EVALUATION OF CHEMOPREVENTIVE RESPONSE OF PENTOXIPHYLLINE AND SILDENAFIL IN COLORECTAL CARCINOMA EXPERIMENTALLY INDUCEDIN RATS: COMPARATIVE STUDY WITH 5-FLUOROURACIL
Journal Title: International Journal of Pharmacy and Pharmaceutical Sciences - Year 2015, Vol 7, Issue 12
Abstract
Objective: This study was designed to investigate some possible therapeutic mechanisms of pentoxifylline and sildenafil in the treatment of colorectal carcinoma induced by 1, 2 dimethylhydrazines in rats.Methods: Rats were allocated into seven groups, negative control, colon cancer induced by 1,2,dimethylhydrazine, 5-fluorouracil (5-FU) (50 mg/kg)-treated, pentoxifylline (PTX) (50 mg/kg)-treated, sildenafil (0.7 mg/kg)-treated groups; the two other groups set as colon cancer induced group treated with PTX (50 mg/kg) plus 5-FU(50 mg/kg) and sildenafil (0.7 mg/kg) plus 5-FU (50 mg/kg), respectively.Results: Biochemical results revealed significant elevation of serum carcinoembryonic antigen (CEA) levels, carbohydrate19-9 antigen (CA19-9) as colon cancer specific antigen markers; and a significant decrease in scaspase-3 (CASP3) as a marker for apoptosis, in the cancer-induced group compared to negative control group. Cancer-induced rats treated with 5-FU, with PTX or sildenafil showed a significant decrease in serum CEA and CA19-9 levels and a significant increase in CASP3 levels compared to cancer induced group. Furthermore, plasma levels of CEA and CA19-9 in 5-FU plus pentoxifylline and in 5-FUplus sildenafil groups were significantly decreased and plasma levels of CASP3 in 5-FU plus PTX, 5-FU plus sildenafil groups were significantly increased with respect to 5-FU treated group.Conclusion: Results of the present study suggest a good therapeutic approach of the PDE inhibitors, PTX and sildenafil for intervention against progressive colon cancer with special reference to the induction of apoptosis in colon cancer cells.Â
Authors and Affiliations
Ahmed Hamedjwied Ataimish, Nadan. Al-shawi, Mohammed M. Al-qurtas
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Article Has Been Withdraw From Publication
Article Has Been Withdraw From Publication
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