Basic Informations

C.V

Education
Master in Pharmaceutical Sciences (Biochemistry)
-Department of Biochemistry Faculty of Pharmacy, Beni-Suef University, Beni-Suef, Egypt. Oct 2019
- Thesis " A Biochemical Study on The Possible Protective Effect of Tiopronin and Hesperidin on Chemically Induced Liver Carcinoma in Rats."
Pre-master training course May 2016
-Department of Biochemistry Faculty of Pharmacy, Beni-Suef University, Beni-Suef, Egypt. - - Cumulative grade: Excellent, GPA (B+ 3.8/4) Courses included in training: Biochemistry, Molecular biology, Laboratory techniques, Biostatistics, Computer sciences, Nutrition in Disease Prevention and Cure, Seminar.
Bachelor in Pharmaceutical Sciences Faculty of Pharmacy Beni-Suef University Beni-Suef, Egypt.
- Graduated with general grade of excellent with honors, percentage 93.41%
 PROFESSIONAL AND RESEARCH EXPERIENCE 
Teaching Assistant Nov 2019- till present
-Department of Biochemistry, Faculty of Pharmacy, Beni-Suef University, , Beni-Suef, Egypt.
Demonstrator May 2015- Oct 2019
- Department of Biochemistry, Faculty of Pharmacy, Beni-Suef University, Beni-Suef, Egypt.
 PUBLICATIONS
 Research articles
Yomna S. Momen, Kandeil, M.A. & Mahmoud, M.O. (2025). A Novel Cardioprotective Mechanism of Rosuvastatin: Restoring PINK1/Parkin-Mediated Mitophagy via SIRT1/FOXO1 Activation in Doxorubicin-Induced Cardiotoxicity. Cancer Chemotherapy and Pharmacology 95(1):84, 29 August 2025.
Yomna S. Momen, Mohamed A. Kandeil, Mohamed O. Mahmoud. “Forskolin attenuates doxorubicin-induced cardiotoxicity in rats by activating SIRT1/FOXO1/PINK1/Parkin mediated mitophagy”. Scientific African 28, e02765, June 2025.
Yomna S. Mo’men, Rasha M. Hussein, Mohamed A. Kandeil. “Involvement of PI3K/Akt pathway in the protective effect of hesperidin against a chemically induced Liver cancer in rats”. Journal of Biochemical and Molecular Toxicology 33(6), 19 February 2019.
Yomna S. Mo’men, Rasha M. Hussein, Mohamed A. Kandeil. “A novel chemoprotective effect of tiopronin against diethylnitrosamine-induced hepatocellular carcinoma in rats: Role of ASK1/P38 MAPK-P53 signalling cascade”. Clinical and Experimental Pharmacology and Physiology 47 (2), 322 332, 25 October 2019.
 Review articles
Yomna S. Momen, Jayshree Mishra, Narendra Kumar. “Brain-Gut and Microbiota-Gut-Brain Communication in Type-2 Diabetes Linked Alzheimer’s Disease”. Nutrients 2024, 16 (15), 2558.
Yomna S. Momen, “Targeting the NLRP3 Inflammasome: Novel Inhibitors for Cardiovascular Diseases Management”. 
 Abstracts and Posters
 Jayshree Mishra, Yomna Momen, Priyam Kumar, and Narendra Kumar. “Gut-brain Communication in Pathogenesis of Alzheimer’s Disease”. Pathobiology Mechanisms of Disease, Proceedings of Annual Meeting of the American Society for Investigative Pathology, Baltimore, US, 2024, April 20-23; ASIP: Baltimore, US, 2024; Abstract number039, page 42. PRESENTATIONS
Yomna Momen “Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease”. Seminar Series organized by College of Pharmacy, Texas A&M University, May 03, 2023.
GRANT AWARD
Forfeited and Returned to Funding Agency Principle Investigator, “Prevention of Doxorubicin-induced Cardiotoxicity through modulation of Mitophagy”, Support and Project Finance Office, Beni-Suef University, 2021-2022; Total Costs: LE30,000.

