Poonam Thakur1, S N Sanyal. 1. Department of Biophysics, Panjab University, Chandigarh, India. poonamthkur@gmail.com
Abstract
OBJECTIVES: To evaluate the chemopreventive efficacy of Diclofenac, a preferential cyclooxygenase-2 (COX-2) inhibiting non steroidal anti-inflammatory drug (NSAID) in the 9, 10 Dimethylbenz(a)anthracene (DMBA) induced experimental lung carcinogenesis. METHODS: Animals were divided into 4 groups. Control group received normal saline intratratracheally. DMBA group was given DMBA (20 mg/kg of body weight) in the similar manner. DMBA+Diclofenac group was given daily oral dose of Diclofenac (8 mg/kg of body weight) in addition to DMBA while the last group received Diclofenac only. Animals were sacrificed after 24 weeks. COX-2 expression was studied by immunohistochemistry (IHC) and Western immunoblotting. For apoptosis study DNA fragmentation on agarose gel and florescent staining of alveolar macrophages were done. RESULTS: The incidence and burden of tumor were reduced by the Diclofenac treatment. Diclofenac caused the reduction in the COX-2 levels which were increased in the DMBA treated group. It also caused the induction of apoptosis as seen by both techniques. CONCLUSION: From all these results it can be concluded that Diclofenac might have a chemopreventive role for lung carcinogenesis which is mediated by suppression of COX-2 enzyme and induction of apoptosis. Copyright 2010 Elsevier Inc. All rights reserved.
OBJECTIVES: To evaluate the chemopreventive efficacy of Diclofenac, a preferential cyclooxygenase-2 (COX-2) inhibiting non steroidal anti-inflammatory drug (NSAID) in the 9, 10 Dimethylbenz(a)anthracene (DMBA) induced experimental lung carcinogenesis. METHODS: Animals were divided into 4 groups. Control group received normal saline intratratracheally. DMBA group was given DMBA (20 mg/kg of body weight) in the similar manner. DMBA+Diclofenac group was given daily oral dose of Diclofenac (8 mg/kg of body weight) in addition to DMBA while the last group received Diclofenac only. Animals were sacrificed after 24 weeks. COX-2 expression was studied by immunohistochemistry (IHC) and Western immunoblotting. For apoptosis study DNA fragmentation on agarose gel and florescent staining of alveolar macrophages were done. RESULTS: The incidence and burden of tumor were reduced by the Diclofenac treatment. Diclofenac caused the reduction in the COX-2 levels which were increased in the DMBA treated group. It also caused the induction of apoptosis as seen by both techniques. CONCLUSION: From all these results it can be concluded that Diclofenac might have a chemopreventive role for lung carcinogenesis which is mediated by suppression of COX-2 enzyme and induction of apoptosis. Copyright 2010 Elsevier Inc. All rights reserved.