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  1. Article ; Online: Prunus Armeniaca L

    Hosny, Samar / Sahyon, Heba / Youssef, Magdy / Negm, Amr

    Anti-cancer agents in medicinal chemistry

    2020  Volume 21, Issue 5, Page(s) 621–629

    Abstract: Background: Despite significant advances in therapeutic interventions, liver cancer is the leading cause of cancer mortality in the world. Potential phytochemicals have shown to be promising agents against many life-threatening diseases because of their ...

    Abstract Background: Despite significant advances in therapeutic interventions, liver cancer is the leading cause of cancer mortality in the world. Potential phytochemicals have shown to be promising agents against many life-threatening diseases because of their low toxicity and potential effectiveness.
    Objective: The current study aims to conduct an in vitro investigation of the anticancer activity of Apricot Extract (AE) and Amygdalin Containing Fraction (ACF), additionally studying their therapeutic effects on DMBAinduced liver carcinogenesis mice model to highlight their related biochemical and molecular mechanisms.
    Methods and results: Amygdalin was isolated from the seeds of P. armeniaca L. Male mice received AE or ACF, DMBA, DMBA+AE, DMBA+ACF, and vehicles. The oxidative stress and antioxidant markers, cell proliferation by flow cytometric analysis of Proliferating Cell Nuclear Antigen (PCNA) expression, angiogenesis marker (VEGF), inflammatory marker (TNF-α), apoptotic, anti-apoptotic and autophagy genes expression (caspase-3, Bcl-2, and Beclin-1) were investigated. AE and ACF were found to stimulate the apoptotic process by up-regulating caspase-3 expression and down-regulating Bcl-2 expression. They also reduced VEGF and PCNA levels and increased the antioxidant defense system. Moreover, AE and ACF treatments also inhibited HepG2 and EAC cell proliferation and up-regulated Beclin-1 expression.
    Conclusion: This study provides evidence that, in DMBA-induced hepatocarcinogenesis, the key proteins involved in the proliferation, angiogenesis, autophagy, and apoptosis are feasible molecular targets for hepatotherapeutic potential using AE and ACF.
    MeSH term(s) Amygdalin/chemical synthesis ; Amygdalin/chemistry ; Amygdalin/pharmacology ; Animals ; Antineoplastic Agents, Phytogenic/chemistry ; Antineoplastic Agents, Phytogenic/isolation & purification ; Antineoplastic Agents, Phytogenic/pharmacology ; Apoptosis/drug effects ; Cell Proliferation/drug effects ; Dose-Response Relationship, Drug ; Drug Screening Assays, Antitumor ; Hep G2 Cells ; Humans ; Liver Neoplasms/drug therapy ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Liver Neoplasms, Experimental/drug therapy ; Liver Neoplasms, Experimental/metabolism ; Liver Neoplasms, Experimental/pathology ; Male ; Mice ; Mitochondria/drug effects ; Mitochondria/metabolism ; Molecular Structure ; Plant Extracts/chemistry ; Plant Extracts/isolation & purification ; Plant Extracts/pharmacology ; Prunus armeniaca/chemistry ; Seeds/chemistry ; Structure-Activity Relationship
    Chemical Substances Antineoplastic Agents, Phytogenic ; Plant Extracts ; Amygdalin (214UUQ9N0H)
    Language English
    Publishing date 2020-06-03
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2217610-X
    ISSN 1875-5992 ; 1871-5206
    ISSN (online) 1875-5992
    ISSN 1871-5206
    DOI 10.2174/1871520620666200608124003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Oleanolic Acid Suppressed DMBA-Induced Liver Carcinogenesis through Induction of Mitochondrial-Mediated Apoptosis and Autophagy.

    Hosny, Samar / Sahyon, Heba / Youssef, Magdy / Negm, Amr

    Nutrition and cancer

    2020  Volume 73, Issue 6, Page(s) 968–982

    Abstract: Phytochemicals appeared as a rich source of efficient and safe agents against many diseases like cancer. Various herbal sources are rich in oleanolic acid (OA). The scope of this study was to assess the biochemical and molecular mechanisms implicated in ... ...

    Abstract Phytochemicals appeared as a rich source of efficient and safe agents against many diseases like cancer. Various herbal sources are rich in oleanolic acid (OA). The scope of this study was to assess the biochemical and molecular mechanisms implicated in the ameliorative potency of OA against DMBA-induced liver carcinogenesis. Forty-eight male albino mice were assigned randomly to five groups (eight mice each) as follows: control healthy group, olive oil group, OA group, DMBA group, and DMBA with OA. Apoptosis, autophagy, inflammation, proliferation, and angiogenesis were investigated in the tissue samples. Histopathological examination was carried out as well as liver enzymes activity and other hepatic antioxidant and inflammatory biomarkers. The treatment with OA effectively suppressed the DMBA-initiated liver carcinogenesis via modulation of antioxidant status, induction of apoptosis and autophagy through modulating the expression of Caspase-3, Bcl-2 and Beclin-1, inhibiting angiogenesis (VEGF), proliferation (PCNA), and improved liver function and histological picture with a reduction in AFP level. Additionally, OA applies its antitumor effects by inhibition of proinflammatory transcription factor NF-κB and inflammatory markers (TNF-α and Cox-2) associated with DMBA administration. The present study shows that OA treatment efficiently suppressed the DMBA-initiated liver carcinogenesis through induction of mitochondrial-mediated apoptosis and autophagy and modulating inflammation.
    MeSH term(s) 9,10-Dimethyl-1,2-benzanthracene/toxicity ; Animals ; Apoptosis ; Autophagy ; Carcinogenesis ; Liver ; Male ; Mice ; Oleanolic Acid/pharmacology
    Chemical Substances 9,10-Dimethyl-1,2-benzanthracene (57-97-6) ; Oleanolic Acid (6SMK8R7TGJ)
    Language English
    Publishing date 2020-06-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 424433-3
    ISSN 1532-7914 ; 0163-5581
    ISSN (online) 1532-7914
    ISSN 0163-5581
    DOI 10.1080/01635581.2020.1776887
    Database MEDical Literature Analysis and Retrieval System OnLINE

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