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Non Selective Inhibition of COX Activity Reversed Inflammation and Reactive Oxygen Radicals Mediated Prostate Cancer Risk and Decreased Disease Progression in Preclinical Model

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DOI: 10.4236/jct.2016.71005    3,784 Downloads   4,103 Views

ABSTRACT

Prostate cancer (PCa) represents the most frequent urologic diagnosis in elderly males. We have previously shown that exposure of prostate to lipopolysaccharide (LPS) promotes cancer risk. We investigated the effect of non-selective cyclooxygenase (COX) inhibition on prostate inflammation-mediated cancer risk in vivo. The prostates of male rats were inoculated with E. coli as sources of inflammatory molecules (LPS) and were treated with COX inhibitor, aspirin 2 mg/Kg orally for 14 days or PBS. Oxidative stress was induced with two 2 mls of hydrogen peroxide orally twice daily or PBS for 14 days; they were either treated with COX inhibitor or PBS for another 14 days. Blood was collected and analyzed for acid phosphatase and PSA. Data showed presences of LPS in the prostate of the rats resulted in gradual increase in PSA when compared to control (P < 0.0001). However, COX inhibition resulted in statistically significant reduction in concentration of PSA level compared to control group (P < 0.0001). To understand if oxidative stress mechanism was involved in the inflammation mediated increase in PSA, data showed that rats exposed to H2O2 had 2.5 fold increase in acid phosphatase (ACP) compared control (P < 0.0001), and by inhiting COX activity, a statistically significant reduction in ACP from 11.2 IU/L ± 0.67 to 5.7 IU/L ± 0.347 (P < 0.0034) was observed. Thus since increased in PSA was associated to cancer risk, our data suggested that inflammation mediated prostate cancer risk was reversible by Inhibition of COX Activity in rats.

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Omabe, M. , Omabe, K. , Famurewa, C. , Okorocha, A. and Omabe, G. (2016) Non Selective Inhibition of COX Activity Reversed Inflammation and Reactive Oxygen Radicals Mediated Prostate Cancer Risk and Decreased Disease Progression in Preclinical Model. Journal of Cancer Therapy, 7, 41-49. doi: 10.4236/jct.2016.71005.

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