosis. In addition, salidroside abolished MPP þ -induced the production of reactive oxygen species (ROS), the upregulation of NADPH oxidase 2 (NOX2) expression, the down-regulations of superoxide dismutase (SOD) activity and glutathione (GSH) level in SH-SY5Y cells, while these effects were also blocked by sirtinol. Finally, we found that the inhibition of salidroside on MPP þ -induced phosphorylation of p38, extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) were also reversed by sirtinol in SH-SY5Y cells. Taken together, these results indicated that SIRT1 contributes to the neuroprotection of salidroside against MPP þ -induced apoptosis and oxidative stress, in part through suppressing of mitogen-activated protein kinase (MAPK) pathways.

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“…Ota et al reported that upregulation of SIRT1 can exert protective effects against cellular senescence and dysfunction in human endothelial cells [42]. In addition, Tsai et al reported that oxidative stress-induced inhibition of SIRT1 function can promote 6-hydroxydopamine-induced cell death [43]. Notably, SIRT1 is also involved in cerebral ischemia.…”

Section: Discussionmentioning

confidence: 99%

Adiponectin Protects against Glutamate‐Induced Excitotoxicity via Activating SIRT1‐Dependent PGC‐1α Expression in HT22 Hippocampal Neurons

Liang

Zhao

Liu

et al. 2016

Oxidative Medicine and Cellular Longevity

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Glutamate- (Glu-) induced excitotoxicity plays a critical role in stroke. This study aimed to investigate the effects of APN on Glu-induced injury in HT22 neurons. HT22 neurons were treated with Glu in the absence or the presence of an APN peptide. Cell viability was assessed using the MTT assay, while cell apoptosis was evaluated using TUNEL staining. Levels of LDH, MDA, SOD, and GSH-Px were detected using the respective kits, and ROS levels were detected using dichlorofluorescein diacetate. Western blot was used to detect the expression levels of silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), cleaved caspase-3, Bax, and Bcl-2. In addition to the western blot, immunofluorescence was used to investigate the expression levels of SIRT1 and PGC-1α. Our results suggest that APN peptide increased cell viability, SOD, and GSH-Px levels and decreased LDH release, ROS and MDA levels, and cell apoptosis. APN peptide upregulated the expression of SIRT1, PGC-1α, and Bcl-2 and downregulated the expression of cleaved caspase-3 and Bax. Furthermore, the protective effects of the APN peptide were abolished by SIRT1 siRNA. Our findings suggest that APN peptide protects HT22 neurons against Glu-induced injury by inhibiting neuronal apoptosis and activating SIRT1-dependent PGC-1α signaling.

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Investigating the role of Sirt1-modulated oxidative stress in relation to benign paroxysmal positional vertigo and Parkinson's disease

Cited by 34 publications

References 53 publications

The Role of Oxidative Stress and Inflammatory Mediators in Benign Paroxysmal Positional Vertigo

The Role of Oxidative Stress and Inflammatory Mediators in Benign Paroxysmal Positional Vertigo

SIRT1 mediates salidroside‐elicited protective effects against MPP⁺‐induced apoptosis and oxidative stress in SH‐SY5Y cells: involvement in suppressing MAPK pathways

Adiponectin Protects against Glutamate‐Induced Excitotoxicity via Activating SIRT1‐Dependent PGC‐1α Expression in HT22 Hippocampal Neurons

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Investigating the role of Sirt1-modulated oxidative stress in relation to benign paroxysmal positional vertigo and Parkinson's disease

Cited by 34 publications

References 53 publications

The Role of Oxidative Stress and Inflammatory Mediators in Benign Paroxysmal Positional Vertigo

The Role of Oxidative Stress and Inflammatory Mediators in Benign Paroxysmal Positional Vertigo

SIRT1 mediates salidroside‐elicited protective effects against MPP+‐induced apoptosis and oxidative stress in SH‐SY5Y cells: involvement in suppressing MAPK pathways

Adiponectin Protects against Glutamate‐Induced Excitotoxicity via Activating SIRT1‐Dependent PGC‐1α Expression in HT22 Hippocampal Neurons

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SIRT1 mediates salidroside‐elicited protective effects against MPP⁺‐induced apoptosis and oxidative stress in SH‐SY5Y cells: involvement in suppressing MAPK pathways