Resveratrol attenuates high glucose-induced endothelial cell apoptosis via mediation of store-operated calcium entry

Lu, Ting; Zhou, Dayan; Gao, Pan; Si, Liang-Yi; Xu, Qiang

doi:10.1007/s11010-017-3194-7

Cited by 14 publications

(8 citation statements)

References 29 publications

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“…Accordingly, it has become particularly pressing to find an effective treatment to prevent or delay the damage caused by oxidative stress. As a promising anti-oxidative small molecule, the effects of resveratrol on preventing chemical-induced oxidative damage or apoptosis have been extensively studied [ 32 , 33 , 41 , 42 ]. Furthermore, the possible functions of resveratrol in improving oocyte maturation, fertilization and preimplantation embryonic development have also been reported [ 36 – 38 ].…”

Section: Discussionmentioning

confidence: 99%

Resveratrol increases resistance of mouse oocytes to postovulatory aging in vivo

Liang

Lin

Zhang

et al. 2018

Aging

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After ovulation, metaphase II oocytes undergo a time-dependent deterioration in vivo or in vitro, which is referred to as postovulatory oocyte aging, a process during which a series of deleterious molecular and cellular changes occur. In this study, we found that short-term injection of resveratrol (3,5,4'-trihydroxystilbene) effectively ameliorated oxidative stress-induced damage in postovulatory oocyte aging of middle-aged mice in vivo. Resveratrol induced changes that delayed the aging-induced oocyte deterioration including the elevated expression of the anti-aging molecule Sirtuin 1 (SIRT1); it reduced intracellular reactive oxygen species (ROS) level, and improved mitochondria function. In addition, these beneficial changes may also help to prevent apoptosis. Taken together, our data suggest that resveratrol can effectively protect against postovulatory oocyte aging in vivo primarily by preventing ROS production.

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Section: Discussionmentioning

confidence: 99%

Resveratrol increases resistance of mouse oocytes to postovulatory aging in vivo

Liang

Lin

Zhang

et al. 2018

Aging

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“…On this basis, research on SOCE can exclude other influences. Many studies have shown that resveratrol can inhibit SOCE, but its mechanism is diverse [19, 23, 24]. Our research showed that suppressed SOCE was correlated with ORAI1 loss and reduction of ORAI1–STIM1 dimer without expressive difference for STIM1 in FLSs.…”

Section: Discussionmentioning

confidence: 51%

“…Besides, based on our former study, 5 μM H 2 O 2 , rather than higher or lower dose, lead to slight proliferation of fibroblast in vitro, which provided a bio-model to imitate cytoproliferative and oxidative microenvironment in human RA enhancing the reliability of in vitro cell-based study [5]. Recent studies have shown that resveratrol can attenuate high glucose-induced apoptosis of vascular endothelial cells by regulating SOCE, suggesting that resveratrol may be involved in the regulation of specific apoptosis via SOCs [19]. Therefore, based on the previous research, our group further explored the specific mechanism of resveratrol-induced apoptosis in fibroblasts within 5 μM H 2 O 2 , and attempted to elucidate the regulation of resveratrol on SOCE and two essential SOCs, STIM1 and ORAI1.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol reduces store-operated Ca2+ entry and enhances the apoptosis of fibroblast-like synoviocytes in adjuvant arthritis rats model via targeting ORAI1–STIM1 complex

