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      Recent updates on daidzein against oxidative stress and cancer

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          Abstract

           Dear Editor, Daidzein (7-hydroxy-3-(4-hydroxyphenyl)-4H-chromen-4-one) is a naturally occurring compound commonly found in soybeans and some other legumes. Daidzein is an isoflavone by nature and isolated from Pueraria Mirifica, having category of biologically active secondary metabolites commonly produced in the soybean growth and belong to the group of flavonoids. A number of pharmacological activities have been accounted for daidzein, which includes anti-carcinogenesis, anti-fibrotic, anti-diabetic, cholesterol-lowering and cardiovascular activity. Daidzein pretreatment was found to diminish the seriousness of mucosal damage in a portion subordinate way. Some other therapeutic uses of daidzein are weight reduction, decreasing bowels moment, and inflammation associated with histopathological deformities (Amaral et al., 2017[1]). Their structure and function are alike to human estrogen, which can play a massive role in the prevention of osteoporosis, cancer, and postmenopausal syndromes. Uses of daidzein in anticancer activity against ovarian cancer are still limited (Meng et al., 2017[14]). Epidemiological data suggest that increased utilization of soybean in food results in decreased cancer risk. Soybean food is highly recommended in cancer prevention because it has a number of anticarcinogens (Yu et al., 2017[23]). The potent antioxidant activity of daidzein reported in various in vitro and in vivo studies was conclusively shown in this literature (Table 1(Tab. 1); References in Table 1: Amaral et al., 2017[1]; Atiq et al., 2019[2]; Budryn et al., 2018[3]; Chan et al., 2018[4]; Davis et al., 2001[5]; Eskra et al., 2019[6]; Foti et al., 2005[7]; Gundogdu et al., 2018[8]; Hua et al., 2018[9]; Huang et al., 2019[10]; Karale and Kamath, 2017[11]; Liang et al., 2018[12]; Medeiros et al., 2016[13]; Meng et al., 2017[14]; Murata et al., 2004[15]; Park et al., 2016[16]; Poschner et al., 2017[17]; Rigalli et al., 2019[18]; Rohrdanz et al., 2002[19]; Sivoňová et al., 2019[20]; Uifalean et al., 2018[21]; Wei et al., 2019[22]; Zheng et al., 2017[25]; Zheng et al., 2018[24]; Zhu et al., 2018[26]). Conflict of interest The authors declare no conflict of interest.

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          Daidzein exerts anticancer activity towards SKOV3 human ovarian cancer cells by inducing apoptosis and cell cycle arrest, and inhibiting the Raf/MEK/ERK cascade

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            Ameliorative Effect of Daidzein on Cisplatin-Induced Nephrotoxicity in Mice via Modulation of Inflammation, Oxidative Stress, and Cell Death

            Oxidative stress and inflammation are part and parcel of cisplatin-induced nephrotoxicity. The purpose of this work is to study the role of soy isoflavone constituent, daidzein, in cisplatin-induced renal damage. Cisplatin-induced nephrotoxicity was evident by the histological damage in proximal tubular cells and by the increase in serum neutrophil gelatinase-associated lipocalin (NGAL), blood urea nitrogen (BUN), creatinine, and urinary kidney injury molecule-1 (KIM-1). Cisplatin-induced cell death was shown by TUNEL staining and caspase-3/7 activity. Daidzin treatment reduced all kidney injury markers (NGAL, BUN, creatinine, and KIM-1) and attenuated cell death (apoptotic markers). In cisplatin-induced kidney injury, renal oxidative/nitrative stress was manifested by the increase in lipid peroxidation and protein nitration. Cisplatin induced the reactive oxygen species-generating enzyme NOX-2 and impaired antioxidant defense enzyme activities such as glutathione peroxidase (GPX) and superoxide dismutase (SOD) activities. Cisplatin-induced oxidative/nitrative stress was attenuated by daidzein treatment. Cisplatin induced CD11b-positive macrophages in kidneys and daidzein attenuated CD11b-positive cells. Daidzein attenuated cisplatin-induced inflammatory cytokines tumor necrosis factor α (TNFα), interleukin 10 (IL-10), interleukin 18 (IL-18), and monocyte chemoattractant protein-1 (MCP-1). Daidzein attenuated cell death in vitro. Our data suggested that daidzein attenuated cisplatin-induced kidney injury through the downregulation of oxidative/nitrative stress, immune cells, inflammatory cytokines, and apoptotic cell death, thus improving kidney regeneration.
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              Estrogen receptor modulators genistein, daidzein and ERB-041 inhibit cell migration, invasion, proliferation and sphere formation via modulation of FAK and PI3K/AKT signaling in ovarian cancer

