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Empirical Study of Preconditioning Theory on Neuro-Protective

Author: LiMeiYi
Tutor: NiuJingZhong
School: Taishan Medical College
Course: Geriatrics
Keywords: Hypoxic preconditioning Cerebrospinal fluid Brain Tissue Extracts Plasma Adenosine Hippocampal neurons Oxygen and glucose deprivation SOD / MDA Bcl-2/Bax Brain damage
CLC: R743
Type: Master's thesis
Year: 2010
Downloads: 40
Quote: 0
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Abstract

Background hypoxic / ischemic brain injury is a common disease of the nervous system, frequently-occurring disease, affects not only the patients with limb motor function and higher cognitive functions, and has a high morbidity and mortality, serious threat to human health and reduce the quality of life heavy financial and emotional burden to families and society. Hypoxic / ischemic brain damage brain protective treatment is particularly important, and is closely related with the prognosis of patients. Due to hypoxic / ischemic brain injury, cerebral protection treatments or measures have limited efficacy, treatment of cerebral protection is a hot and difficult issues of domestic and foreign research. The preconditioning theory has confirmed brain protection, corresponding mechanism has initially clear. Anoxic / hypoxic / ischemic preconditioning (Hypoxic / Ischemic the preconditioning, HPC / IPC) and pharmacological preconditioning (Pharmacological Preconditioning, PPC) are all theoretical categories preconditioning preconditioning theory clinical application, how to achieve that may increase its clinical The operability is transformed medical problems to be solved. Based on the theory of invention patents (Name: cardiovascular health therapy instrument inventor: Kyrgyzstan Xunming such as hypoxic preconditioning, the advent of Patent No.: 200710176701) theory anti-hypoxia preconditioning / ischemic brain damage that is transforming medical research brought momentum and dawn. Theory preconditioning against hypoxic / ischemic brain damage effect, our previous study found that, overall hypoxic preconditioning has a protective effect on acute cerebral infarction caused by cerebral ischemia injury preconditioning theory clinical application, there are still difficulties ; In order to further increase the clinical operability, we initially confirmed that hypoxic preconditioning mice brain homogenate extract has a protective effect of nerve cells in the large the Shushu embryo hippocampal neurons during hypoxia and reoxygenation. Therefore, in the basis of preliminary studies, the experimental research will continue to explore the preconditioning the theory against hypoxic injury effects, including the following two aspects: (1) hypoxic preconditioning Wistar rat cerebrospinal fluid, brain homogenate extract and plasma on the original Wistar rats hippocampus neurons of oxygen and glucose deprivation injury in cultured and related mechanisms; (2) adenosine pharmacological preconditioning of the role of the Wistar rat primary cultured neonatal rat hippocampus neurons of oxygen and glucose deprivation injury mechanisms. Through this study clearly preconditioning theory anti-hypoxic brain injury effects, the theoretical basis for translational medicine research. Research purposes, to explore hypoxic preconditioning Wistar rat cerebrospinal fluid, brain homogenate extracts and plasma of Wistar rat primary cultured neonatal rat hippocampal neurons oxygen glucose deprivation injury and related mechanisms. Explore adenosine pharmacological preconditioning Wistar primary cultured neonatal rat hippocampal neurons oxygen glucose deprivation injury and related mechanisms. Research methods, experiment used 200-250g of healthy adult Wistar rats of both sexes, conducted hypoxia preconditioning model replication were extracted from the cerebrospinal fluid, brain tissue and blood, producing sterile cerebrospinal fluid and brain homogenate extracts and plasma; birth Wistar rats within 24h, whichever primary cultured hippocampus neurons, and oxygen and glucose deprivation training. 2, cultured neural cells were randomly divided into normal control group (N), pure oxygen and glucose deprivation group (OGD group), normal CSF / Brain Tissue Extracts / plasma intervention oxygen glucose deprivation group (CSF / BH / BP the OGD group) and hypoxic preconditioning CSF / brain tissue extract fluid / plasma intervention oxygen glucose deprivation group (HPC OGD group), Earle's solution containing Na2S2O4 (1 mmol / L) of sugar-free replication neurons of oxygen and glucose deprivation injury model. by colorimetric hypoxia preconditioning and normal cerebrospinal fluid, brain homogenates and plasma SOD and MDA content; AnnexinV / PI double staining and immunofluorescence staining for detection of apoptosis and apoptosis-related protein expression. 