ORIGINAL ARTICLE
Year : 2015  |  Volume : 22  |  Issue : 1  |  Page : 21-29

Terminalia chebula attenuates DMBA/Croton Oil-Induced oxidative stress and inflammation in Swiss albino mouse skin


Department of Medical Elementology and Toxicology, Faculty of Science, Section of Molecular Carcinogenesis and Chemoprevention, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi, India

Correspondence Address:
Sarwat Sultana
Department of Medical Elementology and Toxicology, Faculty of Science, Section of Molecular Carcinogenesis and Chemoprevention, Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi- 110 062
India
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DOI: 10.4103/0971-6580.172252

PMID: 26862256

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Objective: The present study was designed to investigate underlying molecular mechanism for antitumorigenic potential of Terminalia chebula (TC) against chemically-induced skin tumorigenesis in Swiss albino mice. It is used as herbal medicine because it exhibits antioxidant, anti-inflammatory, and anticarcinogenic activity. However, the précised underlying mechanism remains to be elucidated. Materials and Methods: In light of the important role of nuclear factor-kappaB (NF-κB), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (i-NOS), ornithine decarboxylase (ODC), proinflammatory cytokines, oxidative stress in carcinogenesis, chemopreventive efficacy of TC against 7,12-dimethylbenz[a] anthracene (DMBA), and croton oil-induced 2-stage skin carcinogenesis was studied in terms of cytoprotective antioxidant enzymes activity, lipid peroxidation (LPO), inflammatory responses, and expression of various molecular markers in skin tissues. Results: We found that topical application of TC at dose of 30 mg/kg b. wt. mouse effectively suppressed oxidative stress and deregulated activation of inflammatory mediators and tumorigenesis. Histological findings further supported the protective effects of TC against DMBA/croton oil-induced cutaneous damage. Conclusion: The findings of the present study suggest that the chemopreventive effect of TC is associated with upregulation of endogenous cytoprotective machinery and downregulation of inflammatory mediators (interleukin (IL)-6, COX-2, i-NOS, ODC, and NF-κB).


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