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137 results on '"El‐Daly, Mahmoud"'

9. Corrigendum to “Ketogenic diet restores hormonal, apoptotic/proliferative balance and enhances the effect of metformin on a letrozole-induced polycystic ovary model in rats” [Life Sci. 313 (2022) 121285]

Author

Ahmed, Al-Shaimaa F., primary, Sharkawi, Sara S., additional, AbdelHameed, Sara S., additional, Bayoumi, Asmaa M., additional, Moussa, Rabab S., additional, Alhakamy, Nabil A., additional, Al Sadoun, Hadeel, additional, Mansouri, Rasha A., additional, El-Moselhy, Mohamed A., additional, El-Daly, Mahmoud, additional, and Anter, Aliaa F., additional

Published
2023
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14. Corrigendum: The severity of acute kidney and lung injuries induced by cecal ligation and puncture is attenuated by menthol: Role of proliferating cell nuclear antigen and apoptotic markers

Author

Anter, Aliaa, primary, Ahmed, Al-Shaimaa F., additional, Hammad, Asmaa S. A., additional, Almalki, Waleed Hassan, additional, Abdel Hafez, Sara Mohamed Naguib, additional, Kasem, AlShaimaa W., additional, El-Moselhy, Mohamed A., additional, Alrabia, Mohammad W., additional, Ibrahim, Ahmed R. N., additional, and El-Daly, Mahmoud, additional

Published
2022
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19. Protective effects of menthol against sepsis-induced hepatic injury: Role of mediators of hepatic inflammation, apoptosis, and regeneration

Author

Matouk, Asmaa I., primary, El-Daly, Mahmoud, additional, Habib, Heba A., additional, Senousy, Shaymaa, additional, Naguib Abdel Hafez, Sara Mohamed, additional, Kasem, AlShaimaa W., additional, Almalki, Waleed Hassan, additional, Alzahrani, Abdulaziz, additional, Alshehri, Ahmed, additional, and Ahmed, Al-Shaimaa F., additional

Published
2022
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21. The Severity of Acute Kidney and Lung Injuries Induced by Cecal Ligation and Puncture Is Attenuated by Menthol: Role of Proliferating Cell Nuclear Antigen and Apoptotic Markers

Author

Anter, Aliaa, primary, Ahmed, Al-Shaimaa F., additional, Hammad, Asmaa S. A., additional, Almalki, Waleed Hassan, additional, Abdel Hafez, Sara Mohamed Naguib, additional, Kasem, AlShaimaa W., additional, El-Moselhy, Mohamed A., additional, Alrabia, Mohammad W., additional, Ibrahim, Ahmed R. N., additional, and El-Daly, Mahmoud, additional

Published
2022
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24. Anti-androgenic potential of the fruit extracts of certain Egyptian Sabal species and their genetic variability studies: a metabolomic-molecular modeling approach

Author

Abd Almaksoud, Hanan M., primary, El-Hawary, Seham S., additional, Atia, Mohamed A. M., additional, Sayed, Ahmed M., additional, El-Daly, Mahmoud, additional, Kamel, Amr Abdallah, additional, Elimam, Hanan, additional, Abdelmohsen, Usama Ramadan, additional, and Saber, Fatema R., additional

Published
2022
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35. Angiotensin aldosterone inhibitors improve survival and ameliorate kidney injury induced by sepsis through suppression of inflammation and apoptosis.

Author

Al‐Kadi, Alaa, El‐Daly, Mahmoud, El‐Tahawy, Nashwa F. G., Khalifa, Mohamed Montaser A., and Ahmed, Al‐Shaimaa F.

Subjects
*SEPSIS, *RENIN-angiotensin system, *KIDNEY injuries, *ANGIOTENSINS, *ACUTE kidney failure, *INTENSIVE care units
Abstract

Sepsis is an extensive life‐threatening illness that occurs due to an abnormal host response that extends through the initial storm of inflammation and oxidative stress and terminates at the late stage of immunosuppression. Among global intensive care units, sepsis‐induced acute kidney injury is reported with high mortality rate. The purpose of this study was to evaluate the protective effect of the renin angiotensin aldosterone system (RAAS) inhibition on sepsis outcomes. Cecal ligation and puncture (CLP) procedure was applied for sepsis induction. The experimental design constituted of five groups of rats: sham, CLP‐nontreated and CLP‐treated with ramipril (10 mg/kg, p.o.), losartan (20 mg/kg, i.p.) and spironolactone (25 mg/kg, p.o.). Twenty‐four hours after surgery, rats were euthanized for blood and tissue samples, which were used for assessment of serum inflammatory markers, and oxidative stress parameters, as well as to kidney function parameters. The tissue samples were used for histological and caspase‐3 assessment. A survival study was conducted using another set of animals. Our results showed that the different RAAS inhibitors showed protective effects evidenced by enhanced overall survival following sepsis (80% in ramipril and spironolactone‐treated and 60% in losartan‐treated vs. 10% in the septic group), in addition to improved renal function parameters and reduction of oxidative stress and inflammation. The timely use of RAAS inhibitors during sepsis might represent a new therapeutic approach in septic patient. [ABSTRACT FROM AUTHOR]