3, primary cultured Wistar neonatal rat hippocampal neurons were randomly divided into normal control group (N), pure oxygen and glucose deprivation group (OGD group), the low concentration of adenosine preconditioning role of oxygen and glucose deprivation (ADL OGD group ), the concentration of adenosine preconditioning oxygen glucose deprivation effect (ADM OGD group) oxygen glucose deprivation effect (ADH OGD group) and high concentrations of adenosine preconditioning AnexinV / PI double staining and immunofluorescence staining observed low, three adenosine concentration pretreatment on apoptosis and apoptosis-related protein expression in neurons of oxygen and glucose deprivation injury. Results, compared with the normal rat cerebrospinal fluid, hypoxic preconditioning in rat cerebrospinal fluid SOD increased (P lt; 0.01), MDA decreased (P lt; 0.05); to extract liquid phase with normal rat brain homogenates ratio of hypoxic preconditioning in rat brain homogenates extract SOD were significantly increased (P lt; 0.01), MDA decreased (P lt; 0.01); compared with normal rat plasma, hypoxic preconditioning in rat plasma SOD increased (P lt; 0.01), MDA content significantly decreased (P lt; 0.01). 2, laser confocal microscope AnnexinV / PI double staining results show occasional apoptosis: N group, OGD group apoptotic neurons. The normal rat cerebrospinal fluid (P lt; 0.01) and hypoxia preconditioning in cerebrospinal fluid (P lt; 0.01) oxygen and glucose deprivation injury of neurons have a protective effect, the latter exhibited higher (P lt; 0.01); rat brain homogenate extract weak protective effect (P lt; 0.05) hypoxic preconditioning rat brain tissue extract of damaged neurons was significantly protective effect (P lt; 0.01); neuronal injury in the normal rat plasma to protect nerve antioxidant glucose deprivation injury (P lt; 0.01), hypoxic preconditioning in rat plasma traumatic neuronal apoptosis (P lt; 0.01) can be reduced to greater extent. Flow cytometry is consistent with the above results. 3, Bcl-2 and Bax protein expression detected: N group only a very small amount of Bcl-2 and Bax proteins expression in the OGD group is a very small amount of protein expression of Bcl-2 and Bax protein expression. Normal cerebrospinal fluid and cerebrospinal fluid could hypoxic preconditioning significantly increased the expression of Bcl-2 protein (P lt; 0.01), to reduce the expression of Bax protein (P lt; 0.01), elevated Bcl-2/Bax ratio; normal rat brain homogenate extract could increase to some extent, the Bcl-2 protein expression (P lt; 0.05), significantly reduced Bax expression (P lt; 0.01), compared with the normal rat brain tissue extract of hypoxic preconditioning rat brain homogenate extract could significantly increase the Bcl-2 protein expression (P lt; 0.01), to further reduce the expression of Bax protein (P lt; 0.05); normal rat plasma increases the Bcl-2 protein expression (P lt; 0.05 ), Bax protein had no effect (P = 0.063), hypoxic preconditioning plasma not only to a greater extent to enhance the Bcl-2 protein expression (P lt; 0.01), but also significantly reduced Bax protein expression (P lt; 0.01 ) 4, adenosine preconditioning hippocampal neurons detect: Compared with pure oxygen and glucose deprivation group, low-dose adenosine preconditioning neurons can not produce oxygen and glucose deprivation damage protective effect; in dose adenosine preconditioning can reduce oxygen glucose deprivation induced the number of neuronal apoptosis, Bcl-2 protein expression (P lt; 0.01), to reduce the expression of Bax protein (P lt; 0.01); high-dose adenosine preconditioning has a more significant cytoprotective effects, can further improve the Bcl- 2/Bax ratio. Conclusions hypoxic preconditioning induced cerebrospinal fluid, brain tissue extract fluid and plasma SOD activity and MDA content decreased. 2, hypoxia preconditioning cerebrospinal fluid, brain homogenate extracts and plasma can be varying degrees of confrontation neurons of oxygen and glucose deprivation damage-induced apoptosis, which may be raised the Bcl-2 protein expression by reducing the level of oxidative stress, and to reduce the expression of Bax protein. 3, high dose of adenosine preconditioning can induce the hypoxic neuronal glucose tolerance improve, reduce neuronal apoptosis by to elevated Bc1-2/Bax ratio play against hypoxic brain damage effects.

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