Effects Of TCST On The Expression Of HSP70 And Brain Histopathology After Focal Ischemic Damage In Rats

Cerebral vascular disease stands as one of the three leadingcauses of death, with high morbidity and mortality. It makes greatdemands on patients, who must not only survive the complicationsof the acute stages, but must cope then with the great physical andeconomic costs of long-term disabilities. Great progress has beenmade on therapeutics of cerebral ischemia with the furtherinvestigation on the pathogenesis. Various strategies have been usedto reduce stroke morbidity and mortality, one of which has beenthrombolysis with vasodilating agent to restore cerebral blood flowto ischemic brain tissue.The characteristic and physiological effects of stellateganglion block is dilating of blood vessel and accelerating bloodflow in the distributed area.Alleviating the increase of vascularresistance and stagnation of circulation due to the excitation ofsympathetic system. enhancing brain blood flow and increasingperfusion pressure, improving brain ischemia and hypoxia, changingpenumbra tissue to normal, saving agonal brain tissue and decreasingthe infaction area.Besides used for pain related disease, SGB alsogets better response from ischemic cerebrovascular disease. but theunderlying mechanism is unclear. In this project, we take themolecular to explore the mechanism to its neuroprotective effects.Methods: 96 healthy Wistar rats (weight from 250g to 300g)were recruited to establith the middle cerebral artery occlusion(MCAO) model by the ligation of the right carotid artery. The focalischmic tissue was fixed, dehydrated, and paraffin-embedded inregular way at the time 6h,24h,48h,72h after the occlusion of MCArespectively. The expression of HSP70 in focal ischemic tissue ofdifferent times after MCAO was assayed by immunohistochemistry.The neurological defects and cerebral pathological changes areobserved.Results: The results of immunohistochemistry revealed that theexpression of HSP70 is low in the common brain tissue. Theexpression of HSP70 in the controlled and treatment group increasedfrom 6h after the MCAO, and reached their peaks at the time of 24hafter ischemia respectively. The expression of HSP70 in thetreatment group is less than that of controlled group.Conclusion:TCST ease the neurological defects of the animalmodels,ameliorate the pathological changes of the ischemic tissues,reduce the expression of HSP70. It is neuroprotective and is good tothe rehibition of the neurological function.The experiment focused on the recent development of thestudies of focal cerebral ischemia, and studied further on theexpression of HSP70 in the focal cerebral ischemia of MCAO modelusing modern immunohistochemistry techniques.The expression ofHSP70 in the treatment group is less than that of controlled group.Combined with our experiment, we are certain that SGB hasneuroprotective effects to the ischemic damage.Further study of themechanism of how SGB in the focal ischemia and then exploringnew effective ways to treat cerebral vascular diseases in the earlystage is our next aim.