Published
2022
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41. Heat shock protein‐27 and sex‐selective regulation of muscarinic and proteinase‐activated receptor 2‐mediated vasodilatation: differential sensitivity to endothelial NOS inhibition

Author

Pulakazhi Venu, Vivek Krishna, Saifeddine, Mahmoud, Mihara, Koichiro, El‐Daly, Mahmoud, Belke, Darrell, Dean, Jonathan L E, O'Brien, Edward R, Hirota, Simon A, and Hollenberg, Morley D

Subjects
Male, Mice, Knockout, Oxadiazoles, animal structures, Dose-Response Relationship, Drug, Nitric Oxide Synthase Type III, HSP27 Heat-Shock Proteins, Research Papers, Receptors, Muscarinic, Mice, Inbred C57BL, Vasodilation, Mice, Structure-Activity Relationship, NG-Nitroarginine Methyl Ester, Quinoxalines, Animals, Receptor, PAR-2, Female, Endothelium, Vascular, Enzyme Inhibitors
Abstract

BACKGROUND AND PURPOSE: Previously, we demonstrated that exogenous heat shock protein 27 (HSP27/gene, HSPB1) treatment of human endothelial progenitor cells (EPCs) increases the synthesis and secretion of VEGF, improves EPC‐migration/re‐endothelialization and decreases neo‐intima formation, suggesting a role for HSPB1 in regulating EPC function. We hypothesized that HSPB1 also affects mature endothelial cells (ECs) to alter EC‐mediated vasoreactivity in vivo. Our work focused on endothelial NOS (eNOS)/NO‐dependent relaxation induced by ACh and the coagulation pathway‐activated receptor, proteinase‐activated receptor 2 (PAR2). EXPERIMENTAL APPROACH: Aorta rings from male and female wild‐type, HSPB1‐null and HSPB1 overexpressing (HSPB1o/e) mice were contracted with phenylephrine, and NOS‐dependent relaxation responses to ACh and PAR2 agonist, 2‐furoyl‐LIGRLO‐NH(2), were measured without and with L‐NAME and ODQ, either alone or in combination to block NO synthesis/action. Tissues from female HSPB1‐null mice were treated in vitro with recombinant HSP27 and then used for bioassay as above. Furthermore, oestrogen‐specific effects were evaluated using a bioassay of aorta isolated from ovariectomized mice. KEY RESULTS: Relative to males, HSPB1‐null female mice exhibited an increased L‐NAME‐resistant relaxation induced by activation of either PAR2 or muscarinic ACh receptors that was blocked in the concurrent presence of both L‐NAME and ODQ. mRNAs (qPCR) for eNOS and ODQ‐sensitive guanylyl‐cyclase were increased in females versus males. Treatment of isolated aorta tissue with HSPB1 improved tissue responsiveness in the presence of L‐NAME. Ovariectomy did not affect NO sensitivity, supporting an oestrogen‐independent role for HSPB1. CONCLUSIONS AND IMPLICATIONS: HSPB1 can regulate intact vascular endothelial function to affect NO‐mediated vascular relaxation, especially in females.

Published
2018

46. Heat shock protein-27 and sex-selective regulation of muscarinic and proteinase-activated receptor 2-mediated vasodilatation: differential sensitivity to endothelial NOS inhibition

Author

Pulakazhi Venu, Vivek Krishna, primary, Saifeddine, Mahmoud, additional, Mihara, Koichiro, additional, El-Daly, Mahmoud, additional, Belke, Darrell, additional, Dean, Jonathan L E, additional, O'Brien, Edward R, additional, Hirota, Simon A, additional, and Hollenberg, Morley D, additional

Published
2018
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47. Minimizing Hyperglycemia-Induced Vascular Endothelial Dysfunction by Inhibiting Endothelial Sodium-Glucose Cotransporter 2 and Attenuating Oxidative Stress: Implications for Treating Individuals With Type 2 Diabetes

Author

Pulakazhi Venu, Vivek Krishna, El-Daly, Mahmoud, Saifeddine, Mahmoud, Hirota, Simon A., Ding, Hong, Triggle, Chris R., and Hollenberg, Morley D.

