Does the full text show promise and what did your doctors and stroke hospital do with that information? Sit on it like lazy asses? If you had a functioning stroke hospital there would be a research analyst to ask about that. But I bet you don't have one, whose only job is to evaluate stroke research and implement the good stuff in the hospital. Each hospital would not need to have a research analyst if we had great stroke associations rather than the fucking failures of stroke associations we have now
Multi-Targeting Andrographolide, a Novel NF-κB Inhibitor, as a Potential Therapeutic Agent for Stroke
1 Department of Pharmacology, Taipei Medical University, Taipei 110, Taiwan
2 Division of Cardiology, Department of Internal Medicine, Cathay General Hospital, Taipei 200, Taiwan
3 Department of Life Science, College of Life Sciences, National Chung Hsing University, Taichung 402, Taiwan
4 Department of Ocular Microbiology, Institute of Ophthalmology, Joseph Eye Hospital, Tiruchirappalli 620001, Tamil Nadu, India
5 Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei 110, Taiwan
*
Authors to whom correspondence should be addressed.
Int. J. Mol. Sci. 2017, 18(8), 1638; https://doi.org/10.3390/ijms18081638
Received: 4 July 2017
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Revised: 24 July 2017
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Accepted: 26 July 2017
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Published: 27 July 2017
(This article belongs to the Special Issue Neuroprotective Strategies 2017)
A key focus in the field of drug discovery has been motivated by the
neuroprotection of natural compounds. Cerebral ischemia is a
multifaceted pathological process with a series of mechanisms, and a
perspective for the development of neuroprotectants from traditional
herbal medicine or natural products is a promising treatment for this
disease. Natural compounds with the effects of anti-oxidation,
anti-inflammation, anti-apoptosis, and neurofunctional regulation
exhibit therapeutic effects on experimental ischemic brain injury.
Conferring to the pharmacological mechanisms underlying neuroprotection,
a study found that androgapholide, a diterpene lactone compound,
exhibits varying degrees of neuroprotective activities in both in vitro
and in vivo experimental models of stroke. The neuroprotective
mechanisms of andrographolide are suggested as: (I) increasing nuclear
factor E2-related factor 2-heme oxygenase (Nrf2-HO-1) expression through
p38-mitogen activated protein kinase (MAPK) regulation, (II) inducing
cerebral endothelial cells (CEC) apoptosis and caspase-3 activation,
(III) down regulating Bax, inducible nitric oxide synthase (iNOS), and
(IV) inhibiting hydroxyl radical (OH−) formation, and
activating transcription factor NF-κB signaling pathways. Recently,
several researchers have also been trying to unveil the principal
mechanisms involved in the neuroprotective effects of andrographolide.
Therefore, this review aims to summarize an overview on the
neuroprotective effects of andrographolide and exemplifies the essential
mechanisms involved. This paper can provide information that
andrographolide drug discovery may be a promising strategy for the
development of a novel class of neuroprotective drug.
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Keywords:
andrographolide; neuroprotection; stroke; multi-targets; signaling pathways
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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.
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