Effect of Isocryptolepine Derivative on Ehrlich Ascites Carcinoma Cells in Mice via Regulation of Oxidative Stress and MAPK/JNK/mTOR Signaling Pathway | ||
| Egyptian Journal of Chemistry | ||
| Articles in Press, Accepted Manuscript, Available Online from 15 September 2025 | ||
| Document Type: Original Article | ||
| DOI: 10.21608/ejchem.2025.409048.12118 | ||
| Authors | ||
| Bishoy El-Aarag* 1; Mohamed Essam shams ElDeen2; Wafaa Ibrahim3; Abdullah Ahmed Sayed Ahmed4; Ibrahim Tantawy5 | ||
| 1Biochemistry Division, Chemistry Department, Faculty of Science, Menoufia University, Egypt | ||
| 2Biochemistry Division, Department of Chemistry, Faculty of Science, Menoufia University, Shebin El-Koom, 32512, Egypt | ||
| 3Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Tanta University, Tanta, Egypt | ||
| 4Department of Chemistry, Faculty of Science, Menoufia University, Shebin El-Kom 32512, Menoufia, Egypt; | ||
| 5Chemistry Department, Faculty of Science, El Menoufeia University, Shebin El Koom, Egypt | ||
| Abstract | ||
| Ehrlich ascites carcinoma (EAC) is mammary adenocarcinoma model that is highly sensitive to chemotherapy. Major signaling cassettes of the mitogen-activated protein kinase (MAPK) signaling pathway include the c-Jun N-terminal kinase (JNK) and p38 pathways. They function in the number of cellular processes regulation, involving apoptosis, embryonic development, and proliferation. Isocryptolepine derivatives were examined for their anti-tumor properties because of their interaction with DNA base pairs and topoisomerase II. The present trail objectives to investigate the anticancer potency of the as prepared 6-aminopropyl amino isocryptolepine (6-APAI) on EAC in mice and its impact on JNK and p38 pathways via assessment of EAC cell viability, ascites volume, malondialdehyde, catalase activity and total antioxidant capacity, in addition, the mTOR and caspase-8 concentrations in EACs were determined, and JNK and p38 expression levels were also assessed. The findings indicated that 6-APAI has a cytotoxic effect on the viability of EAC cells and decreases the volume of ascites. Additionally, 6-APAI promotes oxidative stress and apoptosis. Moreover, it upregulates the expression of JNK and p38 in EACs indicated that the anticancer 6-APAI activity against EACs in mice is mediated by the JNK and p38 signaling pathways regulation. | ||
| Keywords | ||
| Isocrypotolepine derivative; Ehrlich ascites carcinoma; mTOR; Caspase-8; JNK; p38 | ||
|
Statistics Article View: 4 |
||
