Protective effect of telmisartan against oxidative damage induced by high glucose in neuronal PC12 cell

Eslami, Habib; Sharifi, Ali Mohammad; Rahimi, Hamzeh; Rahati, Maryam

doi:10.1016/j.neulet.2013.10.057

Cited by 40 publications

(33 citation statements)

References 30 publications

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“…Previous studies have shown that ROS leads to caspase‐3 activation and has a specialized role in the promotion of hyperglycemia‐induced neuronal damage . Furthermore, caspase activation (including caspase‐3 and ‐9) is enhanced in high‐glucose situations .…”

Section: Discussionmentioning

confidence: 99%

Leptin attenuates oxidative stress and neuronal apoptosis in hyperglycemic condition

Kaeidi

Hajializadeh

Jahandari

et al. 2018

Fundamemntal Clinical Pharma

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One of the main pathological mechanisms of neurotoxicity in diabetic situation is oxidative stress promoted by hyperglycemia. It has been shown that leptin has neuroprotective effects and may provide neuronal survival signals. This study was designed to reveal the possible neuroprotective effects of leptin in hyperglycemic conditions. Pheochromocytoma (PC12) cell viability was assessed via the MTT test. Cellular reactive oxygen species (ROS) generation was determined by DCFH-DA analysis. The malondialdehyde (MDA) and glutathione (GSH) levels were measured in high-glucose-treated PC12 cells with and without leptin cotreatment. Western blotting was performed to measure apoptosis markers (Cleaved caspase-3 and Bax/Bcl2 ratio). Elevation of glucose levels (100 mmol/L) consecutively increased intracellular ROS and MDA level, and apoptosis in PC12 cells after 24 h leptin administration (12 and 24 nmol/L) decreased the high-glucose-induced cell toxicity, caspase-3 activation, and Bax/Bcl-2 ratio. Also, cotreatment with leptin (12 and 24 nmol/L) significantly reduced oxidative damage to PC12 cells in high-glucose condition, as reflected by the diminution in MDA and ROS levels and the increase in GSH content. Our finding demonstrates that leptin has protective effects against hyperglycemia-induced neural damage. This could be related to the attenuation of oxidative stress and neural apoptosis.

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Section: Discussionmentioning

confidence: 99%

Leptin attenuates oxidative stress and neuronal apoptosis in hyperglycemic condition

Kaeidi

Hajializadeh

Jahandari

et al. 2018

Fundamemntal Clinical Pharma

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“…However, little information about the protective effect of Se against hyperglycemia-induced toxicity and apoptosis is available, especially the molecular mechanism. PC12 derived from rat pheochromocytoma cells was considered as an optimal model in vitro to simulate neuron to explore the underlying mechanism [30,31]. After all, PC12 cell line is a cancer cell line, the in vivo effect and mechanism of DSePA need further evaluation.…”

Section: Discussionmentioning

confidence: 99%

DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

Wang

et al. 2015

Mol Neurobiol

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Hyperglycemia as the major hallmark of diabetic neuropathy severely limited its therapeutic efficiency. Evidences have revealed that selenium (Se) as an essential trace element could effectively reduce the risk of neurological diseases. In the present study, 3,3'-diselenodipropionic acid (DSePA), a derivative of selenocystine, was employed to investigate its protective effect against high glucose-induced neurotoxicity in PC12 cells and evaluate the underlying mechanism. The results suggested that high glucose showed significant cytotoxicity through launching mitochondria-mediated apoptosis in PC12 cells, accompanied by poly (ADP-ribose) polymerase (PARP) cleavage, caspase activation, and mitochondrial dysfunction. Moreover, high glucose also triggered DNA damage and dysregulation of MAPKs and AKT pathways through reactive oxygen species (ROS) overproduction. p53 RNA interference partially suppressed high glucose-induced cytotoxicity and apoptosis, indicating the role of p53 in high glucose-induced signal. However, DSePA pretreatment effectively attenuated high glucose-induced cytotoxicity, inhibited the mitochondrial dysfunction through regulation of Bcl-2 family, and ultimately reversed high glucose-induced apoptotic cell death in PC12 cells. Attenuation of caspase activation, PARP cleavage, DNA damage, and ROS accumulation all confirmed its protective effects. Moreover, DSePA markedly alleviated the dysregulation of AKT and MAPKs pathways induced by high glucose. Our findings revealed that the strategy of using DSePA to antagonize high glucose-induced neurotoxicity may be a highly effective strategy in combating high glucose-mediated neurological diseases.

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“…Oxidative stress plays an important role in the neuronal damage of many central nervous system (CNS) diseases, including Alzheimer's disease, Parkinson's disease, cerebral ischemia, and traumatic brain injury (TBI) (Shibata and Kobayashi 2008;Eslami et al 2014;Sun et al 2013;Cornelius et al 2013). Excessive accumulation of reactive oxygen species (ROS), such as superoxide anion (O 2 -) and hydrogen peroxide (H 2 O 2 ), can attack proteins, lipid membranes, and nucleic acids, causing oxidative injury to neural cells (Chan 2001;Prasad et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Propofol Protects Against H2O2-Induced Oxidative Injury in Differentiated PC12 Cells via Inhibition of Ca2+-Dependent NADPH Oxidase

et al. 2015

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Propofol (2,6-diisopropylphenol) is a widely used general anesthetic with anti-oxidant activities. This study aims to investigate protective capacity of propofol against hydrogen peroxide (H2O2)-induced oxidative injury in neural cells and whether the anti-oxidative effects of propofol occur through a mechanism involving the modulation of NADPH oxidase (NOX) in a manner of calcium-dependent. The rat differentiated PC12 cell was subjected to H2O2 exposure for 24 h to mimic a neuronal in vitro model of oxidative injury. Our data demonstrated that pretreatment of PC12 cells with propofol significantly reversed the H2O2-induced decrease in cell viability, prevented H2O2-induced morphological changes, and reduced the ratio of apoptotic cells. We further found that propofol attenuated the accumulation of malondialdehyde (biomarker of oxidative stress), counteracted the overexpression of NOX core subunit gp91(phox) (NOX2) as well as the NOX activity following H2O2 exposure in PC12 cells. In addition, blocking of L-type Ca(2+) channels with nimodipine reduced H2O2-induced overexpression of NOX2 and caspase-3 activation in PC12 cells. Moreover, NOX inhibitor apocynin alone or plus propofol neither induces a significant downregulation of NOX activity nor increases cell viability compared with propofol alone in the PC12 cells exposed to H2O2. These results demonstrate that the protective effects of propofol against oxidative injury in PC12 cells are mediated, at least in part, through inhibition of Ca(2+)-dependent NADPH oxidase.

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Protective effect of telmisartan against oxidative damage induced by high glucose in neuronal PC12 cell

Cited by 40 publications

References 30 publications

Leptin attenuates oxidative stress and neuronal apoptosis in hyperglycemic condition

Leptin attenuates oxidative stress and neuronal apoptosis in hyperglycemic condition

DSePA Antagonizes High Glucose-Induced Neurotoxicity: Evidences for DNA Damage-Mediated p53 Phosphorylation and MAPKs and AKT Pathways

Propofol Protects Against H2O2-Induced Oxidative Injury in Differentiated PC12 Cells via Inhibition of Ca2+-Dependent NADPH Oxidase

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