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  1. Article ; Online: Therapeutic effect of Arthrocnemum machrostachyum methanolic extract on Ehrlich solid tumor in mice.

    Sharawi, Zeina W

    BMC complementary medicine and therapies

    2020  Volume 20, Issue 1, Page(s) 153

    Abstract: Background: The anti-cancer effect of the halophyte Arthrocnemum indicum, a member of Arthrocnemum family of salt-tolerant plants, was evaluated against colorectal cancer cell, CaCo2. However, the anti-cancer effect of another halophyte Arthrocnemum ... ...

    Abstract Background: The anti-cancer effect of the halophyte Arthrocnemum indicum, a member of Arthrocnemum family of salt-tolerant plants, was evaluated against colorectal cancer cell, CaCo2. However, the anti-cancer effect of another halophyte Arthrocnemum machrostachyum was not investigated yet. Herein, the anticancer effect of A. machrostachyum methanolic extract (AME) was evaluated against Ehrlich solid tumor (EST) in mice and the potential mechanism of action was also studied.
    Methods: Male Swiss albino mice (n = 28) were randomly divided into 4 groups (n = 7/group). Group 1 (negative control group); group 2 (EST) injected intramuscularly by 0.2 mL Ehrlich ascitic carcinoma (2 × 10
    Results: Treatment with AME induced anti-tumor effects against EST as indicated by 1) notable reduction in tumor size; 2) elevation in tissue necrosis and apoptosis, as confirmed histologically; 3) increased DNA fragmentation; 4) decreased expression of the apoptotic genes (p53, Bax and caspase 3), and increased expression of the anti-apoptotic marker Bcl2; 5) significantly upregulated cell cycle regulatory genes Cdc2 and connexin26, and; 6) decreased TNFa levels in tumor tissues. Interestingly, a high dose of AME exhibited a more potent anti-tumor effect against EST.
    Conclusion: These findings indicate that AME has a potent antitumor effect against EST and could be used as an adjuvant to anticancer drugs to combat tumor, but after application of further confirmatory clinical trials.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Caco-2 Cells ; Carcinoma, Ehrlich Tumor/drug therapy ; Carcinoma, Ehrlich Tumor/genetics ; Chenopodiaceae/chemistry ; DNA Fragmentation/drug effects ; Disease Models, Animal ; Egypt ; Humans ; Male ; Methanol ; Mice ; Plant Extracts/pharmacology ; Tumor Necrosis Factor-alpha/drug effects
    Chemical Substances Antineoplastic Agents ; Plant Extracts ; Tumor Necrosis Factor-alpha ; Methanol (Y4S76JWI15)
    Language English
    Publishing date 2020-05-24
    Publishing country England
    Document type Journal Article
    ISSN 2662-7671
    ISSN (online) 2662-7671
    DOI 10.1186/s12906-020-02947-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Therapeutic effect of Arthrocnemum machrostachyum methanolic extract on Ehrlich solid tumor in mice

    Sharawi, Zeina W.

    BMC Complement Med Ther. 2020 Dec., v. 20, no. 1 p.153-153

    2020  

    Abstract: BACKGROUND: The anti-cancer effect of the halophyte Arthrocnemum indicum, a member of Arthrocnemum family of salt-tolerant plants, was evaluated against colorectal cancer cell, CaCo2. However, the anti-cancer effect of another halophyte Arthrocnemum ... ...

    Abstract BACKGROUND: The anti-cancer effect of the halophyte Arthrocnemum indicum, a member of Arthrocnemum family of salt-tolerant plants, was evaluated against colorectal cancer cell, CaCo2. However, the anti-cancer effect of another halophyte Arthrocnemum machrostachyum was not investigated yet. Herein, the anticancer effect of A. machrostachyum methanolic extract (AME) was evaluated against Ehrlich solid tumor (EST) in mice and the potential mechanism of action was also studied. METHODS: Male Swiss albino mice (n = 28) were randomly divided into 4 groups (n = 7/group). Group 1 (negative control group); group 2 (EST) injected intramuscularly by 0.2 mL Ehrlich ascitic carcinoma (2 × 10⁶ cells); and groups 3 and 4 injected intratumorally with AME (180 and 360 mg/kg body weight, respectively) at D12 trice weekly for 2 weeks. Gene expression, protein expression, DNA damage, and TNFa level in tumors were determined by real-time PCR, western blot, comet assay, and Elisa, respectively. RESULTS: Treatment with AME induced anti-tumor effects against EST as indicated by 1) notable reduction in tumor size; 2) elevation in tissue necrosis and apoptosis, as confirmed histologically; 3) increased DNA fragmentation; 4) decreased expression of the apoptotic genes (p53, Bax and caspase 3), and increased expression of the anti-apoptotic marker Bcl2; 5) significantly upregulated cell cycle regulatory genes Cdc2 and connexin26, and; 6) decreased TNFa levels in tumor tissues. Interestingly, a high dose of AME exhibited a more potent anti-tumor effect against EST. CONCLUSION: These findings indicate that AME has a potent antitumor effect against EST and could be used as an adjuvant to anticancer drugs to combat tumor, but after application of further confirmatory clinical trials.
    Keywords DNA damage ; DNA fragmentation ; Western blotting ; adjuvants ; albino ; antineoplastic activity ; apoptosis ; body weight ; carcinoma ; caspase-3 ; cell cycle ; colorectal neoplasms ; comet assay ; complement ; gene expression ; halophytes ; males ; mechanism of action ; necrosis ; neoplasm cells ; protein synthesis ; quantitative polymerase chain reaction ; salt tolerance ; therapeutics
    Language English
    Dates of publication 2020-12
    Size p. 153.
    Publishing place BioMed Central
    Document type Article ; Online
    ISSN 2662-7671
    DOI 10.1186/s12906-020-02947-y
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  3. Article: Calcium Activation of the Androgen Receptor in Prostate Cells.

