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      Investigation of the anti-cataractogenic mechanisms of curcumin through in vivo and in vitro studies

      research-article
      1 , 2 , 2 ,
      BMC Ophthalmology
      BioMed Central
      Curcumin, Cataract, Reactive oxygen, Cell viability, Cell apoptosis

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          Abstract

          Background

          Cataract is the leading cause of blindness in elderly people worldwide, especially in developing countries. Studies to identify strategies that can prevent or retard cataract formation are urgently required. This study aimed to investigate the potential mechanism of the cytoprotective effects of curcumin in in vivo and in vitro experiments.

          Methods

          Male Wistar rats were randomly divided into three groups: the control group, the model group (administered 20 μmol/kg sodium selenite), and the curcumin group (pretreated with 75 mg/kg body weight curcumin 24 h prior to the administration of sodium selenite). The expression levels of heat shock protein 70 (HSP70), the activities of 8-hydroxy-2-deoxyguanosine (8-OHdG), catalase (CAT), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were assessed by using RT-PCR assay and ELISA. In addition, the cell viability, cell apoptosis, and cell cycle were assessed using a CCK-8 assay and flow cytometry in in vitro studies, followed by RT-PCR analysis to identify the mRNA expression levels of caspase 3, Bcl-2 associated X (Bax), B-cell lymphoma 2 (Bcl-2), cyclooxygenase (Cox-2), c-met, and Slug.

          Results

          Cataract was successfully established in rats of the model group and the curcumin group through intraperitoneal injection of sodium selenite. The expression levels of HSP70 and the activities of 8-OHdG and MDA in the curcumin group were decreased compared with those in the model group, whereas the activities of CAT, SOD, and GSH-Px were significantly higher than those in the model group ( P < 0.05). In the in vitro studies, the cell viability and cell apoptosis significantly increased and decreased, respectively, in the curcumin group compared with the model group. Correspondingly, the mRNA expression of caspase-3, Bax, and Cox-2 was lower in the curcumin group than in the model group ( P < 0.05).

          Conclusions

          This study suggested that curcumin attenuated selenite-induced cataract through the reduction of the intracellular production of reactive oxygen species and the protection of cells from oxidative damage.

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          Most cited references33

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          Cell death in development.

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            Important causes of visual impairment in the world today.

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              Oxidative stress-induced cataract: mechanism of action.

              This review examines the hypothesis that oxidative stress is an initiating factor for the development of maturity onset cataract and describes the events leading to lens opacification. Data are reviewed that indicate that extensive oxidation of lens protein and lipid is associated with human cataract found in older individuals whereas little oxidation (and only in membrane components) is found in control subjects of similar age. A significant proportion of lenses and aqueous humor taken from cataract patients have elevated H2O2 levels. Because H2O2, at concentrations found in cataract, can cause lens opacification and produces a pattern of oxidation similar to that found in cataract, it is concluded that H2O2 is the major oxidant involved in cataract formation. This viewpoint is further supported by experiments showing that cataract formation in organ culture caused by photochemically generated superoxide radical, H2O2, and hydroxyl radical is completely prevented by the addition of a GSH peroxidase mimic. The damage caused by oxidative stress does not appear to be reversible and there is an inverse relationship between the stress period and the time required for loss of transparency and degeneration of biochemical parameters such as ATP, GPD, nonprotein thiol, and hydration. After exposure to oxidative stress, the redox set point of the single layer of the lens epithelial cells (but not the remainder of the lens) quickly changes, going from a strongly reducing to an oxidizing environment. Almost concurrent with this change is extensive damage to DNA and membrane pump systems, followed by loss of epithelial cell viability and death by necrotic and apoptotic mechanisms. The data suggest that the epithelial cell layer is the initial site of attack by oxidative stress and that involvement of the lens fibers follows, leading to cortical cataract.
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                Author and article information

                Contributors
                +86-0539-8078312 , wangmeng1985218@163.com
                Journal
                BMC Ophthalmol
                BMC Ophthalmol
                BMC Ophthalmology
                BioMed Central (London )
                1471-2415
                17 February 2018
                17 February 2018
                2018
                : 18
                : 48
                Affiliations
                [1 ]GRID grid.415946.b, Department of pharmacy, , Linyi People’s hospital of Shandong University, ; LinYi, 276003 China
                [2 ]GRID grid.415946.b, Department of Ophthalmology, , Linyi People’s hospital of Shandong University, ; No. 27, Jiefang road, LinYi, Shandong 276003 China
                Article
                711
                10.1186/s12886-018-0711-8
                5816369
                29454324
                a7e33e27-51e7-4bea-80c9-b57794b03d2e
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 19 March 2017
                : 8 February 2018
                Categories
                Research Article
                Custom metadata
                © The Author(s) 2018

                Ophthalmology & Optometry
                curcumin,cataract,reactive oxygen,cell viability,cell apoptosis
                Ophthalmology & Optometry
                curcumin, cataract, reactive oxygen, cell viability, cell apoptosis

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