%0 Journal Article
%T Trianthema portulacastrum Linn. Displays Anti-Inflammatory Responses during Chemically Induced Rat Mammary Tumorigenesis through Simultaneous and Differential Regulation of NF-百B and Nrf2 Signaling Pathways
%A Animesh Mandal
%A Anupam Bishayee
%J International Journal of Molecular Sciences
%P 2426-2445
%D 2015
%I MDPI AG
%R 10.3390/ijms16022426
%X 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-百B) and nuclear factor erythroid 2-related factor 2 (Nrf2). Mammary tumors were harvested from our previous study in which TPE (50每200 mg/kg) was found to inhibit mammary tumorigenesis in a dose-response manner. The expressions of intratumor COX-2, HSP90, NF-百B, inhibitory kappaB-alpha (I百B汐) and Nrf2 were determined by immunohistochemistry. TPE downregulated the expression of COX-2 and HSP90, blocked the degradation of I百B汐, hampered the translocation of NF-百B 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-百B and Nrf2 signaling pathways.
%K breast tumor
%K DMBA
%K Trianthema portulacastrum
%K COX-2
%K HSP90
%K NF-百B
%K Nrf2
%K anti-inflammatory mechanisms
%U http://www.mdpi.com/1422-0067/16/2/2426