Resveratrol Protects PC12 Cells from High Glucose-Induced Neurotoxicity Via PI3K/Akt/FoxO3a Pathway

Liu, Mi‐Hua; Yuan, Cong; He, Jun; Tan, Tian‐Ping; Wu, Shao‐Jian; Fu, Hong‐Yun; Liu, Jun; Yu, Shan; Chen, Yu‐Dan; Le, Qun-Fang; Tian, Wei; Hu, Heng‐Jing; Zhang, Yuan; Lin, Xiaolan

doi:10.1007/s10571-014-0147-5

Cited by 55 publications

(43 citation statements)

References 34 publications

(38 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…PI3/Akt is a pro-survival pathway, and its activation leads to cell survival. Different in vitro and in vivo studies showed that RES poses protective effect on the heart, brain and liver and some cell lines including PC12 and ovarian cancer cells (Chong et al, 2015;Gwak et al, 2015;Liu et al, 2015;Wang et al, 2015). In a review article, Bastianetto and colleagues listed the neuroprotective effects of RES (Bastianetto et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Neuro‐Protective Effects of Resveratrol on Carbon Monoxide‐Induced Toxicity in Male Rats

Tabrizian

Shahraki

Bazzi

et al. 2017

Phytotherapy Research

View full text Add to dashboard Cite

Acute carbon monoxide (CO) poisoning causes neurotoxicity through induction of necrosis, apoptosis, lipid peroxidation and oxidative stress. Resveratrol (RES) is a natural polyphenolic phytoalexin that exhibits neuroprotective effects in ischemia/reperfusion due to its anti-apoptotic, anti-necrotic and strong anti-oxidant properties as well as its ability to activate pro-survival pathways. In this study, rats were exposed to CO 3000 ppm for 1 h. Immediately after poisoning and on the next four consecutive days, RES (1, 5 and 10 mg/kg) was administered intraperitoneally. On the fifth day, animals' brains were excised, and necrosis, lipid peroxidation level and the level of Akt, BAX and BCL2 expression were evaluated. The results showed that RES 10 mg/kg significantly reduced lipid peroxidation, but RES 1 and 5 mg/kg had no significant effect on this parameter. Furthermore, RES 5 and 10 mg/kg significantly increased Akt expression level, while BAX/BCL2 ratio was reduced by RES 1, 5 and 10 mg/kg. Moreover, RES reduced necrotic foci in the brain, but the best results were seen following treatment with RES 10 mg/kg. In summary, RES showed neuroprotective effect in CO-poisoned rats as it decreased necrosis and BAX/BCL2 ratio and increased Akt expression levels. Copyright © 2017 John Wiley & Sons, Ltd.

show abstract

Section: Discussionmentioning

confidence: 99%

Neuro‐Protective Effects of Resveratrol on Carbon Monoxide‐Induced Toxicity in Male Rats

Tabrizian

Shahraki

Bazzi

et al. 2017

Phytotherapy Research

View full text Add to dashboard Cite

show abstract

“…Accumulated studies suggest that ROS overproduction and subsequent induction of oxidative damage were both involved in high glucose-induced neurotoxicity [23]. Therefore, intracellular ROS accumulation was measured by a fluoresceinlabeled dye, DCFH-DA.…”

Section: Dsepa Blocks High Glucose-induced Mitochondrial Dysfunction mentioning

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

View full text Add to dashboard Cite

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.

show abstract

“…RES is a polyphenol that is primarily found in red wine and possesses comprehensive physiological actions, including cardioprotective, anti-platelet and anti-inflammatory properties (7,8). RES inhibits DOX-induced cardiotoxicity by reducing oxidative stress and decreasing the severity of cardiac dysfunction (9).…”

Section: Introductionmentioning

confidence: 99%

Resveratrol inhibits doxorubicin-induced cardiotoxicity via sirtuin 1 activation in H9c2 cardiomyocytes

Liu

Shan

et al. 2016

Experimental and Therapeutic Medicine

Self Cite

View full text Add to dashboard Cite

Abstract. Doxorubicin (DOX) is an efficient drug used in cancer therapy; however, it can induce severe cytotoxicity, which limits its clinical application. In the present study, the effects of resveratrol (RES) on sirtuin 1 (SIRT1) activation in mediating DOX-induced cytotoxicity in H9c2 cardiac cells was investigated. H9c2 cells were exposed to 5 µM DOX for 24 h to establish a model of DOX cardiotoxicity. Apoptosis of H9c2 cardiomyocytes was assessed using the MTT assay and Hoechst nuclear staining. The results demonstrated that pretreating H9c2 cells with RES prior to the exposure of DOX resulted in increased cell viability and a decreased quantity of apoptotic cells. Western blot analysis demonstrated that DOX decreased the expression level of SIRT1. These effects were significantly alleviated by co-treatment with RES. In addition, the results demonstrated that DOX administration amplified forkhead box O1 (FoxO1) and P53 expression levels in H9c2 cells. RES was also found to protect against DOX-induced increases of FoxO1 and P53 expression levels in H9c2 cells. Furthermore, the protective effects of RES were arrested by the SIRT1 inhibitor nicotinamide. In conclusion, the results demonstrated that RES protected H9c2 cells against DOX-induced injuries via SIRT1 activation.

show abstract

Resveratrol Protects PC12 Cells from High Glucose-Induced Neurotoxicity Via PI3K/Akt/FoxO3a Pathway

Cited by 55 publications

References 34 publications

Neuro‐Protective Effects of Resveratrol on Carbon Monoxide‐Induced Toxicity in Male Rats

Neuro‐Protective Effects of Resveratrol on Carbon Monoxide‐Induced Toxicity in Male Rats

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

Resveratrol inhibits doxorubicin-induced cardiotoxicity via sirtuin 1 activation in H9c2 cardiomyocytes

Contact Info

Product

Resources

About