    Sharawi, Zeina W / Khatrawi, Sawsan M / Wang, Qiaochu / Zhou, Hongzhao / Cyrus, Kedra / Yan, Gai / Hoxter, Becky / Haddad, Bassem R / Martin, Mary Beth

    International journal of endocrinology

    2023  Volume 2023, Page(s) 9907948

    Abstract: Background: Although prostate cancer patients initially respond to androgen deprivation therapy, most patients progress to a resistant phenotype. Castration resistance is due, in part, to intratumoral and/or adrenal synthesis of androgens, ... ...

    Abstract Background: Although prostate cancer patients initially respond to androgen deprivation therapy, most patients progress to a resistant phenotype. Castration resistance is due, in part, to intratumoral and/or adrenal synthesis of androgens, overexpression or mutation of the androgen receptor (AR), stabilization of AR by chaperones, and ligand-independent activation of AR. Increasing evidence also links disruption of calcium homeostasis to progression of prostate cancer. Our previous study shows that heavy metal cadmium activates the AR through a ligand-independent mechanism. Cadmium mimics calcium in biological systems due to their similar ionic charge and radius. This study determines whether calcium activates AR and whether first- and second-generation antiandrogens block the ability of calcium to activate the receptor.
    Methods: The expression of androgen-responsive genes and calcium channels was measured in prostate cells using a quantitative real-time polymerase chain reaction assay. Cell growth was measured.
    Results: To ask whether calcium activates AR, prostate cells were treated with calcium in the absence and presence of the first-generation antiandrogens hydroxyflutamide and bicalutamide and the second-generation antiandrogen enzalutamide, and the expression of androgen-responsive genes and cell growth was measured. In the normal PWR-1E cells and HEK293T cells transiently expressing AR, treatment with calcium increased the expression of androgen-responsive genes by approximately 3-fold. The increase was blocked by enzalutamide but was not consistently blocked by the first-generation antiandrogens. In LNCaP cells which contain a mutant AR, treatment with calcium also increased the expression of androgen-responsive genes by approximately 3-fold, and the increase was more effectively blocked by enzalutamide than by hydroxyflutamide or bicalutamide. Treatment with calcium also increased cell growth that was blocked by enzalutamide. To ask whether dysregulation of calcium channels is associated with castration resistance, calcium channels were measured in the normal PWR-1E prostate cells, the hormone-responsive LNCaP cells, and the castration-resistant VCaP and 22RV1 cells. Compared to normal prostate cells, the hormone-responsive and hormone-resistant cells overexpressed several calcium channels.
    Conclusions: The results of this study show that calcium activates AR and increases cell growth and that calcium channels are overexpressed in hormone-responsive and hormone-resistant prostate cancer cells. Taken together, the results suggest a novel role of calcium in the castration-resistant phenotype.
    Language English
    Publishing date 2023-12-13
    Publishing country Egypt
    Document type Journal Article
    ZDB-ID 2502951-4
    ISSN 1687-8345 ; 1687-8337
    ISSN (online) 1687-8345
    ISSN 1687-8337
    DOI 10.1155/2023/9907948
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  4. Article ; Online: Buspirone attenuated methotrexate-induced hippocampal toxicity in rats by regulating Nrf2/HO-1, PPAR-γ, NF-κB/nNOS, and ROS/NLRP3/caspase-1 signaling pathways.

    Althagafy, Hanan S / Sharawi, Zeina W / Batawi, Ashwaq H / Almohaimeed, Hailah M / Al-Thubiani, Wafa S / Hassanein, Emad H M / Rateb, Amal

    Journal of biochemical and molecular toxicology

    2023  Volume 37, Issue 9, Page(s) e23414

    Abstract: Methotrexate (MTX) is a chemotherapeutic agent widely used to treat a variety of tumors. Nonetheless, MTX-induced hippocampal neurotoxicity is a well-defined dose-limiting adverse effect that limits clinical utility. Proinflammatory cytokine production ... ...

