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العنوان
Potential anti-hepatocellular carcinoma effect of Bee venom-loaded chitosan nanoparticles /
المؤلف
Hanoura, Nouf Mostafa Ahmed.
هيئة الاعداد
مشرف / Prof.Dr.Mahmoud Mahamed Balbaa
مشرف / Ass.Prof. Mohamed Abdel mohsen El-Kersh
مشرف / Prof.Dr.Ayman Ibrahim Ahmed Elkady
مشرف / Dr.Marwa Bassiouny Gomaa
الموضوع
Chitosan. Bee.
تاريخ النشر
2022.
عدد الصفحات
44 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الكيمياء الحيوية ، علم الوراثة والبيولوجيا الجزيئية
تاريخ الإجازة
12/12/2022
مكان الإجازة
جامعة الاسكندريه - كلية العلوم - Biochemistry
الفهرس
Only 14 pages are availabe for public view

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Abstract

Hepatocellular carcinoma (HCC) is one of the world’s most risky diseases due to the lack of clear and cost-effective therapeutic targets. Currently, the toxicity of conventional chemotherapeutic medications and the development of multidrug resistance is driving research into targeted therapies. The nano-biomedical field’s potential for developing an effective therapeutic nano-sized drug delivery system is viewed as a significant pharmaceutical trend for the encapsulation and release of numerous anticancer therapies. In this regard, current research is centered on the creation of biodegradable chitosan nanoparticles (CSNPs) for the selective and sustained release of bee venom into liver cancer cells. Furthermore, surface modification with polyethylene glycol (PEG) and GE11 peptide-conjugated bee venom CSNPs allows for the targeting of EGFR-overexpressed liver cancer cells. A series of in vitro and in vivo cellular analyses were used to investigate the antitumor effects and mechanisms of targeted bee venom-CSNPs. Targeted bee venom-CSNPs, in particular, were found to have higher cytotoxicity against HepG2 cells than SMMC-7721 cells, as well as stronger cellular uptake and a substantial reduction in cell migration, leading to improved cancer suppression. It also promotes cancer cell death in EGFR overexpressed HepG2 cells by boosting reactive oxygen species, activating mitochondria-dependent pathways inhibiting EGFR-stimulated MEK/ERK pathway, and elevating p38-MAPK in comparison to native bee venom. In hepatocellular carcinoma (HCC)-induced mice, it has anti-cancer properties against tumor tissue. It also improved liver function and architecture without causing any noticeable toxic side effects, as well as inhibiting tumor growth by activating the apoptotic pathway. The design of this cancer-targeted nanoparticle establishes GE11-bee venom-CSNPs as a potential chemotherapeutic treatment for EGFR over-expressed malignancies Finally, our work elucidates the molecular mechanism underlying the anticancer selectivity of targeted bee venom-CSNPs and outlines therapeutic strategies to target liver cancer.