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Original Research Article | OPEN ACCESS

Prophylactic effects of triptolide on colon cancer development in azoxymethane/dextran sulfate sodium-induced mouse model

Yizhou Zhou1, Li Sun1, Lei Cui2, Yu Feng1

1Department of Oncology; 2Department of Cardiology, Xuzhou Central Hospital, Xuzhou 221009, China.

For correspondence:-  Yu Feng   Email: fengyu889@hotmail.com   Tel:+8618068709060

Accepted: 8 October 2017        Published: 30 November 2017

Citation: Zhou Y, Sun L, Cui L, Feng Y. Prophylactic effects of triptolide on colon cancer development in azoxymethane/dextran sulfate sodium-induced mouse model. Trop J Pharm Res 2017; 16(11):2659-2665 doi: 10.4314/tjpr.v16i11.13

© 2017 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate effects of triptolide on colon cancer cell growth and its capacity to prevent tumor development in an azoxymethane (AOM)/dextran sulfate sodium (DSS) mouse model of colon cancer.
Methods: HCT116 cell viability and migration potential were assessed. Control and AOM/DSS-treated mice (with and without triptolide) were analyzed for tumor development. The animals were divided into five groups (n = 5). Normal control group was given saline, animals in the untreated control group received AOM and DSS while animals in the treatment groups received 10, 50 and 100 mg/kg doses of triptolide intraperitoneally alternately for 2 months after AOM and DSS injection.
Results: Triptolide enhanced nuclear material condensation, significantly (p < 0.05) increased the levels of cleaved poly (ADP-ribose) polymerase, reduced the levels of pro-caspase-3 and pro-caspase-8 in HCT116 cells. Triptolide also significantly (p < 0.05) decreased the expression of pIκBα, activated peroxisome proliferator-activated receptor γ, and markedly reduced the activity of both metalloproteinase-2 and metalloproteinase-9. Treatment of AOM/DSS mice with triptolide significantly reduced adenocarcinoma multiplicity compared to the control group.
Conclusion: Triptolide administration suppresses growth of HCT116 cells and colon cancer development in mice by inhibiting inflammatory responses. Therefore, triptolide has potentials to be developed for colon cancer therapy
 

Keywords: Cell viability, Condensation, Metalloproteinase, Apoptotic, Triptolide, Adenocarcinoma, Colon cancer

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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