              Background Ovarian cancer is the most lethal gynaecological malignancy. Chemotherapy is the main stay of treatment for metastatic disease, with modest response rates but significant side effects. Therefore, there is a need for alternative therapies that can control the disease while offering good quality of life. Ovarian cancer cells express both estrogen receptor subtypes (ERα and ERβ). There is growing evidence that ERβ is anti-oncogenic. Genistein and daidzein are phytoestrogens found in soybeans and they display higher affinity to bind ERβ. ERB-041 is a potent selective ERβ agonist. In this study, we aimed to investigate the effects of genistein, daidzein and ERB-041 on ovarian cancer. Methods Ovarian cancer cell lines were treated with genistein, daidzein and ERB-041 in pharmacological doses. Cell migration, invasion, proliferation, cell cycle arrest, apoptosis and sphere formation were assessed by Transwell migration and invasion assays, XTT assay, focus formation, flow cytometry and sphere formation assay, respectively. Immunoblotting analysis was performed to determine the downstream signaling pathways. Results We found that genistein, daidzein and ERB-041 significantly inhibited ovarian cancer cell migration, invasion, proliferation, as well as induced cell cycle arrest and apoptosis. Significantly inhibitory effect on the size and number of sphere formed in genistein, daidzein and ERB-041 treated cells was also demonstrated. Moreover, genistein, daidzein and ERB-041 treatment reduced p-FAK, p-PI3K, p-AKT, p-GSK3β, p21 or cyclin D1 expression in ovarian cancer cells. Conclusion Genistein, daidzein and ERB-041 decreased ovarian cancer cell migration, invasion, proliferation and sphere formation, and induced cell cycle arrest and apoptosis with altered FAK and PI3K/AKT/GSK signaling and p21/cyclin D1 expression, suggesting their roles on ovarian cancer cell metastasis, tumorigenesis and stem-like properties and their potential as alternative therapies for ovarian cancer patients. Electronic supplementary material The online version of this article (10.1186/s12935-018-0559-2) contains supplementary material, which is available to authorized users.
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                Author and article information

                Journal
                EXCLI J
                EXCLI J
                EXCLI J
                EXCLI Journal
                Leibniz Research Centre for Working Environment and Human Factors
                1611-2156
                21 October 2019
                2019
                : 18
                : 950-954
                Affiliations
                [1 ]School of Pharmacy, Suresh Gyan Vihar University, Mahal Road, Jagatpura, Jaipur, India
                Author notes
                *To whom correspondence should be addressed: Gaurav Gupta, School of Pharmacy, Suresh Gyan Vihar University, Mahal Road, Jagatpura, Jaipur, India, E-mail: gauravpharma25@ 123456gmail.com
                Article
                2019-1847 Doc950
                10.17179/excli2019-1847
                6868922
                31762721
                cb55ec16-8a0d-4899-b5b4-e20883048ea6
                Copyright © 2019 Rawat et al.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Licence ( http://creativecommons.org/licenses/by/4.0/) You are free to copy, distribute and transmit the work, provided the original author and source are credited.

                History
                : 26 September 2019
                : 10 October 2019
                Categories
                Letter to the Editor

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