New Discovery of Curcumin Combination Therapy and Action Mechanism

Notice the words neuroprotective, angiogenesis,  and protect against apoptotic cell death. But you can't do anything with this on your own until after your death since nothing will occur with this by creating a stroke protocol on it until maybe your children and grandchildren are dead. That is how fucking bad stroke leadership is.  

New Discovery of Curcumin Combination Therapy and Action Mechanism

Chongshan Dai ,1 Xiuying Zhang,2 and Keyu Zhang3 1Department of Surgery, University of Texas Southwestern Medical Center, Harry Hines Blvd, Dallas, TX 5323, USA 2Department of Basic Veterinary Science, College of Veterinary Medicine, Northeast Agricultural University, Harbin, Heilongjiang 150030, China 3Key Laboratory of Veterinary Chemical Drugs and Pharmaceutics, Ministry of Agriculture, Shanghai Veterinary Research Institute, Chinese Academy of Agricultural Sciences, No. 518 Ziyue Road, Minhang District, Shanghai 200241, China Correspondence should be addressed to Chongshan Dai; chongshan.dai@utsouthwestern.edu Received 24 February 2020; Accepted 24 February 2020; Published 10 March 2020 Copyright © 2020 Chongshan Dai et al. 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.
Curcumin(diferuloylmethane, a yellow pigment in spice turmeric) is a natural product polyphenol extracted from the rhizome of Curcuma longa.  Curcumin has been shown to elicit a strong antioxidant activity by directly scavenging free radicals, even more effectively than vitamin E. It has been widely used in pharmaceutical and medical applications based on the broad spectrum of biological actions, including antibacterial, antiviral, antifungal, and anti-inflammatory activities. Direct curcumin targets include cyclooxygenase 2 (COX-2), lipoxygenase, nuclear factor erythroid 2-related factor 2, toll-like receptor (TLR) 4, transforming growth factorbeta (TGF-β)/smad signaling pathway, focal adhesion kinase, glutathione, glycogen synthase kinase- (GSK-) 3 β, phosphorylase-3 kinase, xanthine oxidase, pp60 src tyrosine kinase, and ubiquitin isopeptidase, which play important roles in oxidative stress, inflammation, autophagy, ferroptosis, and apoptosis. Therefore, curcumin has been proposed to increase the therapeutic efficiency of some drugs, albeit the potential molecular mechanisms remain unclear. Importantly, available preclinical and phase I/II data suggest that curcumin is well tolerated and has a good safety profile. A classic example is the combination between curcumin and polymyxins whereby in addition to its synergistic antimicrobial activity, curcumin could potentially ameliorate polymyxin induced unwanted neurotoxicity. With the
proposal of concept on precision medicine in the clinic, the underlying molecular mechanism and potential target for the combination therapy are much emphasized. In this special issue, investigators contribute original research articles and review articles that would facilitate the understanding of the basic mechanisms of curcumin as well as the development of new and promising complementary and alternative strategies for curcumin combination. Wang et al. reported the neuroprotective effect of curcumin against oxygen-glucose deprivation/reoxygenation (OGD/R)injury in HT22 neuronal cells. They suggested that curcumin can protect OGD/R-induced neuronal apoptotic cell death by inhibiting intracellular ROS accumulation and mitochondria dysfunction. Knockdown of SOD2 by RNA interference (RNAi) attenuated the protective effect of curcumin on OGD/R-induced neuronal cell death, suggesting that SOD2 may be a target of curcumin death. Wang and Chen reviewed the bidirectional action of curcumin and curcuminoids as well as synthetic curcumin analog on angiogenesis based on the current research findings. They review paper summarized the antiangiogenesis effect of curcumin. Curcumin could regulate multiple factors, including proangiogenesis factor vascular endothelia growth factor (VEGF), matrix metalloproteinase (MMPs), and fibroblast growth factors (FGF), both in vivo and in vitro, and promote angiogenesis under certain circumstances via these factors.