Yang

Zheng

et al. 2019

Biol Res

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Background Resveratrol was reported to trigger the apoptosis of fibroblast-like synoviocytes in adjuvant arthritis rats but the subcellular mechanism remains unclear. Since ER stress, mitochondrial dysfunction and oxidative stress were involved in the effects of resveratrol with imbalance of calcium bio-transmission, store operated calcium entry (SOCE), a novel intracellular calcium regulatory pathway, may also participate in this process. Results In the present study, Resveratrol was found to suppress ORAI1 expression of a dose dependent manner while have no evident effects on STIM1 expressive level. Besides, resveratrol had no effects on ATP or TG induced calcium depletion but present partly dose-dependent suppression of SOCE. On the one hand, microinjection of ORAI1 overexpressed vector in sick toe partly counteracted the therapeutic effects of resveratrol on adjuvant arthritis and serum inflammatory cytokine including IL-1, IL-6, IL-8, IL-10 and TNF-α. On the other hand, ORAI1 SiRNA injection provided slight relief to adjuvant arthritis in rats. In addition, ORAI1 overexpression partly diminished the alleviation of hemogram abnormality induced by adjuvant arthritis after resveratrol treatment while ORAI1 knockdown presented mild resveratrol-like effect on hemogram in rats model. Conclusion These results indicated that resveratrol reduced store-operated Ca 2+ entry and enhanced the apoptosis of fibroblast-like synoviocytes in adjuvant arthritis rats model via targeting ORAI1–STIM1 complex, providing a theoretical basis for ORAI1 targeted therapy in future treatment with resveratrol on rheumatoid arthritis. Electronic supplementary material The online version of this article (10.1186/s40659-019-0250-7) contains supplementary material, which is available to authorized users.

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“…RESV is a polyphenol naturally found in a variety of plant species such as grapes, apples, berries, and peanuts. It is well known to have bene cial effects, including anti-in ammatory, anti-oxidative stress and anti-apoptosis [9,18]. The anti-apoptotic effects of RESV have been widely investigated in multiple organs, including lungs.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol attenuates cigarette smoke induced endothelial apoptosis by activating Notch1 signaling mediated autophagy

Zong

Liu

et al. 2021

Preprint

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Background: Increasing evidences have showed that endothelial apoptosis contributes to cigarette smoke (CS)-induced disease progression, such as chronic obstructive pulmonary disease (COPD). Our previous studies have validated Notch1 as an anti-apoptotic signaling in CS-induced endothelial apoptosis. Resveratrol (RESV) is a naturally occurring polyphenol that exhibits an anti-apoptotic activity in endothelial cells that exposed to many kinds of destructive stimulus. However, the effects of resveratrol on Notch1 signaling in CS-induced endothelial apoptosis have not yet been fully elucidated. Therefore, the aim of this study was to examine whether RESV can protect endothelial cells from CS-induced apoptosis via regulating Notch1 signaling. Methods: Human umbilical vein endothelial cells (HUVECs) were pretreated with RESV for 2 h, followed by cotreatment with 2.5%CSE for 24h to explore the role of RESV in CSE induced endothelial apoptosis. 3-methyladenine (3-MA) or rapamycin was used to alter autophagic levels. Lentivirus Notch1 intracellular domain (LV-N1ICD) or γ-secretase inhibitor (DAPT) were used to change Notch1 expression. The expression of Notch1, autophagic and apoptotic markers were examined by Western blot and the apoptosis rate was detected by Flow cytometry analysis.Results: Our results showed that activating autophagy reduced CSE-induced endothelial apoptosis, while blocking autophagy promoted cell apoptosis in HUVECs. RESV pretreatment attenuated the CSE-induced endothelial apoptosis and activated Notch1 signaling. RESV pretreatment also increased LC3b-II and Beclin1 production, decreased p62 and mTOR expression. 3-MA treatment inhibited autophagy and aggravated CSE induced apoptosis, while rapamycin promoted autophagy, led to a decrease in cell apoptosis. LV-N1ICD transfection upregulated autophagy and reduced apoptosis. However, this protective effect was abolished by 3-MA treatment. In cells treated with DAPT, autophagy was decreased, while apoptosis was increased. RESV partly rescued the DAPT induced apoptosis by activating Notch1 signaling. Conclusion: In HUVECs, RESV attenuates CSE induced endothelial apoptosis by inducing autophagy in a Notch1-dependent manner.

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Resveratrol attenuates high glucose-induced endothelial cell apoptosis via mediation of store-operated calcium entry

Cited by 14 publications

References 29 publications

Resveratrol increases resistance of mouse oocytes to postovulatory aging in vivo

Resveratrol increases resistance of mouse oocytes to postovulatory aging in vivo

Resveratrol reduces store-operated Ca2+ entry and enhances the apoptosis of fibroblast-like synoviocytes in adjuvant arthritis rats model via targeting ORAI1–STIM1 complex

Resveratrol attenuates cigarette smoke induced endothelial apoptosis by activating Notch1 signaling mediated autophagy

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