Abstract

This overview deals with mechanisms whereby hyperglycemia-induced oxidative stress compromises vascular endothelial function and provides a background for a recently published study illustrating the beneficial impact of endothelial sodium-glucose cotransporter 2 (SGLT2) inhibitors in attenuating hyperglycemia-induced vascular dysfunction in vitro. The data provide new insight that can possibly lead to improved drug therapy for people with type 2 diabetes. The working hypotheses that underpinned the experiments performed are provided, along with the findings of the study. For the causes of hyperglycemia-induced vascular endothelial dysfunction, the findings point to the key roles of: 1) functional endothelial SGLT2; 2) oxidative stress-induced signalling pathways including mammalian sarcoma virus kinase, the EGF receptor-kinase and protein kinase C; and 3) mitochondrial dysfunction triggered by hyperglycemia was mitigated by an SGLT2 inhibitor in the hyperglycemic mouse aorta vascular organ cultures. The overview sums up the approaches implicated by the study that can potentially counteract the detrimental impact of hyperglycemia on vascular function in people with diabetes, including the clinical use of SGLT2 inhibitors for those with type 2 diabetes already being treated, for example, with metformin, along with dietary supplementation with broccoli-derived sulforaphane and tetrahydrobiopterin. The caveats associated with the study for extending the findings from mice to humans are summarized, pointing to the need to validate the work using vascular tissues from humans. Suggestions for future clinical studies are made, including the assessment of the impact of the therapeutic strategies proposed on measurements of blood flow in subjects with diabetes.

Published
2024
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49. Effects of ticagrelor, empagliflozin and tamoxifen against experimentally-induced vascular reactivity defects in rats in vivoand in vitro

Author

Moustafa Ahmed, Yasmin, Shehata Messiha, Basim Anwar, El-Sayed El-Daly, Mahmoud, and Abo-Saif, Ali Ahmed

Abstract

In the current investigation, the effects of the P2Y12 blocker ticagrelor, the sodium/glucose transporter-2-inhibitor empagliflozin, and the selective estrogen receptor modulator tamoxifen were examined against rheumatoid arthritis (RA)/diabetes mellitus (DM)-co-morbidity-induced defects in vascular reactivity.

Published
2019
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50. Effects of ticagrelor, empagliflozin and tamoxifen against experimentally-induced vascular reactivity defects in rats in vivoand in vitro

Author

Ahmed, Yasmin Moustafa, Anwar, Basim, El-Daly, Mahmoud El-Sayed, and Abo-Saif, Ali Ahmed

Abstract

Background: In the current investigation, the effects of the P2Y12 blocker ticagrelor, the sodium/glucose transporter-2-inhibitor empagliflozin, and the selective estrogen receptor modulator tamoxifen were examined against rheumatoid arthritis (RA)/diabetes mellitus (DM)-co-morbidity-induced defects in vascular reactivity. Methods: After model setting, rats were allocated into a normal control, an RA/DM-co-morbidity, and three treatment groups receiving ticagrelor, empagliflozin and tamoxifen. Aorta tissue was isolated for enzyme-linked immunosorbent assay (ELISA) and western blot estimation of the pro-inflammatory molecules angiotensin-II (Ang-II) and endothelin-1 (ET-1), the adhesion molecules P-selectin and vascular cell adhesion molecule-1 (VCAM-1), the energy preserving molecule adenosine-5’-mono-phosphate-activated protein kinase (AMPK), and the anti-inflammatory molecule vasoactive intestinal peptide (VIP). Estimations of endothelial nitric oxide synthase (eNOS) and matrix metalloproteinase (MlVIP)-2 were performed immunohistochemically, together with histopathological examination using hematoxylin and eosin and Masson trichrome staining. An in vitrostudy on rat aortic strips was conducted to assess aorta vasorelaxation. Results: Ticagrelor, empagliflozin and tamoxifen significantly increased aorta tissue AMPK and eNOS and decreased Ang-II, ET-1, P-selectin, VCAM-1 and VIP levels compared with RA/DM-co-morbidity, coupled with improved acetylcholine vasorelaxation in vitro. Conclusion: Ticagrelor, empagliflozin and tamoxifen may correct vascular reactivity defects, where modulation of vascular AMPK, eNOS, Ang-II, ET-1, P-selectin, VCAM-1 and MMP-2 underline their protective effects.

Published
2019
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