Resveratrol provides neuroprotection by inhibiting phosphodiesterases and regulating the cAMP/AMPK/SIRT1 pathway after stroke in rats

Wan, Dan; Zhou, Yehan; Wang, Ke; Hou, Yongying; Hou, Ruihang; Ye, Xiufeng

doi:10.1016/j.brainresbull.2016.02.011

Cited by 106 publications

(67 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Resveratrol (3,5,4'-trihydroxy-stilbene, RS) is a stilbenoid, a natural polyphenolic agent, which has been demonstrated to eliminate free radicals and ROS, reduce inflammatory response and modulate programmed cell death (9). Particularly, administration of resveratrol has potent neuroprotection effects in various animal models including cerebral ischemia reperfusion injury (10), stroke (11), and TBI (12). However, the mechanisms through which resveratrol exerts protective effect following TBI require further examination.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol pretreatment attenuates traumatic brain injury in rats by suppressing NLRP3 inflammasome activation via SIRT1

Zou

Liu

Li³

et al. 2017

Mol Med Report

View full text Add to dashboard Cite

The inflammatory response in the cerebral cortex serves an important role in the progression of secondary injury following traumatic brain injury (TBI). The NLR family pyrin domain containing 3 (NLRP3) inflammasome is necessary for initiating inflammation and is involved in various central nervous system disorders. The aim of the present study was to investigate the neuroprotective effect of resveratrol and elucidate the underlying mechanisms of resveratrol associated regulation of the NLRP3 inflammasome in TBI. The results demonstrated that the activation of NLRP3, caspase‑1 and sirtuin 1 (SIRT1), enhanced the production of inflammatory cytokines and reactive oxygen species (ROS) following TBI. Administration of resveratrol alleviated the degree of TBI, as evidenced by the reduced neuron‑specific enolase (NSE) and brain water content (WBC). Resveratrol pretreatment also inhibited the activation of NLRP3 and caspase‑1, and reduced the production of inflammatory cytokines and ROS. In addition, resveratrol further promoted SIRT1 activation. Furthermore, the suppressing effect of resveratrol on the NLRP3 inflammasome and ROS was blocked by the SIRT1 inhibitor, sirtinol. The results revealed that the activation of the NLRP3 inflammasome and the subsequent inflammatory responses in the cerebral cortex were involved in the process of TBI. Resveratrol may attenuate the inflammatory response and relieve TBI by reducing ROS production and inhibiting NLRP3 activation. The effect of resveratrol on NLRP3 inflammasome and ROS may also be SIRT1 dependent.

show abstract

Section: Introductionmentioning

confidence: 99%

Resveratrol pretreatment attenuates traumatic brain injury in rats by suppressing NLRP3 inflammasome activation via SIRT1

Zou

Liu

Li³

et al. 2017

Mol Med Report

View full text Add to dashboard Cite

show abstract

“…It was found that resveratrol inhibits PDE (Takizawa et al 2015), including PDE1 and PDE4 (Wang et al 2016, Rauf et al 2017. These features explain the neuroprotective properties of resveratrol in ischemia (Wan et al 2016). Inhibition of PDE3 explains the enhancement of myocardial contractility without an arrhythmogenic effect.…”

Section: Resultsmentioning

confidence: 95%

L-NAME-induced Preeclampsia: correction of functional disorders of the hemostasis system with Resveratrol and Nicorandil

Ступакова¹,

Лазарева²,

Гуреев³

et al. 2019

RRP

View full text Add to dashboard Cite

Introduction. Preeclampsia is a formidable disease of the second half of pregnancy, leading to severe complications, including disability and even death. Many authors have recognized the correlation between the severity of preeclampsia and the degree of disturbances in the hemostasis system. In this regard, the objective of this study was to assess inhibition of platelet aggregation and the possibility of its correction with resverаtrol and nicorandil. Materials and methods. The study was performed on 250 mature white Wistar female rats weighing 250–300 g. The platelet aggregation induced by ADP, collagen, ristomycin, adrenaline was determined, as well as PTT, TT, aPTT, fibrinogen, and the clotting time. Results and discussion. Introduction of resverаtrol and nicorandil resulted in a decrease in thrombocyte aggregation capacity from 53.8 ± 2.60% to 22.1 ± 1.25% and 37.1 ± 1.79%, respectively, when using ADP as an inducer. The clotting time was from 841 ± 42 s up to 1135 ± 33 s and 1034 ± 26 s, respectively. In addition, there was an increase in temporal parameters of plasma-coagulation hemostasis and a decrease in plasma fibrinogen content. The use of glibenclamide resulted in partial cancellation of the positive effects of resverаtrol and nicorandil, with an increase in platelet aggregation to 28.9 ± 1.8% and 43.9 ± 1.2% when using ADP as an inducer and a decrease in the thrombosis time to 988 ± 26 s and 950 ± 22 s, respectively. Conclusion. In animals with experimental preeclampsia, there were disturbances in the hemostasis system, comparable to those in the clinical situation. The use of resverаtrol and nicorandil leads to a pronounced correction of hemostasis parameters. The positive effects of the studied pharmacological agents are mediated by several mechanisms, including K+ATP channels.

