Polydatin inhibits the oxidative stress-induced proliferation of vascular smooth muscle cells by activating the eNOS/SIRT1 pathway

Ma, Yi; Gong, Xun; Mo, Yingli; Wu, Saizhu

doi:10.3892/ijmm.2016.2554

Cited by 42 publications

(21 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The upregulation of SIRT1 activity is closely related to certain health benefits [34]. In addition, the activation of the SIRT1 pathway contributes to the proliferation of vascular smooth muscle cells [35-37]. In contrast, multiple researchers have revealed that SIRT1 can induce cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Protects Against Pulmonary Arterial Hypertension in Rats via Activation of Silent Information Regulator 1

Jia

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Objectives: The polyphenol resveratrol (Rev) has been found to exhibit various beneficial effects including prevention of pulmonary arterial hypertension (PAH). The present study was designed to investigate the action and potential mechanism of Rev on PAH, focusing on the role of SIRT1 (Silent Information Regulator 1) in apoptosis of pulmonary artery smooth muscle cells (PASMCs). Methods: PAH rats were established by exposure to hypoxia for 21 days. Rev and SRT1720 (a selective SIRT1 activator) were used to reverse PAH by gavaging rats. PASMCs were confronted with hypoxia for 24 h or 48 h and were then treated with Rev or SRT1720 in vitro. Western blot was performed to detect the protein expression of SIRT1. CCK-8 and scratch wound experiments were carried out to verify cell proliferation. In addition, the TUNEL positive assay and flow cytometry assay were used to measure PASMC apoptosis. Mitochondrial permeability transition (mPT) was identified by confocal microscopy. Right ventricular systolic pressure (RVSP) was determined with a Gould pressure transducer, and right ventricular hypertrophy (RVH) was determined by weighing the cardiac muscle. Results: We demonstrated that Rev could reverse the remodelling of the pulmonary vasculature, thus contributing to alleviating the severity of PAH. Down-regulation of SIRT1 was observed in PAH, but administration of Rev had no obvious effect on the protein expression of SIRT1. In addition, Rev could induce mitochondrial swelling and nuclear pyknosis, leading to small, dense, and dysmorphic mitochondria in rats exposed to hypoxia alone. Rev treatment inhibited PASMC proliferation in a dose-dependent manner in vitro. Incubation with SRT1720, a specific activator of SIRT1, significantly retarded PASMC proliferation and promoted PASMC apoptosis in vitro. The mechanism could be associated with inducing mPT damage in PASMCs. Rev and SRT1720 treatment mitigated RVSP and reduced RVH. Conclusion: Rev produced a beneficial effect partially by enhancing the activation of SIRT1, thus improving RVSP and reducing RVH. SIRT1 activation increased PASMC apoptosis by inducing mPT dysfunction, which might be a novel future strategy for the treatment of PAH.

show abstract

Section: Discussionmentioning

confidence: 99%

Resveratrol Protects Against Pulmonary Arterial Hypertension in Rats via Activation of Silent Information Regulator 1

Jia

et al. 2017

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Wang [64] illustrates that polydatin is the main substance in serum after intragastric administration with polydatin or resveratrol, and the mutual transformation between polydatin and resveratrol keeps balance; they both have the ability of antioxidative stress in vivo, and polydatin has a better effect than resveratrol, which hints that polydatin may be a substitute for resveratrol as antioxidant for clinical use. Ma et al [65] demonstrated that polydatin inhibited the oxidative stress-induced proliferation of vascular smooth muscle cells (VMSCs) by activating the endothelial nitric oxide synthetase (eNOS/SIRT1) pathway.…”

Section: Polydatinmentioning

confidence: 99%

BIOLOGICALLY ACTIVE COMPOUNDS OF KNOTWEED (Reynoutria spp.)

Patočka¹,

Navrátilová²,

Ovando³

2017

Mil. Med. Sci. Lett.

