Preventive effect of acemannan on DMBA-induced mouse skin tumorigenesis by modulating inflammatory cytokines and apoptosis pathways: molecular docking and molecular dynamic simulation approaches
- 1Department of Clinical Pharmacy, College of Pharmacy, Jouf University, Sakaka 72341, Al-Jouf, Saudi Arabia.
- 2Department of Pharmaceutics, College of Pharmacy, Jouf University, Sakaka 72341, Al-Jouf, Saudi Arabia.
- 3Department of Pharmacology, College of Pharmacy, Jouf University, Aljouf, Sakaka 72341, Saudi Arabia.
- 4Clinical Laboratory Science, Medical Applied College, Jouf University, Sakaka, Aljouf 72341, Saudi Arabia.
- 5Dnyan Kala Krida & Krushi Prathishthan's, Late Laxmibai Phadtare College of Pharmacy, A/P-Kalamb-Walchandnagar, Indapur, Pune 413114, India.
- 0Department of Clinical Pharmacy, College of Pharmacy, Jouf University, Sakaka 72341, Al-Jouf, Saudi Arabia.
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View abstract on PubMed
Summary
This summary is machine-generated.Acemannan shows promise in preventing skin cancer by reducing tumor growth and regulating oxidative stress and inflammation. This study found acemannan effectively inhibited cancer development in mice treated with DMBA.
Area Of Science
- Oncology
- Dermatology
- Pharmacology
Background
- Skin cancers, including melanoma, are increasingly prevalent, influenced by environmental factors like UV radiation.
- UV radiation induces oxidative stress, a key factor in melanoma development.
- Investigating natural compounds for therapeutic potential against skin cancer is crucial.
Purpose Of The Study
- To evaluate the therapeutic potential of acemannan against 7,12-dimethylbenz[a]anthracene (DMBA)-induced skin cancer in mice.
- To assess acemannan's effects on oxidative stress, inflammation, and apoptosis pathways in skin cancer.
Main Methods
- DMBA-induced skin cancer model in mice, with groups receiving varying doses of acemannan.
- Assessment of tumor burden, oxidative stress markers, antioxidant enzymes, inflammatory cytokines, NF-κB signaling, and apoptosis.
- Histopathological examination, molecular docking, and molecular dynamics simulations were performed.
Main Results
- Acemannan significantly reduced tumor burden, number, and volume in DMBA-treated mice.
- Acemannan modulated oxidative stress, enhanced antioxidant activity, suppressed inflammation, inhibited NF-κB signaling, and induced apoptosis.
- Molecular docking revealed strong binding affinities of acemannan to key proteins involved in inflammation and apoptosis.
Conclusions
- Acemannan demonstrates significant therapeutic potential for skin cancer prevention.
- Its mechanisms involve regulating oxidative stress, inflammation, and apoptosis.
- Acemannan may serve as a promising agent for managing skin cancer.
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