Title:Sesamol Induces Apoptosis by Altering Expression of Bcl-2 and Bax Proteins and Modifies Skin Tumor Development in Balb/c Mice
VOLUME: 17 ISSUE: 5
Author(s):Rishi Bhardwaj, SN Sanyal, Kim Vaiphei, Vandita Kakkar, Parneet Kaur Deol, Indu Pal Kaur* and Tranum Kaur*
Affiliation:Department of Biophysics, Panjab University, Chandigarh, Department of Biophysics, Panjab University, Chandigarh, Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, University Institute of Pharmaceutical Sciences, UGC Centre for Advance Study, Panjab University, Chandigarh-160014, Department of Chemistry and Biochemistry, University of Windsor, Windsor, N9B 3P4 ON
Keywords:Chemoprevention, apoptosis, SLNs, antioxidant, apoptotic proteins.
Abstract:Background: Chemoprevention using natural agents has emerged as a new and promising strategy for
reducing cancer burden. Sesamol, a water soluble lignin, is a potent antioxidant with potential anticancer activities. Its
small size (molecular weight: 138.34g) coupled with easy permeability (log P: 1.29) results in its excessive systemic
loss therefore, compromising local bioavailability. Furthermore, irritant nature of sesamol limits its application on
skin per se.
Objective: Present study aims to evaluate chemopreventive efficacy of free and encapsulated (SLNs) sesamol, at gross
and molecular level, in DMBA induced skin cancer animal model.
Methods: Evaluation is done in terms of tumor burden quantification, histological evaluation of skin, determination of
oxidative stress, and quantification of apoptotic proteins, bcl-2 and bax, using both western blot analysis and
immunofluorescence studies.
Results: Sesamol administration (both in free and encapsulated form) significantly decreased the tumor burden and
lipid peroxidation level and increased anti-oxidant levels, thereby hampering the development and promotion of skin
tumors. Further, downregulation of bcl-2 and stimulation of bax protein expression on treatment with both free and
encapsulated sesamol was responsible for the induction of apoptosis in tumor cells. Encapsulating sesamol into SLNs
not only reduced its irritant nature which limits its direct topical application but also improved its local targeting to
skin.
Conclusion: Both free and encapsulated sesamol demonstrated the inhibition of tumor progression by inducing skin
cell apoptosis via bcl-2/bax mediated pathway.
