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Open AccessArticle

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
Int. J. Mol. Sci. 2015, 16(2), 2426-2445; https://doi.org/10.3390/ijms16022426
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)
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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MDPI and ACS Style

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. https://doi.org/10.3390/ijms16022426

AMA Style

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. International Journal of Molecular Sciences. 2015; 16(2):2426-2445. https://doi.org/10.3390/ijms16022426

Chicago/Turabian Style

Mandal, Animesh; Bishayee, Anupam. 2015. "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. 16, no. 2: 2426-2445. https://doi.org/10.3390/ijms16022426

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