Blog
About

88
views
0
recommends
+1 Recommend
1 collections
    6
    shares
      • Record: found
      • Abstract: found
      • Article: found

      GTS40, an active fraction of Gou Teng-San (GTS), protects PC12 from H 2O 2-induced cell injury through antioxidative properties

      Read this article at

      ScienceOpenPublisher
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Oxidative stress, a predominant cause of apoptosis cascades triggered in neurodegenerative disorders, has been regarded as a critical inducement in the pathogenesis of Alzheimer’s disease (AD). Gou Teng-San (GTS) is a traditional Chinese herbs preparation commonly utilized to alleviate cognitive dysfunction and psychological symptoms of patients with dementia. The present study aimed to investigate the protective effects of GTS40, an active fraction of GTS, on H 2O 2-induced oxidative damage and identify the potential active ingredients. Our results revealed that GTS40 exhibited radical scavenging activity, elevated cell viability, decreased the levels of intracellular reactive oxygen species (ROS), and stabilized mitochondrial transmembrane potential (MMP) in H 2O 2-treated PC12 cells. In addition, GTS40 blocked the apoptotic cascade by reversing the imbalance of Bcl-2/Bax and inhibiting the activity of caspase-3. Furthermore, an HPLC-QTOFMS method was developed to characterize major chemical constituents in GTS40. Our results revealed twenty-seven identified or tentatively characterized compounds through comparing their retention time ( t R) and MS spectra with reference standards. These results suggested that GTS40 was a promising active fraction that may be beneficial in the prevention and treatment of oxidative stress-mediated neurodegenerative disorders.

          Related collections

          Most cited references 24

          • Record: found
          • Abstract: not found
          • Article: not found

          BCL-2 family members and the mitochondria in apoptosis

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Programmed cell death via mitochondria: different modes of dying.

             S Susin,  B Queenan,  J-M Bras (2005)
            Programmed cell death (PCD) is a major component of normal development, preservation of tissue homeostasis, and elimination of damaged cells. Many studies have subdivided PCD into the three categories of apoptosis, autophagy, and necrosis based on criteria such as morphological alterations, initiating death signal, or the implication of caspases. However, these classifications fail to address the interplay between the three types of PCD. In this review, we will discuss the central role of the mitochondrion in the integration of the cell death pathways. Mitochondrial alterations such as the release of sequestered apoptogenic proteins, loss of transmembrane potential, production of reactive oxygen species (ROS), disruption of the electron transport chain, and decreases in ATP synthesis have been shown to be involved in, and possibly responsible for, the different manifestations of cell death. Thus, the mitochondria can be viewed as a central regulator of the decision between cellular survival and demise.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Ginsenoside Rg1 protects against hydrogen peroxide-induced cell death in PC12 cells via inhibiting NF-κB activation.

               Jun-Feng Kou,  Bo Yu,  Qian Liu (2010)
              Oxidative stress is a major cause in neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), and cerebral ischemia. Ginsenoside Rg1, a natural product extracted from Panax ginseng C.A. Meyer, has been reported to exert notable neuroprotective activities, which partly ascribed to its antioxidative activity. However, its molecular mechanism against oxidative stress induced by exogenous hydrogen peroxide (H(2)O(2)) remained unclear. In this study, we investigated its effect on H(2)O(2)-induced cell death and explored possible signaling pathway in PC12 cells. We proved that pretreatment with Rg1 at concentrations of 0.1-10 μM remarkably reduced the cytotoxicity induced by 400 μM of H(2)O(2) in PC12 cells by MTT and Hoechst and PI double staining assay. Of note, we demonstrated the activation of NF-κB signaling pathway induced by H(2)O(2) thoroughly in PC12 cells, and Rg1 suppressed phosphorylation and nuclear translocation of NF-κB/p65, phosphorylation and degradation of inhibitor protein of κB (IκB) as well as the phosphorylation of IκB-kinase complex (IKK) by western blotting or indirect immunofluorescence assay. Besides, Rg1 also inhibited the activation of Akt and the extracellular signal-regulated kinase 1/2 (ERK1/2). Furthermore, the protection of Rg1 on H(2)O(2)-injured PC12 cells was attenuated by pretreatment with two NF-κB pathway inhibitors (JSH-23 or BOT-64). In conclusion, our results suggest that Rg1 could rescue the cell injury by H(2)O(2) via down-regulation NF-κB signaling pathway as well as Akt and ERK1/2 activation, which put new evidence on the neuroprotective mechanism of Rg1 against the oxidative stress and the regulatory role of H(2)O(2) in NF-κB pathway in PC12 cells. Copyright © 2010 Elsevier Ltd. All rights reserved.
                Bookmark

                Author and article information

                Journal
                CJNM
                Chinese Journal of Natural Medicines
                Elsevier
                1875-5364
                20 July 2017
                : 15
                : 7
                : 495-504
                Affiliations
                1Department of Natural Medicinal Chemistry, China Pharmaceutical University, Nanjing 210009, China
                2Department of Pharmaceutical Analysis, China Pharmaceutical University, Nanjing 210009, China
                3Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, China
                Author notes
                *Corresponding author: FENG Feng, Tel: 86-25-86185216, E-mail: fengfeng@ 123456cpu.edu.cn ; LIU Wen-Yuan, Tel: 86-25-83271038, E-mail: liuwenyuan8506@ 123456163.com

                These authors have no conflict of interest to declare.

                Article
                S1875-5364(17)30075-4
                10.1016/S1875-5364(17)30075-4
                Copyright © 2017 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81373956
                Award ID: J1310032
                This work was supported by the National Natural Science Foundation of China (Nos. 81373956 and J1310032).

                Comments

                Comment on this article