Recent Advances in the Study on Resveratrol

Nakata, Rieko; Takahashi, Satoru; Inoue, H.

doi:10.1248/bpb.35.273

Cited by 150 publications

(118 citation statements)

References 96 publications

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“…Previous studies proved that DNJ-rich MLE has been potentially used to improve lipid profiles in a human study (Doi et al 2000) and to suppress lipid accumulation through activation of the b-oxidation in vivo (Tsuduki et al 2009). In addition, resveratrol has properties to decrease ROS ) and stimulate PPARa involved in fatty acid oxidation (Nakata et al 2012). Moreover, previous studies reported that resveratrol improved insulin resistance by promoting HO-1 protein through mediating Nrf2 level in HepG2 cell (Cheng et al 2012).…”

Section: Discussionmentioning

confidence: 98%

Mulberry leaves (Morus alba L.) ameliorate obesity-induced hepatic lipogenesis, fibrosis, and oxidative stress in high-fat diet-fed mice

2015

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Obesity is associated with chronic diseases such as fatty liver, type 2 diabetes, cardiovascular disease, and severe metabolic syndrome. Obesity causes metabolic impairment including excessive lipid accumulation and fibrosis in the hepatic tissue as well as the increase in oxidative stress. In order to investigate the effect of mulberry leaf (Morus alba L.) extract (MLE) on obesity-induced oxidative stress, lipogenesis, and fibrosis in liver, MLE has been gavaged for 12 weeks in high-fat diet (HFD)-induced obese mice. MLE treatment significantly ameliorated LXRa-mediated lipogenesis and hepatic fibrosis markers such as a-smooth muscle actin, while MLE up-regulated lipolysis-associated markers such as lipoprotein lipase in the HFD-fed mice. Moreover, MLE normalized the activities of antioxidant enzymes including heme oxygenase-1 and glutathione peroxidase in accordance with protein levels of 4-hydroxynonenal in the HFDfed mice. MLE has beneficial effects on obesity-related fatty liver disease by regulation of hepatic lipid metabolism, fibrosis, and antioxidant defense system. MLE supplementation might be a potential therapeutic approach for obesity-related disease including non-alcoholic fatty liver disease.

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Section: Discussionmentioning

confidence: 98%

Mulberry leaves (Morus alba L.) ameliorate obesity-induced hepatic lipogenesis, fibrosis, and oxidative stress in high-fat diet-fed mice

2015

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“…Resveratrol is a parent compound of a family of molecules including glucosides and polymers (Cal et al, 2003), existing in cis and transconfigurations in narrow range of spermatophytes of which vines, peanuts and pines are the prime representatives (Kiselev et al, 2011;Nakata et al, 2012;Neves et al, 2012). Previous studies have reported that resveratrol exerted antitumor activities at various stages of tumor initiation, promotion and progression (Cimino et al, 2012;Stefanska et al, 2012;Whitlock et al, 2012), including in esophageal squamous cell carcinoma (Tang et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Inhibits Oesophageal Adenocarcinoma Cell Proliferation via AMP-activated Protein Kinase Signaling

Guanghua

Wang²,

Yang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Resveratrol has been examined in several model systems for potential effects against cancer. Adenosine monophosphate-activated protein kinase (AMPK) is reported to suppress proliferation in most eukaryocyte cells. Whether resveratrol via AMPK inhibits proliferation of oesophageal adenocarcinoma cells (OAC) is unknown. The aim of this study was to determine the roles of AMPK in the protective effects of resveratrol in OAC proliferation and to elucidate the underlying mechanisms. Treatment of cultured OAC derived from human subjects or cell lines with resveratrol resulted in decreased cell proliferation. Further, inhibition of AMPK by pharmacological reagent or genetical approach abolished resveratrol-suppressed OAC proliferation, reduced the level of p27 Kip1 , a cyclin-dependent kinase inhibitor, and increased the levels of S-phase kinase-associated protein 2 (Skp2) of p27 Kip1 -E3 ubiquitin ligase and 26S proteasome activity reduced by resveratrol. Furthermore, gene silencing of p27 Kip1 reversed resveratrol-suppressed OAC proliferation. In conclusion, these findings indicate that resveratrol inhibits Skp2-mediated ubiquitylation and 26S proteasome-dependent degradation of p27 Kip1 via AMPK activation to suppress OAC proliferation.

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“…In the in vitro situation, resveratrol activates several anti-aging genes and play anti-oxidative effect to delay cell replicative senescence. 11,13) But in the in vivo study, we administrated resveratrol on 3-month old mice, which is far from aging. Therefore, resveratrol rescued HDF-induced inflammatory response and oxidative stress which will strongly induce renal fibrosis.…”

Section: Hfd and Hg Culture Comparisonmentioning

confidence: 99%

“…7) Activation of SIRT1 protects mice from diet-induced obesity, metabolic disorders and oxidative injury, 8) while SIRT1 inactivation is associated with lipid accumulation, cell injury and diabetic nephropathy. 9,10) Resveratrol (3,5,4′-trihydroxystilbene), a natural plant polyphenol first isolated from the roots of white hellebore, 11) is reported as an activator of SIRT1. 12) Several evidences indicated the therapeutic potential of resveratrol, such as its antioxidant activity, cardioprotective effects and anticancer properties.…”

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confidence: 99%

Resveratrol Protects against High-Fat Diet Induced Renal Pathological Damage and Cell Senescence by Activating SIRT1

Zhang

et al. 2016

Biological & Pharmaceutical Bulletin

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Obesity-related renal diseases have been a worldwide issue. Effective strategy that prevents high fat-diet induced renal damage is of great significance. Resveratrol, a natural plant polyphenol, is famous for its antioxidant activity, cardioprotective effects and anticancer properties. However whether resveratrol can play a role in the treatment of renal diseases is unknown. In this study, we added resveratrol in normal glucose or high glucose medium and provide evidences that resveratrol protects against high-glucose triggered oxidative stress and cell senescence. Moreover, mice were fed with standard diet, standard diet plus resveratrol, high-fat diet or high-fat diet plus resveratrol for 3 months, and results show that resveratrol treatment prevents high-fat diet induced renal pathological damage by activating SIRT1, a key member in the mammalian sirtuin family that response to calorie restriction life-extension method. This research confirms the potential role of resveratrol in the treatment of renal diseases and may provide an effective and convenient method to mimic the beneficial effects of calorie restriction.

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Recent Advances in the Study on Resveratrol

Cited by 150 publications

References 96 publications

Mulberry leaves (Morus alba L.) ameliorate obesity-induced hepatic lipogenesis, fibrosis, and oxidative stress in high-fat diet-fed mice

Mulberry leaves (Morus alba L.) ameliorate obesity-induced hepatic lipogenesis, fibrosis, and oxidative stress in high-fat diet-fed mice

Resveratrol Inhibits Oesophageal Adenocarcinoma Cell Proliferation via AMP-activated Protein Kinase Signaling

Resveratrol Protects against High-Fat Diet Induced Renal Pathological Damage and Cell Senescence by Activating SIRT1

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