Study On Intervening Effect Of Chlorogenic Acid On Cerebral Ischemia Reperfusion Rats And Mice Model

Objective:Through observing levels of intercellular adhesion molecule1(ICAM-1), tumor necrosis factor a(TNF-a), Bcl-2associated X protein (Bax), B-cell lymphoma gene(Bcl-2), Cysteine protease3(Caspase-3), ATP enzyme, vascular cell adhesion molecule (VCAM-1), erythropoietin (EPO), hypoxia-inducible factor1α(HIF-1α), nerve growth factor (NGF) in brain tissue and levels of neuron specific enolase (NSE), myeloperoxidase (MPO), S100β protein in serum of cerebral ischemia reperfusion rats and mice mode, and effect on neurological deficiency score, brain infarction area, brain morphology, to explore the defense mechanism of chlorogenic acid to cerebral ischemia reperfusion injury.Method:Firstly blocked the bilateral common carotid artery (CCA) for10minutes, restored perfusion for10minutes, and then blocked bilateral carotid artery occlusion for10minutes, to copy the repeated cerebral ischemia reperfusion mice model. Before operation, nimodipine, high, medium, low dosage groups were gave corresponding medicine by using intragastric administration, sham-operated group and model group were gave the same volume of0.5%CMC by using intragastric administration,1times a day,7days in a row. Copied the repeated cerebral ischemia reperfusion mice model after1h by the last administration, reperfusion24h after the operation, caculated death rate, determined ICAM-1, TNF-α levels in mouse brain tissue, NSE, MPO levels in serum, and observed morphological changes of mouse brain tissue.To copy the focal cerebral ischemia reperfusion mice model by blocking the left middle cerebral artery. Before operation, nimodipine, high, medium, low dosage groups were gave corresponding medicine by using intragastric administration, sham-operated group and model group were gave the same volume of0.5%CMC by using intragastric administration,1times a day,7days in a row. Copied the focal cerebral ischemia reperfusion mice model after1h by the last administration, reperfusion22h after the operation, caculated death rate, evaluated neural function deficient by using neurological deficiency score, determined S100β level in serum, stained brain tissue slices by TTC, and then calculated the area of cerebral infarction.To copy the focal cerebral ischemia reperfusion mice model by blocking the left middle cerebral artery. Before operation, nimodipine, high, medium, low dosage groups were gave corresponding medicine by using intragastric administration, sham-operated group and model group were gave the same volume of0.5%CMC by using intragastric administration,1times a day,7days in a row. Copied the focal cerebral ischemia reperfusion mice model after1h by the last administration, reperfusion22h after the operation, caculated death rate, evaluated neural function deficient by using neurological deficiency score, determined Bax, Bcl-2, Caspase-3, ATP enzyme level in mouse brain tissue, observed morphological changes of mouse brain tissue.To copy the focal cerebral ischemia reperfusion rats model by blocking the left middle cerebral artery. Before operation, nimodipine, high, medium, low dosage groups were gave corresponding medicine by using intragastric administration, sham-operated group and model group were gave the same volume of0.5%CMC by using intragastric administration,1times a day,7days in a row. Copied the focal cerebral ischemia reperfusion rats model after1h by the last administration, reperfusion22h after the operation, caculated death rate, evaluated neural function deficient by using neurological deficiency score, determined NSE level in serum, TTC stained lmm brain tissue slice which located at intersection of optic nerve, calculated the area of cerebral infarction. Determined ICAM-1, VCAM-1, EPO, HIF-1α level in rat brain tissue, checked NGF by immunohistochemistry, and observed morphological changes of mouse brain tissue.Result:Repeated cerebral ischemia reperfusion mice model, focal cerebral ischemia reperfusion mice model, focal cerebral ischemia reperfusion rats model were copied successfully. Chlorogenic acid could significantly reduce death rate, neurological deficiency score, cerebral infarction area, ICAM-1, TNF-α, Bax, Caspase-3, VCAM-1levels in brain tissue, NSE, MPO, S100β levels in serum of mice and rats. Chlorogenic acid could significantly increase Bcl-2, ATP enzyme, EPO, HIF-1α, BDNF, NGF level in brain tissue of mice and rats. Chlorogenic acid could significantly ameliorate hippocampus and cortex pathology injury in brain tissue of mice and rats.Conclusion:Chlorogenic acid could reduce cerebral ischemia reperfusion injury and protect brain tissue. The mechanisms are protecting brain from the injury of inflammatory factor, reducing apoptosis of nerve cells, increasing neuronal growth factors, improving the energy metabolism in brain tissue, activating the self protection mechanism of brain cells, protecting nerve cell, ameliorating hippocampus and cortex pathology injury in brain tissue, reducing cerebral infarction area, etc.