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Text
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URL Address
<a href="http://doi.org/10.1155/2014/769515" target="_blank" rel="noreferrer noopener">http://doi.org/10.1155/2014/769515</a>
Pages
769515–769515
Volume
2014
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Apocynum Tablet Protects against Cardiac Hypertrophy via Inhibiting AKT and ERK1/2 Phosphorylation after Pressure Overload.
Publisher
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Evidence-based complementary and alternative medicine : eCAM
Date
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2014
1905-07
Creator
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Qi Jianyong; Liu Qin; Gong Kaizheng; Yu Juan; Wang Lei; Guo Liheng; Zhou Miao; Wu Jiashin; Zhang Minzhou
Description
An account of the resource
Background. Cardiac hypertrophy occurs in many cardiovascular diseases. Apocynum tablet (AT), a traditional Chinese medicine, has been widely used in China to treat patients with hypertension. However, the underlying molecular mechanisms of AT on the hypertension-induced cardiac hypertrophy remain elusive. The current study evaluated the effect and mechanisms of AT on cardiac hypertrophy. Methods. We created a mouse model of cardiac hypertrophy by inducing pressure overload with surgery of transverse aortic constriction (TAC) and then explored the effect of AT on the development of cardiac hypertrophy using 46 mice in 4 study groups (combinations of AT and TAC). In addition, we evaluated the signaling pathway of phosphorylation of ERK1/2, AKT, and protein expression of GATA4 in the cardioprotective effects of AT using Western blot. Results. AT inhibited the phosphorylation of Thr202/Tyr204 sites of ERK1/2, Ser473 site of AKT, and protein expression of GATA4 and significantly inhibited cardiac hypertrophy and cardiac fibrosis at 2 weeks after TAC surgery (P \textless 0.05). Conclusions. We experimentally demonstrated that AT inhibits cardiac hypertrophy via suppressing phosphorylation of ERK1/2 and AKT.
Identifier
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<a href="http://doi.org/10.1155/2014/769515" target="_blank" rel="noreferrer noopener">10.1155/2014/769515</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2014
Evidence-based complementary and alternative medicine : eCAM
Gong Kaizheng
Guo Liheng
Liu Qin
Qi Jianyong
Wang Lei
Wu Jiashin
Yu Juan
Zhang Minzhou
Zhou Miao
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1155/2013/371813" target="_blank" rel="noreferrer noopener">http://doi.org/10.1155/2013/371813</a>
Pages
371813–371813
Volume
2013
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Pomegranate Bioactive Constituents Suppress Cell Proliferation and Induce Apoptosis in an Experimental Model of Hepatocellular Carcinoma: Role of Wnt/ beta -Catenin Signaling Pathway.
Publisher
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Evidence-based complementary and alternative medicine : eCAM
Date
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2013
1905-07
Creator
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Bhatia Deepak; Thoppil Roslin J; Mandal Animesh; Samtani Karishma A; Darvesh Altaf S; Bishayee Anupam
Description
An account of the resource
Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide, and chemoprevention represents a viable approach in lowering the mortality of this disease. Pomegranate fruit, an abundant source of anti-inflammatory phytochemicals, is gaining tremendous attention for its wide-spectrum health benefits. We previously reported that a characterized pomegranate emulsion (PE) prevents diethylnitrosamine (DENA)-induced rat hepatocarcinogenesis though inhibition of nuclear factor-kappaB (NF- kappa B). Since NF- kappa B concurrently induces Wnt/ beta -catenin signaling implicated in cell proliferation, cell survival, and apoptosis evasion, we examined antiproliferative, apoptosis-inducing and Wnt/ beta -catenin signaling-modulatory mechanisms of PE during DENA rat hepatocarcinogenesis. PE (1 or 10 g/kg) was administered 4 weeks before and 18 weeks following DENA exposure. There was a significant increase in hepatic proliferation (proliferating cell nuclear antigen) and alteration in cell cycle progression (cyclin D1) due to DENA treatment, and PE dose dependently reversed these effects. PE substantially induced apoptosis by upregulating proapoptotic protein Bax and downregulating antiapoptotic protein Bcl-2. PE dose dependently reduced hepatic beta -catenin and augmented glycogen synthase kinase-3 beta expression. Our study provides evidence that pomegranate phytochemicals exert chemoprevention of hepatic cancer through antiproliferative and proapoptotic mechanisms by modulating Wnt/ beta -catenin signaling. PE, thus, targets two interconnected molecular circuits (canonical NF- kappa B and Wnt/ beta -catenin pathways) to exert chemoprevention of HCC.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1155/2013/371813" target="_blank" rel="noreferrer noopener">10.1155/2013/371813</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2013
Bhatia Deepak
Bishayee Anupam
Darvesh Altaf S
Department of Pharmaceutical Sciences
Evidence-based complementary and alternative medicine : eCAM
Mandal Animesh
NEOMED College of Pharmacy
Samtani Karishma A
Thoppil Roslin J