The Effects Of Heat Shock Pretreatment On The Neurocyte Apoptosis And The Expressed Heat Shock Protein 70 In Acute Alcoholism Neonatal Rats

Backgrounds and Purposes:Ethanol is a neurotropism toxicant,also main component of liquor. The majority ethylism is betided to drink liquor. Ethanol has severe injury effect in the developmenting cerebrum, nevertheless, the mechanism of action is still dimness.Recently study mostly emphasized on the chronic effect of alcohol in mature animal. The research team lead by Drs Olney , medical college of University of Washington in American , discovered that alcohol can obstruct NMDA receptor and over activation GAB A receptor double mechanism , extensively evoke neuron apoptosis in cerebrum.The most sensitive period of alcohol damage is during the brain growth spurt (BGS), the last trimenon of mankind fetation and the first two postnatal weeks in the rat. Pregnant women drink in this period has strong damage effect ,even one time exposure also can induce fetal death, malformation or dysnoesia(Fetal Alcohol Syndrome,FAS). To establish animal model of acute alcoholism in this period, will advantage to us to further study FAS.Heat shock respond is a cell stress reaction controlledby gene expression when organic cell meet stress stimulus such as transient high temperature , hypoxia and so on .The proteins generate in this period of time are known as heat shock protin. There are some literatures report that HSP can protect cell in many kinds of stress reaction such as palsy, neural degeneration disease, epilepepilepsy, oxidation stress, infection, trauma and metabolic poison . The protection of hsp70 is the most notable . The stress stimulate hsp70 expressed increase to guide us to study and research its potential protective effect in induction tolerance .(A phenomenon , preliminary sublethal dose injury can relieve the follow Major injury).Some research found heat shock pretreatment can agonistic intoxication damage such as cerebellum culturaled in glutamate; can protective cell avoid the subsequently cerebral ischemia and hypoxia damage. Whether heat shock pretreatment can reduce fetus acute alcoholism brain injured is still study less .The present study is aim to investigate the protection of heat shock pretreatment in fetus alcoholism brain cell from morphology and molecular biology. Materials and Methods:Thirty first class quality standard , postnatal between 8 and 14 day,healthy male Sprague-Dawley rats , weighing between 13 and 25 (18.4 + 3.8) grams, were divided randomizedly into three group: simple Sodium Chloride group, simple alcohol group , heat shock pretreatment add alcohol group . First,we refer Blake method of preparation to make heat shock pretreatment model rats,after 24h, Anhydrous alcohol(2.5g/kg,99.7%) was give to Simple alcoholgroup and heat shock pretreatment add alcohol group by peritoneal injection. Sodium Chloride was given to simple Sodium Chloride group by peritoneal injection.The rats were killed after 6h and the samples of the brain tissue were taken immediately to be fixed in 4% paraformaldehyde ,embedded in paraffin and then made into sections in 5 u m thick.HE staining and Nissl body staining were carried out to observe the basic pathology change of the brain. Neurocyte apoptosis was detected with the method of terminal-deoxynucleotidyl transferase mediated d-UTP nick end labeling (TUNEL) and the expression of heat shock protein 70 was tested with the method of immunohistochemistry(ABC).statistical analysis: All the data were expressed in mean卤SD. Data analysis was performed by Wilcoxon rank sum test and spearman linear correlation analysis ,and the strength of the relationship is reported as r2 . The acceptable level of significance(p)was less than 0.05. The ststistic precessions were carried out in spss 11.0 for windows. Results: 1. The general state of the rats:The neogenesis rats were administration toxic dose alcoh...