    Abstract Methotrexate (MTX) is a chemotherapeutic agent widely used to treat a variety of tumors. Nonetheless, MTX-induced hippocampal neurotoxicity is a well-defined dose-limiting adverse effect that limits clinical utility. Proinflammatory cytokine production and oxidative stress are possible mechanisms for MTX-induced neurotoxicity. Buspirone (BSP), a partial agonist of the 5-HT1a receptor (5-HT1aR), has emerged as an anxiolytic drug. BSP has been shown to possess antioxidant and anti-inflammatory effects. The current study investigated BSP's potential anti-inflammatory and antioxidant effects in attenuating MTX-induced hippocampal toxicity. Rats received either BSP (1.5 mg/kg) orally for 10 days and MTX (20 mg/kg) i.p. on Day 5. BSP administration markedly protected hippocampal neurons from drastic degenerated neuronal changes induced by MTX. BSP significantly attenuated oxidative injury by downregulating Kelch-like ECH-associated protein 1 expression while potently elevating hippocampal Nrf2, heme oxygenase-1, and peroxisome proliferator-activated receptor expression. BSP dampened inflammation by reducing NO
    MeSH term(s) Rats ; Animals ; NF-kappa B/metabolism ; Methotrexate/toxicity ; NF-E2-Related Factor 2/metabolism ; Reactive Oxygen Species ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Buspirone/pharmacology ; Caspase 1/metabolism ; PPAR gamma/metabolism ; Signal Transduction ; Antioxidants/pharmacology ; Oxidative Stress ; Anti-Inflammatory Agents/pharmacology
    Chemical Substances NF-kappa B ; Methotrexate (YL5FZ2Y5U1) ; NF-E2-Related Factor 2 ; Reactive Oxygen Species ; NLR Family, Pyrin Domain-Containing 3 Protein ; Buspirone (TK65WKS8HL) ; Caspase 1 (EC 3.4.22.36) ; PPAR gamma ; Antioxidants ; Anti-Inflammatory Agents
    Language English
    Publishing date 2023-06-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1410020-4
    ISSN 1099-0461 ; 1095-6670
    ISSN (online) 1099-0461
    ISSN 1095-6670
    DOI 10.1002/jbt.23414
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    Zs.A 2201: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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  5. Article ; Online: Baicalin and lung diseases.

    Sharawi, Zeina W / Ibrahim, Islam M / Abd-Alhameed, Esraa K / Althagafy, Hanan S / Jaber, Fatima A / Harakeh, Steve / Hassanein, Emad H M

    Naunyn-Schmiedeberg's archives of pharmacology

    2023  Volume 397, Issue 3, Page(s) 1405–1419

    Abstract: Studies focusing on natural products have been conducted worldwide, and the results suggest that their natural ingredients effectively treat a wide range of illnesses. Baicalin (BIA) is a glycoside derived from the flavonoid baicalein present in ... ...

    Abstract Studies focusing on natural products have been conducted worldwide, and the results suggest that their natural ingredients effectively treat a wide range of illnesses. Baicalin (BIA) is a glycoside derived from the flavonoid baicalein present in Scutellaria baicalensis of the Lamiaceae family. Interestingly, BIA has been shown to protect the lungs in several animal models used in numerous studies. Therefore, we fully analyzed the data of the studies that focused on BIA's lung protective function against various injuries and included them in this review. Interestingly, BIA exhibits promising effects against acute lung injury, lung fibrosis, pulmonary embolism, and lung remodelling associated with COPD, LPS, and paraquat insecticide. BAI exhibits anticancer activity against lung cancer. Additionally, BIA potently attenuates lung damage associated with infections. BIA primarily exerts its therapeutic effects by suppressing inflammation, oxidative stress immune response, and apoptosis pathways. Nrf2/HO-1, PI3K/Akt, NF-κB, STAT3, MAPKs, TLR4, and NLRP3 are important targets in the pulmonary therapeutic effects of BIA on different lung disease models. Consequently, we recommend using it in future potential clinical applications, its contribution to treatment guidelines, and translating its promising effects to clinical practice in lung diseases.
    MeSH term(s) Animals ; Phosphatidylinositol 3-Kinases/metabolism ; Flavonoids/pharmacology ; Flavonoids/therapeutic use ; NF-kappa B/metabolism ; Lung ; Acute Lung Injury/metabolism ; Lipopolysaccharides/pharmacology
    Chemical Substances baicalin (347Q89U4M5) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Flavonoids ; NF-kappa B ; Lipopolysaccharides
    Language English
    Publishing date 2023-09-19
    Publishing country Germany
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 121471-8
    ISSN 1432-1912 ; 0028-1298
    ISSN (online) 1432-1912
    ISSN 0028-1298
    DOI 10.1007/s00210-023-02704-1
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  6. Article ; Online: Nrf2/HO-1 as a therapeutic target in renal fibrosis.

