| Hypoxic-ischemic encephalopathy has become endanger people's lives and health, global public health problem, but its pathogenesis remains unclear, the lack of clinical pathology can block the process of effective drugs. Recently found that the activation of microglia cell-mediated inflammatory response is hypoxic-ischemic encephalopathy pathological an important component of the process. If drug use in the cerebral ischemia and hypoxia different pathological stage reasonable regulation of microglial cell activation, we can largely reduce its mediated neuronal damage, and to achieve effective prevention and treatment of hypoxic-ischemic encephalopathy Objective.Ancient Chinese medicine ginsenoside Rb1 on hypoxic-ischemic encephalopathy is a potential therapeutic value, but its mechanism has yet clear, therefore, the present study was to investigate brain ischemia and hypoxia state ginsenoside Rb1 on activation of microglia and the cell-mediated neuronal damage in hypoxia, with a view to basic theoretical research and lay the foundation for clinical drug development.The choice of topics of hypoxia-inducible microglia activation of the medium N9 in vitro culture of the original SD fetal rat hippocampus neurons to establish a total training system, to prepare activated state N9 cell-mediated hippocampus neurons hypoxic injury the cell model, and application of ginsenoside Rb1 intervention, from the proliferation of cell growth, nerve toxicity expression, mitochondrial oxidative stress damage to explore three aspects of ginsenoside Rb1 on the activation of hypoxia-induced cell-mediated hippocampus N9 Neurons hypoxic injury and the role of possible mechanisms. The results show that:1, hypoxia inducible N9 cell activation, as follows: dynamic changes in cell growth and proliferation, neurotoxicity expression increased, such as O2-, TNF-α, Inos, mitochondrial membrane potential and cytochrome C distribution changes;2, SD rats hypoxia can inhibit the growth of hippocampus neurons proliferation activity, and induced apoptosis, and accompanied by Caspase-3 activity increased; 3, the same N9 is the application of hypoxic cells cultured in vitro cell culture of the establishment of the Department, through the medium of neurotoxicity O2-, TNF-α, NO and the expression of neuronal apoptosis levels (TUNEL-positive cell count and Caspase - 3 activity), the results suggest that hypoxia were much higher than the conventional system of training system of single neurons and training system;4, whether it is preventive or therapeutic treatment administration, ginsenoside Rb1 could inhibit N9 hypoxic cell activation: cell growth and proliferation effectively alleviate the decline in vigor, reduced high expression of TNF-α, O2-, NO, iNOS, and to stability in varying degrees, mitochondrial membrane potential and intracellular distribution of cytochrome C;5, ginsenoside Rb1 can inhibit SD rat hippocampus neurons Caspase-3 activity and change its apoptosis; also N9 cell activation by inhibiting the generation of high expression of TNF-α, O2-, NO, reduced nerve Caspase-3 activity yean to reduce hippocampus neuronal apoptosis degree.From the research findings, conclusions are as follows:1, further evidence of hypoxic cells can be induced by the stress of microglia activation of microglia activation by the neurotoxicity factor (TNF-α, NO, iNOS, O2-) for the effect of important elements, including TNF -αWays and signal transduction pathway JNK/SAPK- NF-κB-related, NO, iNOS, O2- way role, such as oxygen free radicals associated with mitochondrial function.2, further proof of hypoxia-inducible SD rat hippocampus neuronal apoptosis, the activation of Caspase-3 may be an important pathway of apoptosis in one.3, the present study is the first to prove that ginsenoside Rb1 by inhibiting hypoxia-induced activation of microglia activation state by reducing response of microglia cell-mediated SD rat hippocampus neurons hypoxic injury. |
