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Int. J. Mol. Sci. 2015, 16(2), 2426-2445; doi:10.3390/ijms16022426

Trianthema portulacastrum Linn. Displays Anti-Inflammatory Responses during Chemically Induced Rat Mammary Tumorigenesis through Simultaneous and Differential Regulation of NF-κB and Nrf2 Signaling Pathways

1
Cancer Therapeutics and Chemoprevention Group, Department of Pharmaceutical Sciences, College of Pharmacy, Northeast Ohio Medical University, Rootstown, OH 44272, USA
2
Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, California Northstate University, Elk Grove, CA 95757, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Sanjay K. Srivastava
Received: 10 December 2014 / Accepted: 13 January 2015 / Published: 22 January 2015
(This article belongs to the Special Issue Bioactive Phytochemicals in Functional Foods for Cancer Prevention)
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Abstract

Trianthema portulacastrum, a medicinal and dietary plant, has gained substantial importance due to its various pharmacological properties, including anti-inflammatory and anticarcinogenic activities. We have recently reported that a characterized T. portulacastrum extract (TPE) affords a considerable chemoprevention of 7,12-dimethylbenz(a)anthracene (DMBA)-induced rat mammary tumorigenesis though the underlying mechanisms are not completely understood. The objective of this study was to investigate anti-inflammatory mechanisms of TPE during DMBA mammary carcinogenesis in rats by monitoring cyclooxygenase-2 (COX-2), heat shock protein 90 (HSP90), nuclear factor-kappaB (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2). Mammary tumors were harvested from our previous study in which TPE (50–200 mg/kg) was found to inhibit mammary tumorigenesis in a dose-response manner. The expressions of intratumor COX-2, HSP90, NF-κB, inhibitory kappaB-alpha (IκBα) and Nrf2 were determined by immunohistochemistry. TPE downregulated the expression of COX-2 and HSP90, blocked the degradation of IκBα, hampered the translocation of NF-κB from cytosol to nucleus and upregulated the expression and nuclear translocation of Nrf2 during DMBA mammary carcinogenesis. These results in conjunction with our previous findings suggest that TPE prevents DMBA-induced breast neoplasia by anti-inflammatory mechanisms mediated through simultaneous and differential modulation of two interconnected molecular circuits, namely NF-κB and Nrf2 signaling pathways. View Full-Text
Keywords: breast tumor; DMBA; Trianthema portulacastrum; COX-2; HSP90; NF-κB; Nrf2; anti-inflammatory mechanisms breast tumor; DMBA; Trianthema portulacastrum; COX-2; HSP90; NF-κB; Nrf2; anti-inflammatory mechanisms
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Mandal, A.; Bishayee, A. Trianthema portulacastrum Linn. Displays Anti-Inflammatory Responses during Chemically Induced Rat Mammary Tumorigenesis through Simultaneous and Differential Regulation of NF-κB and Nrf2 Signaling Pathways. Int. J. Mol. Sci. 2015, 16, 2426-2445.

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