Wang Peng1, Li Changlu1, Seshadri Sriram2, Jiangang Liu1. 1. Department of General Surgery, Affiliated Hospital of Taishan Medical University, Taian, Shandong Province, China. 2. Department of General Surgery, Affiliated Hospital of Taishan Medical University, Taian, Shandong Province, China; Institute of Science, Nirma University, Chharodi, Ahmedabad, India.
Abstract
BACKGROUND: In the present study, we tried to understand the crosstalk between prostaglandins-COX-mediated rectal tumors and toll- like receptors in rats. METHODS: The tumor was induced using nicotine (100 μL/mL). Following the induction, the serum and rectal tissue were analyzed for Lipo-polysaccharides (LPS) and prostaglandin E2 in serum, and tissue expression of inflammatory mediators like TLR2,4, NFkB; cancer markers like Matrix metalloproteases 2 (MMP2), 9 and Cyclo-oxygenases 2 (COX-2) were estimated. The gut microflora analysis was carried out using the fresh fecal samples of both the study groups. RESULTS: In nicotine-induced group, there was a significant alteration in the gut microflora toward high Gram-negative strains and a decline in Gram-positive populations. All the inflammatory as well as cancer prognostic markers were significantly increased in the tumor-induced animals. CONCLUSION: From the present study, it could be concluded that nicotine significantly induced rectal cancer in the mice model by modu- lating gut microflora and increasing COX-2 and prostaglandin E2 levels.
BACKGROUND: In the present study, we tried to understand the crosstalk between prostaglandins-COX-mediated rectal tumors and toll- like receptors in rats. METHODS: The tumor was induced using nicotine (100 μL/mL). Following the induction, the serum and rectal tissue were analyzed for Lipo-polysaccharides (LPS) and prostaglandin E2 in serum, and tissue expression of inflammatory mediators like TLR2,4, NFkB; cancer markers like Matrix metalloproteases 2 (MMP2), 9 and Cyclo-oxygenases 2 (COX-2) were estimated. The gut microflora analysis was carried out using the fresh fecal samples of both the study groups. RESULTS: In nicotine-induced group, there was a significant alteration in the gut microflora toward high Gram-negative strains and a decline in Gram-positive populations. All the inflammatory as well as cancer prognostic markers were significantly increased in the tumor-induced animals. CONCLUSION: From the present study, it could be concluded that nicotine significantly induced rectal cancer in the mice model by modu- lating gut microflora and increasing COX-2 and prostaglandin E2 levels.