Resveratrol attenuates methylglyoxal-induced mitochondrial dysfunction and apoptosis by Sestrin2 induction

Seo, Kyuhwa; Seo, Suho; Han, Jae Yun; Ki, Sung Hwan; Shin, Sook

doi:10.1016/j.taap.2014.08.011

Cited by 46 publications

(34 citation statements)

References 60 publications

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“…We observed that its expression was lower in day 16 p53 d/d deciduae, which was substantially improved by Met treatment ( Figure 6G). This corroborates other findings that Met or Rsv increases Sesn2 expression (39)(40)(41). We next asked whether p53 can directly regulate the expression of Sesn2.…”

Section: Met or Rsv Inversely Regulates Ampk And Mtorc1 Signaling In supporting

confidence: 90%

p53 coordinates decidual sestrin 2/AMPK/mTORC1 signaling to govern parturition timing

Deng¹,

Cha²,

Yuan³

et al. 2016

Journal of Clinical Investigation

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Section: Met or Rsv Inversely Regulates Ampk And Mtorc1 Signaling In supporting

confidence: 90%

p53 coordinates decidual sestrin 2/AMPK/mTORC1 signaling to govern parturition timing

Deng¹,

Cha²,

Yuan³

et al. 2016

Journal of Clinical Investigation

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“…Cheng et al conducted a study to examine the effect of RSV on MGO‐treated pancreatic cells in the presence or absence of RSV; they reported that RSV had an inhibitory effect on MGO‐mediated expression of a negative regulator of insulin production and oxidative stress . Seo et al found that RSV reduced MGO‐induced oxidative stress, mitochondrial dysfunction, and apoptosis in HepG2 cells . In a study by Ohtsu et al, various dosages of RSV abated AGE‐induced IL‐6 production in mice macrophages and inhibited differentiation of macrophages into the inflammatory M1 phenotype .…”

Section: Resultsmentioning

confidence: 99%

The impact of resveratrol on toxicity and related complications of advanced glycation end products: A systematic review

et al. 2019

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Accumulation of advanced glycation end products (AGEs) promotes the generation of free radicals, which leads to chronic oxidative stress predisposing to chronic oxidative stress, inflammation, and related diseases. This systematic review aimed to determine the effect of resveratrol (RSV) on AGE‐induced toxicity and its deleterious consequences. A comprehensive search was performed through literature were published until December 2018 using relevant keywords. The databases that were used for the search were PubMed, Scopus, Embase, ProQuest, and Google Scholar. A total of 29 eligible studies were found and included in the review for the analysis. Except one, all studies showed suppressing effects for RSV on the production of AGEs or receptor for advanced glycation end products (RAGE) and its detrimental consequences including oxidative stress, inflammatory response, cellular immune reactions, insulin response, and atherosclerosis. RSV exerts its effects through influencing RAGE, nuclear factor kappa B (NF‐κB), peroxisome proliferator‐activated receptor (PPAR) γ, and transforming growth factor (TGF)‐β activities. This review suggests that RSV has got potential to decrease AGEs toxicity and inhibit the AGE‐induced complications. More clinical trials are suggested to evaluate the beneficial effect of RSV on AGEs in chronic metabolic diseases.

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“…Resveratrol also functions as a phytoestrogen, regulating the reproductive systems by changing the level of estrogen through estrogen receptors (ERs) binding, increasing progesterone secretion as well as mRNA levels of Sirt1, LH receptor, and steroidogenic regulatory protein in cells [26, 27]. More notably, resveratrol could develop a powerful anti-apoptotic effect in organisms through its action on several different pathways including interleukin family [28], p53 signal [29], and ROS-dependent pathways [30]. …”

Section: Introductionmentioning

confidence: 99%

Protective effects of resveratrol against mancozeb induced apoptosis damage in mouse oocytes

Liu

Wang

et al. 2016

Oncotarget

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Mancozeb, a mixture of ethylene-bis-dithiocarbamate manganese and zinc salts, is one of the most widely used fungicides in agriculture. Mancozeb could lead to mitochondria dysfunction, cellular anti-oxidation enzymes depletion and apoptotic pathways activation. Previous studies indicated the exposure of mancozeb through mother would lead to irregular estrous cycles, decreased progesterone levels, reduced litter sizes, and more frequent delivery of dead fetuses. In this study, we investigated mancozeb inducing reproductive toxicity, especially focusing on its apoptotic effect and epigenetic modifications. We also showed that resveratrol, a kind of phytoalexin found in peanuts and grapes, can alleviate mancozeb's adverse effects, such as declined fertility, decreased ovary weight and primary follicles. Besides, mancozeb treated oocytes displayed suboptimal developmental competence and this can also be improved by treatment of resveratrol. More detailed investigation of these processes revealed that mancozeb increased reactive oxygen species, causing cell apoptosis and abnormal epigenetic modifications, and resveratrol can block these cytotoxic changes. Collectively, our results showed that resveratrol can alleviate mancozeb induced infertility and this was mainly through the correction of apoptotic tendency and the abnormity of cellular epigenetic modification.

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Resveratrol attenuates methylglyoxal-induced mitochondrial dysfunction and apoptosis by Sestrin2 induction

Cited by 46 publications

References 60 publications

p53 coordinates decidual sestrin 2/AMPK/mTORC1 signaling to govern parturition timing

p53 coordinates decidual sestrin 2/AMPK/mTORC1 signaling to govern parturition timing

The impact of resveratrol on toxicity and related complications of advanced glycation end products: A systematic review

Protective effects of resveratrol against mancozeb induced apoptosis damage in mouse oocytes

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