View full text Add to dashboard Cite

Knotweeds (Reynoutria Houtt.) are plants native to the Far East. Japanese knotweed was introduced from Japan to the unsuspecting West by the horticultural activities of Philippe von Siebold via his nursery at Leiden in the 1840s. By 1854, the plant had arrived at the Royal Botanic Gardens in Edinburgh. The plants were then sold by a large number of commercial nursery gardens around the country. Further vegetative spread followed naturally along watercourses. The knotweed is currently extremely persistant invasive plant. There is also an important source of many bioactive substances which could be used in biomedicine. The article discusses biomedically relevant constituents and its pharmacological and toxicological properties.

show abstract

“…SIRT1 is a member of the sirtuin family, which is involved in many diseases and bioprocesses such cancer development, cell proliferation, oxidative stress, and pyroptosis . SIRT1 is also an upstream protein on PGC‐1α/Nrf2 signaling.…”

Section: Introductionmentioning

confidence: 99%

“…SIRT1 is a member of the sirtuin family, which is involved in many diseases and bioprocesses such cancer development, cell proliferation, oxidative stress, and pyroptosis. [14][15][16][17] SIRT1 is also an upstream protein on PGC-1α/Nrf2 signaling. Studies reported that the SIRT1/PGC-1α/Nrf2 signaling could mediate oxidative stress in rat liver 18 and brain.…”

mentioning

confidence: 99%

Chlorpyrifos activates cell pyroptosis and increases susceptibility on oxidative stress‐induced toxicity by miR‐181/SIRT1/PGC‐1α/Nrf2 signaling pathway in human neuroblastoma SH‐SY5Y cells

Zhao

Yang

Zhao

2019

Environmental Toxicology

View full text Add to dashboard Cite

Background The insecticide exposure has been linked to Parkinson's disease (PD). In the present study, we used a most widely used cell line in study of PD, the SH‐SY5Y cells, to investigate mechanisms of chlorpyrifos (CPF) induced cell toxicity and the possible roles of cell pyroptosis and oxidative stress in SH‐SY5Y cells, as well as role of miR‐181/SIRT1/PGC‐1α/Nrf2 signaling pathway in this process. Methods SH‐SY5Y cells were treated with different concentrations of CPF. Cell viability was measured using CCK‐8 assay. Cell pyroptosis was determined by immunofluorescence of caspase‐1 and TUNEL assay. The miR‐181 (has‐miR‐181‐5p) level was determined by qRT‐PCR. Expression of SIRT1, PGC‐1α, Nrf2, and pyroptosis related proteins NLRP3, caspase‐1, IL‐1β, and IL‐18 was determined by both qRT‐PCR and Western blotting. Results Cell viability was found to be decreased with the increased CPF concentrations. The pyroptosis related proteins, ROS levels, as well as level of caspase‐1 and the TUNEL positive cells were all significantly up‐regulated by CPF. Meanwhile, expression of miR‐181 and pyroptosis proteins was also enhanced, while the SIRT1/PGC‐1α/Nrf2 signaling was inhibited by CPF. Knockdown of Nrf2 significantly up‐regulated the expression of pyroptosis related proteins, ROS level, caspase‐1, and the TUNEL positive cells, while over‐expression of Nrf2 resulted in opposite results. The expression of PGC‐1α and Nrf2 was significantly down‐regulated when SIRT1 was inhibited, while over‐expressed SIRT1 led to increased PGC‐1α and Nrf2 levels. Besides, miR‐181 promoted the CPF induced activation of pyroptosis and oxidative stress, as well as down‐regulated SIRT1/PGC‐1α/Nrf2 signaling, while inhibition of miR‐181 led to opposite results. Conclusions Chlorpyrifos could inhibit cell proliferation, activate cell pyroptosis and increase susceptibility on oxidative stress‐induced toxicity by elevating miR‐181 through down‐regulation of the SIRT1/PGC‐1α/Nrf2 pathway in human neuroblastoma SH‐SY5Y cells. This study might give deeper insights for mechanisms of CPF induced toxicity and might give some novel research targets for PD treatment.

show abstract

Polydatin inhibits the oxidative stress-induced proliferation of vascular smooth muscle cells by activating the eNOS/SIRT1 pathway

Cited by 42 publications

References 48 publications

Resveratrol Protects Against Pulmonary Arterial Hypertension in Rats via Activation of Silent Information Regulator 1

Resveratrol Protects Against Pulmonary Arterial Hypertension in Rats via Activation of Silent Information Regulator 1

BIOLOGICALLY ACTIVE COMPOUNDS OF KNOTWEED (Reynoutria spp.)

Chlorpyrifos activates cell pyroptosis and increases susceptibility on oxidative stress‐induced toxicity by miR‐181/SIRT1/PGC‐1α/Nrf2 signaling pathway in human neuroblastoma SH‐SY5Y cells

Contact Info

Product

Resources

About