Mohamed Kamel Abogolayel

Dr. Mohamed Kamel Abogolayel

Biochemistry Department, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia;
orcid

Research Focus & Metrics

Academic Career Length

9Years (2018-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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7 March 2019 in Evidence-Based Complementary and Alternative Medicine
Verified
Journal Article
Open access
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MZMazin Zamzami
Mazin Zamzami
OBOthman A.S. Baothman
Othman A.S. Baothman
FSFatma Samy
Fatma Samy
MAMohamed Kamel Abogolayel
Mohamed Kamel Abogolayel
The current study aimed to evaluate the probable protective effect ofLepidium sativumseeds (LSS) against CCl4induced hepatic injury in New-Zealand rabbits. Rabbits were randomly divided into two main groups; group-A (noninjured group, n=15) was divided to subgroups A1 (untreated control) and A2 and A3 which received 200 & 400 mg/kg bw of LSS, respectively, in their diet daily. Group-B (injured group, n=30) were subcutaneously injected with CCl4(0.5 ml/kg bw) starting from day one of the experiment and were equally divided into 3 subgroups: B1 received normal standard diet and B2 & B3 received 200 & 400 mg/kg bw of LSS, respectively, in their diet daily. Five rabbits of all subgroups were decapitated 5 and 10 weeks after experimental running. Biochemical analysis revealed significant decrease in serum levels of transaminases,γ-GT, ALP, total bilirubin, cholesterol, triglycerides associated with significant increase in the serum levels of T protein and albumin of 200 and 400 mg/kg bw of LSS protected rabbits for 5 and 10 weeks as compared with CCl4treated rabbits. Oxidative stress and depressed antioxidant system of the liver tissues were markedly obvious in the CCl4treated group. LSS administration reversed these results towards normalization. Histopathological examination of LSS protected rabbits (200 mg/kg bw of LSS for 10 weeks) showed improvement of the histoarchitectural changes of the liver induced by CCl4to the normal aspect, showing regenerating hepatocytes with no steatosis, discrete chronic venous congestion, and discrete inflammatory infiltrate. The current findings provide new evidence that LSS could reverse the hepatotoxic effects of CCl4and repair the liver functions.

27 January 2023 in Food Science & Nutrition
Verified
Journal Article
Open access
OBOthman A.S. Baothman
Othman A.S. Baothman
HAHisham Altayeb
Hisham Altayeb
MZMustafa Adnan Zeyadi
Mustafa Adnan Zeyadi
SHSalman Hosawi
Salman Hosawi
MAMohamed Kamel Abogolayel
Mohamed Kamel Abogolayel
The purpose of this study is to evaluate the likely defensive impact of Ajwa date aqueous extract (AJDAE) in alleviating the nephrotoxicity generated by doxorubicin (DOX) injection in rats. Sixty male Wister albino rats were randomly and equally separated into six groups (n = 10), and they were treated as follows: untreated control group, extract groups administered with 0.75 and 1.5 mg kg bw of AJDAE, toxicant control group administered with DOX, and prophylactic groups were treated with 0.75 and 1.5 mg/kg of AJDAE and 15 mg/kg DOX. Biochemical parameters, antioxidant enzymes, renal functions, DNA integrity, and histopathology were studied to evaluate the nephroprotective activity of AJDAE. Furthermore, bioactive compounds were utilized for in silico molecular docking. AJDAE treatment resulted in significant improvements in the amended renal biomarkers (urea, creatinine, calcium, phosphorous, and uric acid), antioxidative markers, and MDA. Noticeable histopathological improvements supported this result. Results of in silico studies revealed that d‐Mannitol, 6TMS derivative, palmitic acid, and TMS derivative had a higher docking score with human soluble epoxide hydrolase (−10.9 kcal/mol) and NF‐κB‐DNA (−7 kcal/mol). The present findings indicated that AJDAE could decrease ROS generation and lipid peroxidation (LPO) and repair the DOX injection‐related DNA damage.

12 September 2018 in Biomedical and Pharmacology Journal
Verified
Journal Article
Open access
MSMeaad F. Sabbah
Meaad F. Sabbah
FAFawzia Abdulaziz Alshubaily
Fawzia Abdulaziz Alshubaily
OBOthman A. S. Baothman
Othman A. S. Baothman
MZMazin A. Zamzami
Mazin A. Zamzami
LSLobna Shash
Lobna Shash
MAMohamed Kamel Abogolayel
Mohamed Kamel Abogolayel
Doxorubicin (DOX) is one of the most potent and widely used chemotherapeutic agents to treat several malignancies. However, the clinical use of DOX is seriously restricted due to its acute and chronic cardiotoxic side effects This study investigated the protective effect of (Ajwa) date aqueous extract (AJDAE) against doxorubicin-induced cardiotoxicity in rats. Sixty Wister albino male rats (150-200 gms.) were comprised in our study and divided into six equal groups: group I (untreated control), group II, group III, rats were orally received AJDAE (0.75 & 1.5 gm/ kg.bw) respectively, for 4 weeks, rats of groups IV, V and VI were intraperitoneally injected with one dose of doxorubicin (5 mg/kg.bw) at the end of the 4th week of the study to induce cardiotoxicity, rats of groups V & VI were orally received AJDAE (0.75 & 1.5 gm/ kg.bw) respectively. Cardiac enzymes, lipid profile, SOD, GR, GST, GPx, CAT and MDA in rats’ hearts homogenate, urinary 8OHdG as well as DNA integrity and histopathological changes were investigated in all studied rats.Oral administration of AJDAE (0.75 & 1.5 gm/ kg.bw) attenuated the cardiotoxicity of DOX, improved the cardiac enzymes, lipid profile, reduced the urinary 8OHdG and prohibited the depletion of endogenous antioxidants and suppressed lipid peroxidation (MDA). Moreover, AJDAE enhanced DNA integrity. Histological findings showed that AJDAE (0.75 & 1.5 gm/ kg.bw) administration reduced cardiomyocytes alterations, congestion, edema and the intense cellular stress exerted on myocardial fibers as well as restored the cardiomyocytes architecture. Our data showed that AJDAE obviously resulted in protective effects against DOX-induced cardiotoxicity in rat’s heart. It can be concluded that Ajwa date offers a considerable protection against DOX-induced cardiotoxicity.