Chung Kuang Lu worked as an Assistant Research Fellow, National Museum of Marine Biology & Aquarium, Assistant Professor, Institute of Marine Biotechnology, National Dong Hwa University and Assistant Professor, School Pharmacy, Taipei Medical University. His research project focuses on developing and applying biotechnology to detect, isolate, identify and evaluate novel biologically active metabolites from the highly diverse microbes. To discover new anti-cancer, cardiovascular, and reduction in blood sugar agents from microbes is the priority goal.
The Bu-yang Huan-wu Decoction (BHD), one of the classic traditional Chinese medicine (TCM) formula has been used for improving neurological functional recovery in stroke-induced disability in China for more than 300 years and is the most famous and popular TCM formula clinically used in Taiwan. However, whether and how BHD and its active components can protect mice against ischemic stroke-mediated excite toxicity still lacks the evidence-based study. We have previously reported the BHD can protect acute ischemic stroke (AIS) murine through impeding inflammatory responses via impairing NF-κB and GSK3β signaling, most possibly through activating ERK and PI3K/Akt pathways. This compromises the activation/infiltration of microglial and/or inflammatory cells, and activation of endogenous neurogenesis, respectively. Treatment of mice that have undergone ischemic stroke with BHD (1.0 g/kg, p.o.) at 2 hour after stroke enhanced survival rate and ameliorated neurological deficits, brain infarction, neural dysfunction and massive oxidative stress due to enormous free radial production and severe breakdown of blood-brain barrier (BBB). The goal of this study is to further study whether BHD can promote BBB remodeling through which to mediate neuronal cell survival and neuronal progenitor cell migration for neurogenesis and tissue repair. Our data revealed that BHD decreases BBB leakage through dramatically increasing vascular integrity (BBB remodeling) via up-regulating tight junction protein (occludin) expression and Ang1/Tie2 signaling most possibly through inactivating GSK3 to activate Wnt/-catenin signaling in the ischemic brain after stroke. This results explains why BHD can increase neuroblast( DCX+, a neuroblast marker) survival and migration which is closely associated with vascular remodeling and angiogenesis through enhancing neovascularization (CD34+/BrdU+staining) with upexpression of occludin, Ang1 and Tie2, as well as activation of Wnt/-catenin signaling. Our data provide evidence to show that BHD is superior than t-PA in ameliorating AIS via enhancing angiogenesis through which to massively support neuron survival (Tubβ3/Ang1 and Tie2/Ang1 staining) and promote neuroblast proliferation and migration from sub ventricular zone (SVZ) to ischemic damaged core region and peri-infarct area for neurogenesis and tissue repairmen. Besides, the analysis of UPLC fingerprints among different BHD production batches and the 6 plantamedica suggested two active components, X1 and Y1. The survival rates of ischemic stroke mice which were treated by compound X1 and Y1 together were around 65% in day 3.
Draginja Cvetkovic graduated from the School of Medicine University of Belgrade, Serbia in 1984. She attended Postgraduate Study in Cardiology at the University of Belgrade and was a research associate at the Institute for Medical Research in Belgrade. She had special interest in pharmacological treatment in pulmonary hypertension. Upon coming to the USA, she completed internship and residency in Anesthesia at the Beth Israel Medical Center in New York and was fellowship trained in Cardiac Anesthesia at Mt. Sinai Medical Center in New York. In practicing cardiac anesthesia, Dr. Draginja Cvetkovic has focused for 15 years on anesthetizing patients with congenital heart disease. Her certifications are The American Board of Anesthesiology, National Board of Echocardiography, and Subspecialty Certification in Pediatric Anesthesiology. She is now practicing at the Westchester Medical Center in Walhalla, New York. Dr. Draginja Cvetkovic is involved in full range of cardiothoracic surgical procedures including CABG, mitral and aortic valve repair, aortic aneurysm surgery, ventricular assist devices and heart transplants
Stroke after cardiac surgical procedures is a serious and costly healthcare problem with often fatal or disabling outcome. Most neurological events occur in a subset of patients who can be defined before operation. Identification of risk factors for perioperative stroke is important for understanding the pathogenesis of this devastating complication as well as for development of new preventive strategies. The frequency of this complication is reported to be as high as 5% in patients undergoing coronary artery bypass graft (CABG) surgery, almost 9% in CABG patients over 75 years of age, and nearly 16% in patients undergoing valve surgery or those with preexisting cerebrovascular disease. The causes and mechanisms of CNS injury after cardiac operations are complex and multifactorial and many have been proposed, including perioperative embolism from the heart or aortic arch, systemic hypoperfusion, ischemia from large-vessel occlusive disease, or a combination of these factors. New imaging techniques better define the degree and distribution of ischemic injury and may reveal regions of persistent hypoperfusion. It is essential to develop strategies for avoiding injury to the brain, preventing secondary ischemic damage and promoting recovery of brain tissue.