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37 results on '"Elbaset, Marawan A."'

13. Cilostazol Combats Lipopolysaccharide‐Induced Hippocampal Injury in Rats: Role of AKT/GSK3β/CREB Curbing Neuroinflammation.

Author

El-ezz, Doaa Abou, Aldahmash, Waleed, Esatbeyoglu, Tuba, Afifi, Sherif M., Elbaset, Marawan Abd, and Ismail, Norsharina

Subjects
BRAIN degeneration, PROTEIN kinase B, BRAIN damage, PHOSPHODIESTERASE inhibitors, NEUROPLASTICITY
Abstract

Neuroinflammation is important in the pathophysiology of several degenerative brain disorders. This study looked at the potential neuroprotective benefits of cilostazol, a phosphodiesterase inhibitor, against LPS‐induced hippocampus damage in rodents and the principal molecular involvement of AKT/GSK3β/CREB signaling pathways. Behavioral tests revealed that cilostazol successfully corrected LPS‐induced neurobehavioral impairments. Furthermore, cilostazol therapy lowered hippocampal levels of amyloid beta 1–42 (Aβ1‐42) and p‐tau protein, both of which are critical pathological indicators of neurodegenerative disorders. Furthermore, cilostazol administration suppressed LPS‐induced rises in hippocampus caspase‐3 and NF‐κB levels while elevating rat B‐cell/lymphoma 2 (BCL2) and brain‐derived neurotrophic factor (BDNF) levels, which are implicated in neuronal survival and synaptic plasticity. Cilostazol treatment also restored the decreased phosphorylation of protein kinase B (p‐AKT) and reduced the elevated levels of phosphorylated glycogen synthase kinase‐3 beta (p‐GSK3β) and cAMP response element‐binding protein (CREB) in the hippocampus of LPS‐treated rats. Histopathological examination revealed that cilostazol ameliorated LPS‐induced brain damage with reduced neuronal loss and gliosis. Immunohistochemistry analysis showed a decrease in Iba‐1 expression, indicating a reduction in microglial activation in the cilostazol‐treated group compared to the LPS group. The findings advocate that cilostazol exerts neuroprotective effects against LPS‐induced hippocampal injury by modulating the AKT/GSK3β/CREB pathway and curbing neuroinflammation. Cilostazol may hold promise as a therapeutic agent for neuroinflammatory conditions associated with neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

Published
2024
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21. Nrf2/HO‐1, NF‐κB and PI3K/Akt signalling pathways decipher the therapeutic mechanism of pitavastatin in early phase liver fibrosis in rats.

Author

Elbaset, Marawan A., Mohamed, Bassim M. S. A., Hessin, Alyaa, Abd El‐Rahman, Sahar S., Esatbeyoglu, Tuba, Afifi, Sherif M., and Fayed, Hany M.

Subjects
HEPATIC fibrosis, NUCLEAR factor E2 related factor, PI3K/AKT pathway, CELLULAR signal transduction, FIBROSIS, PITAVASTATIN
Abstract

Liver fibrosis is a common chronic hepatic disease. This study aimed to investigate the effect of pitavastatin (Pit) against thioacetamide (TAA)‐induced liver fibrosis. Rats were divided into four groups: (1) control group; (2) TAA group (100 mg/kg, i.p.) three times weekly for 2 weeks; (3 and 4) TAA/Pit‐treated group, in which Pit was administered orally (0.4 and 0.8 mg/kg/day) for 2 weeks following TAA injections. TAA caused liver damage manifested by elevated serum transaminases, reduced albumin and histological alterations. Hepatic malondialdehyde (MDA) was increased, and glutathione (GSH) and superoxide dismutase (SOD) were decreased in TAA‐administered rats. TAA upregulated the inflammatory markers NF‐κB, NF‐κB p65, TNF‐α and IL‐6. Treatment with Pit ameliorated serum transaminases, elevated serum albumin and prevented histopathological changes in TAA‐intoxicated rats. Pit suppressed MDA, NF‐κB, NF‐κB p65, the inflammatory cytokines and PI3K mRNA in TAA‐intoxicated rats. In addition, Pit enhanced hepatic antioxidants and boosted the nuclear factor erythroid 2–related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1) mRNA. Moreover, immunohistological studies supported the ability of Pit to reduce liver fibrosis via suppressing p‐AKT expression. In conclusion, Pit effectively prevents TAA‐induced liver fibrosis by attenuating oxidative stress and the inflammatory response. The hepatoprotective efficacy of Pit was associated with the upregulation of Nrf2/HO‐1 and downregulation of NF‐κB and PI3K/Akt signalling pathways. [ABSTRACT FROM AUTHOR]

