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      Biological Activities of 2,3,5,4′-Tetrahydroxystilbene-2-O- β-D-Glucoside in Antiaging and Antiaging-Related Disease Treatments

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      Oxidative Medicine and Cellular Longevity
      Hindawi Publishing Corporation

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          Abstract

          2,3,5,4′-Tetrahydroxystilbene-2-O- β-D-glucoside (THSG) is active component of the Chinese medicinal plant Polygonum multiflorum Thunb. (THSG). Pharmacological studies have demonstrated that THSG exhibits numerous biological functions in treating atherosclerosis, lipid metabolism, vascular and cardiac remodeling, vascular fibrosis, cardiac-cerebral ischemia, learning and memory disorders, neuroinflammation, Alzheimer and Parkinson diseases, diabetic complications, hair growth problems, and numerous other conditions. This review focuses on the biological effects of THSG in antiaging and antiaging-related disease treatments and discusses its molecular mechanisms.

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          Most cited references63

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          Protection by tetrahydroxystilbene glucoside against cerebral ischemia: involvement of JNK, SIRT1, and NF-kappaB pathways and inhibition of intracellular ROS/RNS generation.

          Many natural polyphenolic compounds have been shown to attenuate reactive oxygen/nitrogen species (ROS/RNS) formation and protect against ischemia/reperfusion injury both in vitro and in vivo. 2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside (TSG), an active component of the rhizome extract from Polygonum multiflorum, exhibits antioxidative and anti-inflammatory effects. Here, we used an in vitro ischemic model of oxygen-glucose deprivation followed by reperfusion (OGD-R) and an in vivo ischemic model of middle cerebral artery occlusion (MCAO) to investigate the neuroprotective effects of TSG on ischemia/reperfusion brain injury and the related mechanisms. We demonstrated that OGD-R-induced neuronal injury, intracellular ROS generation, and mitochondrial membrane potential dissipation were reversed by TSG. The elevation of H2O2-induced [Ca2+]i was also attenuated by TSG. Inhibition of the c-Jun N-terminal kinase (JNK) and Bcl-2 family-related apoptotic signaling pathway was involved in the neuroprotection afforded by TSG. Meanwhile, TSG inhibited iNOS mRNA expression induced by OGD-R, which may be mediated by the activation of SIRT1 and inhibition of NF-kappaB activation. In vivo studies further demonstrated that TSG significantly reduced the brain infarct volume and the number of positive cells by TUNEL staining in the cerebral cortex compared to the MCAO group. Our study indicates that TSG protects against cerebral ischemia/reperfusion injury through multifunctional cytoprotective pathways.
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            In vitro effects of active components of Polygonum Multiflorum Radix on enzymes involved in the lipid metabolism.

            Raw and processed Polygoni Multiflori Radix (PMR and PMRP) are used in the prevention and treatment of non-alcoholic fatty liver disease (NAFLD), hyperlipidemia or related diseases. In our previous research, 2, 3, 5, 4'-tetrahydroxy-stilbene-2-O-β-D-glucoside (TSG) displayed the most important role in the total cholesterol (TC) lowering effect among all the chemical constituents of Polygonum multiflorum. Emodin and physcion displayed more favorable triglyceride (TG) reducing effects than TSG. However, there are few researches focus on the approach and mechanism of how do Polygonum multiflorum exhibit good lipid regulation activity. The targeted sites of active substances of Polygonum multiflorum are still not clearly elucidated. This research pays close attention to how major chemical components of Polygonum multiflorum affect the TC and TG contents in liver cells.
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              Protection by tetrahydroxystilbene glucoside against neurotoxicity induced by MPP+: the involvement of PI3K/Akt pathway activation.

              Oxidative stress plays an important role in the pathogenesis of Parkinson's disease (PD). 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucoside (TSG), which is an active component of the rhizome extract from polygonum multiflorum, shows potent antioxidant properties. In this paper, the neuroprotective effects of TSG on 1-methyl-4-phenylpyridinium (MPP+-induced apoptosis in PC12 cells were investigated. Pretreatment with TSG markedly attenuated MPP+-induced loss of cell viability and release of lactate dehydrogenase (LDH), and reduced MPP+-induced apoptotic cell death in a dose-dependent manner. The anti-apoptotic effects of TSG were probably mediated by the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway since TSG failed to rescue cells from MPP+ injury in the presence of the PI3K inhibitor, LY294002. These results indicate that TSG affords a significant neuroprotective effect against MPP+-induced damage and apoptosis in PC12 cells. The PI3K/Akt signaling pathway might be involved in the TSG-mediated anti-apoptotic effects. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
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                Author and article information

                Journal
                Oxid Med Cell Longev
                Oxid Med Cell Longev
                OMCL
                Oxidative Medicine and Cellular Longevity
                Hindawi Publishing Corporation
                1942-0900
                1942-0994
                2016
                20 June 2016
                : 2016
                : 4973239
                Affiliations
                Murad Research Institute for Modernized Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
                Author notes

                Academic Editor: Ryuichi Morishita

                Author information
                http://orcid.org/0000-0002-2370-169X
                http://orcid.org/0000-0001-6277-6320
                Article
                10.1155/2016/4973239
                4931083
                27413420
                47661cee-47d1-48f9-bd33-7d076000f967
                Copyright © 2016 S. Ling and J.-W. Xu.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 17 April 2016
                : 29 May 2016
                Categories
                Review Article

                Molecular medicine
                Molecular medicine

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