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Protective Effects of [6]-Paradol on Histological Lesions and Immunohistochemical Gene Expression in DMBA Induced Hamster Buccal Pouch Carcinogenesis
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  • Protective Effects of [6]-Paradol on Histological Lesions and Immunohistochemical Gene Expression in DMBA Induced Hamster Buccal Pouch Carcinogenesis
  • Protective Effects of [6]-Paradol on Histological Lesions and Immunohistochemical Gene Expression in DMBA Induced Hamster Buccal Pouch Carcinogenesis
저자명
Mariadoss. Arokia Vijayaanand,Kathiresan. Suresh,Muthusamy. Rajasekar,Kathiresan. Sivakumar
간행물명
Asian Pacific journal of cancer prevention : APJCP
권/호정보
2013년|14권 5호|pp.3123-3129 (7 pages)
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아시아태평양암예방학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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기타언어초록

Background: The search for naturally occurring agents in routinely consumed foods that may inhibit cancer development is of high priority. [6]-Paradol is a pungent phenolic bioactive component from ginger with welldocumented health promoting antioxidant, antimutagenic, antigenotoxic and anti-inflammatory properties. However, anticarcinogenic effects have yet to be fully explored. The objectives of the present study were therefore to assess protective effects against 7,12-dimethylbenz(a)anthracene (DMBA) induced buccal pouch carcinogenesis in male golden Syrian hamsters. Methods: Oral squamous cell carcinomas developed in the left buccal pouch of hamsters on painting with 0.5% of DMBA, three times in a week. To assess the apoptotic associated gene expressing potential of [6]-paradol, it was orally administered to DMBA treated hamsters on alternate days from DMBA painting for 14 weeks. Results: We observed 100% tumor formation with marked levels of neoplastic changes and altered the expression of apoptotic associated gene (p53, bcl-2, caspase-3 and TNF-${alpha}$) was observed in the DMBA alone painted hamsters as compared to control hamsters. Oral administration of [6]-paradol at a dose of 30 mg/kg b.wt to DMBA treated animals on alternative days for 14 weeks significantly reduced the neoplastic changes and improved the status of apoptosis associated gene expression. Conclusion: These observations confirmed that [6]-paradol acts as a tumor suppressing agent against DMBA induced oral carcinogenesis. We also conclude that [6]-paradol also effectively enhances apoptosis- associated gene expression in DMBA treated animals.