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

Sharawi, Zeina W

BMC complementary medicine and therapies

2020 Band 20, Heft 1, Seite(n) 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-Begriff(e)	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
Chemische Substanzen	Antineoplastic Agents ; Plant Extracts ; Tumor Necrosis Factor-alpha ; Methanol (Y4S76JWI15)
Sprache	Englisch
Erscheinungsdatum	2020-05-24
Erscheinungsland	England
Dokumenttyp	Journal Article
ISSN	2662-7671
ISSN (online)	2662-7671
DOI	10.1186/s12906-020-02947-y
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; 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.
Schlagwörter	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
Sprache	Englisch
Erscheinungsverlauf	2020-12
Umfang	p. 153.
Erscheinungsort	BioMed Central
Dokumenttyp	Artikel ; Online
ISSN	2662-7671
DOI	10.1186/s12906-020-02947-y
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel: 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 Band 2023, Seite(n) 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.
Sprache	Englisch
Erscheinungsdatum	2023-12-13
Erscheinungsland	Egypt
Dokumenttyp	Journal Article
ZDB-ID	2502951-4
ISSN	1687-8345 ; 1687-8337
ISSN (online)	1687-8345
ISSN	1687-8337
DOI	10.1155/2023/9907948
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; 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 Band 397, Heft 3, Seite(n) 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-Begriff(e)	Animals ; Phosphatidylinositol 3-Kinases/metabolism ; Flavonoids/pharmacology ; Flavonoids/therapeutic use ; NF-kappa B/metabolism ; Lung ; Acute Lung Injury/metabolism ; Lipopolysaccharides/pharmacology
Chemische Substanzen	baicalin (347Q89U4M5) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Flavonoids ; NF-kappa B ; Lipopolysaccharides
Sprache	Englisch
Erscheinungsdatum	2023-09-19
Erscheinungsland	Germany
Dokumenttyp	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
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; 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 Band 334, Seite(n) 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-Begriff(e)	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
Chemische Substanzen	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)
Sprache	Englisch
Erscheinungsdatum	2023-10-25
Erscheinungsland	Netherlands
Dokumenttyp	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
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; 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 Band 37, Heft 9, Seite(n) 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-Begriff(e)	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
Chemische Substanzen	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
Sprache	Englisch
Erscheinungsdatum	2023-06-21
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	1410020-4
ISSN	1099-0461 ; 1095-6670
ISSN (online)	1099-0461
ISSN	1095-6670
DOI	10.1002/jbt.23414
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Quetiapine attenuates cadmium neurotoxicity by suppressing oxidative stress, inflammation, and pyroptosis.

Althagafy, Hanan S / Harakeh, Steve / Azhari, Sheren A / Farsi, Reem M / Al-Abbas, Nouf S / Shaer, Nehad A / Sharawi, Zeina W / Almohaimeed, Hailah M / Hassanein, Emad H M

Molecular biology reports

2024 Band 51, Heft 1, Seite(n) 660

Abstract: Background: Cadmium (Cd) is a heavy metal with extremely harmful toxic effects on the brain. Quetiapine (QTP) has unique neuroprotective effects with anti-inflammatory and antioxidant actions. However, its neuroprotective effect against Cd-induced ... ...

Abstract	Background: Cadmium (Cd) is a heavy metal with extremely harmful toxic effects on the brain. Quetiapine (QTP) has unique neuroprotective effects with anti-inflammatory and antioxidant actions. However, its neuroprotective effect against Cd-induced neurotoxicity has not been previously studied. Methods: QTP was administered in 10 and 20 mg/kg doses, while Cd was given in a dose of 6.5 mg/kg. Results: In our study, QTP dose-dependently attenuated neuronal injury by downregulating p-tau and β-amyloid. QTP potently attenuates histological abrasions induced by Cd. QTP counteracted oxidative injury by decreasing neuronal MDA and increased GSH levels mediated by downregulating Keap1 and upregulating Nrf2 and HO-1. QTP mitigated inflammation by decreasing MPO and NO Conclusion: In conclusion, QTP mitigates neurotoxicity induced by Cd through suppression of inflammation, pyroptosis, and oxidative stress by controlling the NF-κB, Keap1/Nrf2, and pyroptosis signals.
Mesh-Begriff(e)	Oxidative Stress/drug effects ; Pyroptosis/drug effects ; Animals ; Cadmium/toxicity ; Quetiapine Fumarate/pharmacology ; Inflammation/drug therapy ; Inflammation/metabolism ; Male ; Mice ; Neuroprotective Agents/pharmacology ; NF-E2-Related Factor 2/metabolism ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Neurotoxicity Syndromes/drug therapy ; Neurotoxicity Syndromes/metabolism ; Antioxidants/pharmacology ; Anti-Inflammatory Agents/pharmacology ; NF-kappa B/metabolism
Sprache	Englisch
Erscheinungsdatum	2024-05-15
Erscheinungsland	Netherlands
Dokumenttyp	Journal Article
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-024-09558-7
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; 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 Band 28, Heft 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-Begriff(e)	Animals ; Rats ; AMP-Activated Protein Kinases ; Antioxidants/pharmacology ; Hydrogen Peroxide ; Juglans ; Sirtuin 1/genetics ; Tumor Suppressor Protein p53
Chemische Substanzen	AMP-Activated Protein Kinases (EC 2.7.11.31) ; Antioxidants ; Hydrogen Peroxide (BBX060AN9V) ; Sirtuin 1 (EC 3.5.1.-) ; Tumor Suppressor Protein p53
Sprache	Englisch
Erscheinungsdatum	2023-08-28
Erscheinungsland	Switzerland
Dokumenttyp	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
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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