Master Title

A Biochemical Study on the Possible Protective Effect of Tiopronin and Hesperidin on a Chemically Induced Liver Carcinoma in Rats

Master Abstract

Abstract Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death worldwide. Diethylnitrosamine (DENA) is one of the existing nitrosamines that induces oxidative stress and contributes significantly to HCC pathogenesis. Interestingly,tiopronin is a thiol group-containing compound that is used to control cysteine nephrolithiasis while hesperidin is a flavanone glycoside that is found in the Citrus species. Both tiopronin and hesperidin showed antioxidant activities that protect against several liver diseases. Forty adult male Wistar rats were divided into: Control group (rats were injected with saline), DENA treated group (rats were provided with 100 mg/l of DENA solution in the drinking water for 8 weeks and then DENA-free water from week 9 to week 16), Tiopronin + DENA treated group (rats were injected intraperitoneally with 60 mg/Kg b.wt of tiopronin daily for 16 weeks in addition to DENA as the DENA treated group), Hesperidin+ DENA treated group (rats were given 200 mg/Kg b.wt of hesperidin by oral gavage for 16 weeks and DENA as the DENA treated group). At the end of the experimental period (at week 16), the liver function tests and the oxidative stress markers were assessed. The protein levels of phospho-ASK1, phospho- P38, phospho- P53, PI3K, phospho-Akt and CDK2 were measured in the liver tissues by western blotting analysis. The results showed that tiopronin and hesperidin prevented the elevation of liver function enzymes, serum alpha fetoprotein level and oxidative stress markers such as malondialdehyde, nitric oxide, catalase and glutathione peroxidase. Furthermore, both tiopronin and hesperidin prevented the pathological alterations induced by DENA on the liver tissues macroscopically and microscopically. Remarkably, both tiopronin and hesperidin effectively protected against DENA-induced HCC by different molecular mechanisms. Tiopronin preserved the activity of ASK1/ P38 MAPK/ P53 signaling cascade while hesperidin suppressed DENA-induced up-regulation of PI3K/Akt signaling pathway. Therefore, the use of tiopronin and hesperidin showed a chemoprotective role against the induced hepatocellular carcinoma in rats.

PHD Title

Biochemical Study on the Role of Mitophagy in Doxorubicin Induced Cardiotoxicity in Rats

PHD Abstract

Abstract Despite the advancement of cancer therapy, chemotherapy is still a standard approach in cancer treatment. Doxorubicin (DOX) is a potent chemotherapeutic drug, used for the treatment of both solid and hematological cancers. However, its clinical use is limited due to acute and chronic cardiotoxicity. DOX-induced cardiotoxicity is attributed mainly to mitophagic dysregulation and oxidative stress. Forskolin (FSK), a natural diterpene derived from the roots of Coleus forskohlii, and rosuvastatin (RSV), a lipid-lowering drug, exerted a cardioprotective effect against several cardiac disorders. Therefore, this study aimed to reveal the mechanism by which FSK and RSV protect against DOX-induced cardiotoxicity in Wistar rats. Adult male Wistar rats were divided into eight groups: Control (vehicle only), FSK (20 mg/kg orally for 3 weeks), RSV (20 mg/kg, orally, for 3 weeks), DOX (18 mg/kg intraperitoneally over 2 weeks), FSK + DOX, chloroquine (CQ)+ FSK+ DOX group (CQ 25 mg/kg, intraperitoneally, for 2 weeks beside FSK and DOX as described), RSV + DOX, and CQ+RSV+DOX group. By the end of the third week, serum myocardial injury biomarkers and oxidative stress markers, along with autophagic flux biomarkers (LC3II & P62) in cardiac tissue, were measured via ELISA. Additionally, lncRNA APF gene expression was analyzed using RT PCR, while protein levels of p-SIRT1, FOXO1, p-PINK1, and p-Parkin were determined by western blot. FSK and RSV prevented the DOX-induced elevation of myocardial injury and oxidative stress biomarkers, while restoring the normal autophagic flux. Additionally, FSK and RSV increased lncRNA APF, p-SIRT1, p-PINK1 and p-Parkin expression and decreased FOXO1 expression. CQ, the classical autophagy inhibitor, blunted the cardioprotective effect of both FSK and RSV. These novel findings suggested that FSK and RSV have a cardioprotective effect against DOX-induced cardiotoxicity by normalizing autophagic flux and enhancing PINK1/Parkin-driven mitophagy upon activation of the SIRT1/FOXO1 pathway. Thus, combining FSK or RSV with DOX may enable patients to complete chemotherapy with a reduced risk of cardiotoxicity.