    Hassanein, Emad H M / Ibrahim, Islam M / Abd-Alhameed, Esraa K / Sharawi, Zeina W / Jaber, Fatima A / Althagafy, Hanan S

    Life sciences

    2023  Volume 334, Page(s) 122209

    Abstract: Chronic kidney disease (CKD) is one of the most prevalent chronic diseases and affects between 10 and 14 % of the world's population. The World Health Organization estimates that by 2040, the disease will be fifth in prevalence. End-stage CKD is ... ...

    Abstract Chronic kidney disease (CKD) is one of the most prevalent chronic diseases and affects between 10 and 14 % of the world's population. The World Health Organization estimates that by 2040, the disease will be fifth in prevalence. End-stage CKD is characterized by renal fibrosis, which can eventually lead to kidney failure and death. Renal fibrosis develops due to multiple injuries and involves oxidative stress and inflammation. In the human body, nuclear factor erythroid 2-related factor 2 (Nrf2) plays an important role in the expression of antioxidant, anti-inflammatory, and cytoprotective genes, which prevents oxidative stress and inflammation damage. Heme oxygenase (HO-1) is an inducible homolog influenced by heme products and after exposure to cellular stress inducers such as oxidants, inflammatory chemokines/cytokines, and tissue damage as an outcome or downstream of Nrf2 activation. HO-1 is known for its antioxidative properties, which play an important role in regulating oxidative stress. In renal diseases-induced tissue fibrosis and xenobiotics-induced renal fibrosis, Nrf2/HO-1 has been targeted with promising results. This review summarizes these studies and highlights the interesting bioactive compounds that may assist in attenuating renal fibrosis mediated by HO-1 activation. In conclusion, Nrf2/HO-1 signal activation could have a renoprotective effect strategy against CKD caused by oxidative stress, inflammation, and consequent renal fibrosis.
    MeSH term(s) Humans ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Antioxidants/metabolism ; Fibrosis ; Heme Oxygenase-1/metabolism ; Inflammation/drug therapy ; Inflammation/complications ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress ; Renal Insufficiency, Chronic/drug therapy ; Renal Insufficiency, Chronic/etiology
    Chemical Substances Antioxidants ; Heme Oxygenase-1 (EC 1.14.14.18) ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; HMOX1 protein, human (EC 1.14.14.18)
    Language English
    Publishing date 2023-10-25
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2023.122209
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  7. Article ; Online: Walnut Kernel Oil and Defatted Extracts Enhance Mesenchymal Stem Cell Stemness and Delay Senescence.

    Elsied, Marwa A / Sharawi, Zeina W / Al-Amrah, Hadba / Hegazy, Rabab A / Mohamed, Amro E / Saleh, Rasha M / El-Kholy, Sanad S / Farrag, Foad A / Fayed, Masoud H / El-Magd, Mohammed A

    Molecules (Basel, Switzerland)

    2023  Volume 28, Issue 17

    Abstract: Decreased stemness and increased cellular senescence impair the ability of mesenchymal stem cells (MSCs) to renew themselves, change into different cell types, and contribute to regenerative medicine. There is an urgent need to discover new compounds ... ...

    Abstract Decreased stemness and increased cellular senescence impair the ability of mesenchymal stem cells (MSCs) to renew themselves, change into different cell types, and contribute to regenerative medicine. There is an urgent need to discover new compounds that can boost MSCs' stemness and delay senescence. Therefore, this study aimed to investigate the impact of walnut kernel oil (WKO) and defatted (WKD) extracts on bone marrow (BM)-MSC stemness and senescence. Premature senescence and inflammation were induced in BM-MSCs using H
    MeSH term(s) Animals ; Rats ; AMP-Activated Protein Kinases ; Antioxidants/pharmacology ; Hydrogen Peroxide ; Juglans ; Sirtuin 1/genetics ; Tumor Suppressor Protein p53
    Chemical Substances AMP-Activated Protein Kinases (EC 2.7.11.31) ; Antioxidants ; Hydrogen Peroxide (BBX060AN9V) ; Sirtuin 1 (EC 3.5.1.-) ; Tumor Suppressor Protein p53
    Language English
    Publishing date 2023-08-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1413402-0
    ISSN 1420-3049 ; 1431-5165 ; 1420-3049
    ISSN (online) 1420-3049
    ISSN 1431-5165 ; 1420-3049
    DOI 10.3390/molecules28176281
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    Zs.MO 81: Show issues

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