show abstract

“…39 Moreover, activating AMPK up-regulates SIRT1 expression and activity while suppressing AMPK markedly lowers the resveratrol-mediated SIRT1 level. 40 It was reported that adiponectin up-regulated SIRT1 levels and mitochondrial gene expression for suppressing apoptosis through AMPK/SIRT1/PGC-1α pathway. 41 Our study showed that hypoxia significantly up-regulated SIRT1 level and was suppressed by a depletion of HMGB1.…”

Section: Discussionmentioning

confidence: 99%

<p>Knockdown of HMGB1 Suppresses Hypoxia-Induced Mitochondrial Biogenesis in Pancreatic Cancer Cells</p>

Yang¹,

Ye²,

Zeng³

et al. 2020

OTT

View full text Add to dashboard Cite

Purpose: To explore the regulatory effect of HMGB1 upon hypoxia-induced mitochondrial biogenesis in pancreatic cancer PANC1/CFPAC1 cells. Methods: After a down-regulation of HMGB1 expression by lentivirus-mediated RNAi, the effect of knocking down HMGB1 on hypoxia-induced mitochondrial biogenesis was examined. NRF-1/TFAM expression, mtDNA copy number, ATP content and mitochondrial number/morphology in hypoxia-treated pancreatic cancer cells were detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), Western blot, mtDNA and ATP assay kits and electron microscopy, respectively. Cell proliferation was measured by MTS assay. And protein and acetylation levels of PGC-1α and SIRT1 activity were detected by Western blot, immunoprecipitation (IP) and SIRT1 activity kit. Results: Hypoxia enhanced the expressions of NRF-1/TFAM, boosted mtDNA copy number and ATP content and increased the number of mitochondria in pancreatic cancer cells while induction was suppressed by a knockdown of HMGB1. Knocking down HMGB1 expression lowered hypoxia-induced PGC-1α/SIRT1 expression and activity, phosphorylation of AMPK. PGC-1α over-expression by a plasmid transfection failed to boost mtDNA copy number or ATP content in HMGB1-knockdown cells. A knockdown of HMGB1 attenuated hypoxia with AICAR (an AMPK activator)-induced expression of NRF-1, TFAM, PGC-1α, SIRT1 and the proteins of complexes Ⅰ& Ⅲ and reduced the acetylation level of PGC-1α/SIRT1 activity. Additionally, SRT1720 (a SIRT1 activator)induced elevation in SIRT1 activity boosted hypoxia-induced PGC-1α deacetylation, except in HMGB1-knockdown cells. Conclusion: As a novel regulator of mitochondrial biogenesis via AMPK/SIRT1 pathway under hypoxia, HMGB1 may become a potential drug target for therapeutic interventions in pancreatic cancer.

show abstract

Resveratrol provides neuroprotection by inhibiting phosphodiesterases and regulating the cAMP/AMPK/SIRT1 pathway after stroke in rats

Cited by 106 publications

References 40 publications

Resveratrol pretreatment attenuates traumatic brain injury in rats by suppressing NLRP3 inflammasome activation via SIRT1

Resveratrol pretreatment attenuates traumatic brain injury in rats by suppressing NLRP3 inflammasome activation via SIRT1

L-NAME-induced Preeclampsia: correction of functional disorders of the hemostasis system with Resveratrol and Nicorandil

<p>Knockdown of HMGB1 Suppresses Hypoxia-Induced Mitochondrial Biogenesis in Pancreatic Cancer Cells</p>

Contact Info

Product

Resources

About