Published
2024
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26. Synergistic cardioprotective effects of melatonin and deferoxamine through the improvement of ferritinophagy in doxorubicin-induced acute cardiotoxicity

Author

Hanna, Mira, primary, Seddiek, Hanan, additional, Aboulhoda, Basma Emad, additional, Morcos, George N. B., additional, Akabawy, Ahmed M. A., additional, Elbaset, Marawan Abd, additional, Ibrahim, Abdelsatar Abdelsatar, additional, Khalifa, Mohamed Mansour, additional, Khalifah, Ibtesam Mahmoud, additional, Fadel, Mostafa Said, additional, and Shoukry, Tarek, additional

Published
2022
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36. Immunogenicity and Safety of an Inactivated SARS-CoV-2 Vaccine: Preclinical Studies

Author

Kandeil, Ahmed, primary, Mostafa, Ahmed, additional, Hegazy, Rehab R., additional, El-Shesheny, Rabeh, additional, El Taweel, Ahmed, additional, Gomaa, Mokhtar R., additional, Shehata, Mahmoud, additional, Elbaset, Marawan A., additional, Kayed, Ahmed E., additional, Mahmoud, Sara H., additional, Moatasim, Yassmin, additional, Kutkat, Omnia, additional, Yassen, Noha N., additional, Shabana, Marwa E., additional, GabAllah, Mohamed, additional, Kamel, Mina Nabil, additional, Abo Shama, Noura M., additional, El Sayes, Mohamed, additional, Ahmed, Amira N., additional, Elalfy, Zahraa S., additional, Mohamed, Bassim MSA, additional, Abd El-Fattah, Safa N., additional, El Hariri, Hazem Mohamed, additional, Abdel Kader, Mona, additional, Azmy, Osama, additional, Kayali, Ghazi, additional, and Ali, Mohamed A., additional

Published
2021
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37. Renoprotective Effect of Pitavastatin against TAA-Induced Renal Injury: Involvement of the miR-93/PTEN/AKT/mTOR Pathway

Author

A. Elbaset, Marawan, M. S. A. Mohamed, Bassim, E. Moustafa, Passant, Esatbeyoglu, Tuba, M. Afifi, Sherif, F. Hessin, Alyaa, S. Abdelrahman, Sahar, and M. Fayed, Hany

Abstract

This research investigated if pitavastatin (Pita) might protect rats’ kidneys against thioacetamide (TAA). By altering the PTEN/AKT/mTOR pathway, pitavastatin may boost kidney antioxidant capacity and minimize oxidative damage. Statins have several benefits, including antioxidant and anti-inflammatory characteristics. The principal hypothesis of this study was that Pita can regulate the miR-93/PTEN/AKT/mTOR pathways, which is thought to be responsible for its renoprotective effects. The experiment divided male rats into four groups. Group 1 included untreated rats as the control. Group 2 included rats which received TAA (100 mg/kg intraperitoneally thrice a week for two weeks) to destroy their kidneys. Groups 3 and 4 included rats which received Pita orally at 0.4 and 0.8 mg/kg for 14 days after TAA injections. Renal injury increased BUN, creatinine, and MDA levels and decreased glutathione (GSH) levels. Pitavastatin prevented these alterations. TAA decreased PTEN and increased miR-93, Akt, p-Akt, mTOR, and Stat3 in the kidneys. Pitavastatin also regulated the associated culprit pathway, miR-93/PTEN/Akt/mTOR. In addition, TAA induced adverse effects on the kidney tissue, which were significantly ameliorated by pitavastatin treatment. The findings suggest that pitavastatin can attenuate renal injury, likely by regulating the miR-93/PTEN/Akt/mTOR pathway. This modulation of the pathway appears to contribute to the protective effects of pitavastatin against TAA-induced renal injury, adding to the growing evidence of the pleiotropic benefits of statins in renal health.

Published
2024
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