Hsio-chung ou’s scientific contributions taichung veterans general hospital, taichung (vghtc) and other places brain anoxia

• hypothermia reduces cerebral injury and improves the brain outcome secondary to HI attack [56,58] erythropoietin (EPO) anti-apoptotic, inhibits inflammation, attenuates oxygen free radicals, decreases caspase activation, and increases neurogenesis [59][60][61][62][63][64][65][66]melatonin anti-inflammation, antioxidant, and anti-apoptotic [edaravone creates a radical intermediate that forms stable oxidation products [83][84][85][86]allopurinol a chelator of non-protein bound iron and scavenger of free radicals [87][88][89][90][91]osteopontin (OPN) cleaved caspase-3 inhibition, regulates cerebral cell proliferation, oligodendrocytes differentiation, and is anti-apoptotic [92][93][94]flunarizine dopamine release [95] inos increases iron deposition, inhibits platelet and leukocyte adhesion, and maintains cerebral blood flow [96,97] hydrogen peroxide (H 2 O 2 ) inhibits neuronal apoptosis and attenuates cerebrovascular reactivity [98][99][100][101]IGF-1 GPE attenuates activation of caspases and mitogenic effects [102] connexons mediates the release of paracrine molecules [103,104] naloxone and β-FNA attenuates myeloperoxidase activity and chemokine mrna expression [105] traditional chinese medicines and related extracts such as salvia, paeoniflorin, xinnaoxin, astragalus, safflower, and so on [106] acknowledgments: this work was supported by research grants from the major international (regional) joint research project (2008DFA31140 and 2010DFA32660), chinese science and technology support program (2011BAI11B22), national natural sciences foundation of china (81370230, 81500231, and 81570279), united bank of switzerland-optimus foundation (GIFTS ID 6102), natural sciences foundation of hunan province (2016JJ6118), natural sciences foundation of guangdong province (S2013010014009), key discipline construction fund grant from the third xiangya hospital of central south university, grant from the new xiangya talent project from the third xiangya hospital of central south university (JJ201524), technology foundation for selected overseas chinese scholar, and ministry of human resources and social security of china (ZP), ministry of education, culture, sports, science and technology of japan (grants-in-aid 15F15756 and 15K10043).Brain anoxia


[show abstract] [hide abstract] ABSTRACT: hypoxic-ischemic encephalopathy (HIE) is one of the leading causes of morbidity and mortality in neonates. Because of high concentrations of sensitive immature cells, metal-catalyzed free radicals, non-saturated fatty acids, and low concentrations of antioxidant enzymes, the brain requires high levels of oxygen supply and is, thus, extremely sensitive to hypoxia. Strong evidence indicates that oxidative stress plays an important role in pathogenesis and progression. Following hypoxia and ischemia, reactive oxygen species (ROS) production rapidly increases and overwhelms antioxidant defenses. A large excess of ROS will directly modify or degenerate cellular macromolecules, such as membranes, proteins, lipids, and DNA, and lead to a cascading inflammatory response, and protease secretion.Brain anoxia these derivatives are involved in a complex interplay of multiple pathways (e.G., inflammation, apoptosis, autophagy, and necrosis) which finally lead to brain injury. In this review, we highlight the molecular mechanism for oxidative stress in HIE, summarize current research on therapeutic strategies utilized in combating oxidative stress, and try to explore novel potential clinical approaches.

[show abstract] [hide abstract] ABSTRACT: reperfusion injury, the paradoxical tissue response that is manifested by blood flow-deprived and oxygen-starved organs following the restoration of blood flow and tissue oxygenation, has been a focus of basic and clinical research for over 4-decades. While a variety of molecular mechanisms have been proposed to explain this phenomenon, excess production of reactive oxygen species (ROS) continues to receive much attention as a critical factor in the genesis of reperfusion injury.Brain anoxia as a consequence, considerable effort has been devoted to identifying the dominant cellular and enzymatic sources of excess ROS production following ischemia-reperfusion (I/R). Of the potential ROS sources described to date, xanthine oxidase, NADPH oxidase (nox), mitochondria, and uncoupled nitric oxide synthase have gained a status as the most likely contributors to reperfusion-induced oxidative stress and represent priority targets for therapeutic intervention against reperfusion-induced organ dysfunction and tissue damage. Although all four enzymatic sources are present in most tissues and are likely to play some role in reperfusion injury, priority and emphasis has been given to specific ROS sources that are enriched in certain tissues, such as xanthine oxidase in the gastrointestinal tract and mitochondria in the metabolically active heart and brain.Brain anoxia the possibility that multiple ROS sources contribute to reperfusion injury in most tissues is supported by evidence demonstrating that redox-signaling enables ROS produced by one enzymatic source (e.G., nox) to activate and enhance ROS production by a second source (e.G., mitochondria). This review provides a synopsis of the evidence implicating ROS in reperfusion injury, the clinical implications of this phenomenon, and summarizes current understanding of the four most frequently invoked enzymatic sources of ROS production in post-ischemic tissue.

[show abstract] [hide abstract] ABSTRACT: silymarin is a flavonoid complex extracted from the silybum marianum plant. It acts as a strong antioxidant and free radical scavenger by different mechanisms.Brain anoxia but in addition to antioxidant effects, silymarin/silybin reveals immunomodulatory affects with both immunostimulatory and immunosuppression activities. Different studies have shown that silymarin has the anti-inflammatory effect through the suppression of NF-κb signaling pathway and TNF-α activation. It also has different immunomodulatory activities in a dose and time-dependent manner. As an immunomodulator agent, silymarin inhibits T-lymphocyte function at low doses while stimulates inflammatory processes at high doses. Studies have shown that silymarin has attenuated autoimmune, allergic, preeclampsia, cancer, and immune-mediated liver diseases and also has suppressed oxidative and nitrosative immunotoxicity.Brain anoxia silymarin also has indicated dual effects on proliferation and apoptosis of different cells. In conclusion, based on the current review, silymarin has a broad spectrum of immunomodulatory functions under different conditions. Recognizing the exact mechanisms of silymarin on cellular and molecular pathways would be very valuable for treatment of immune-mediated diseases. Also further studies are needed to assess the utility of silymarin in protection against autoimmune, cancer, allergic and other diseases in human subjects.