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Expression Of Synaptophysin And Neuronal Nitric Oxide Synthase In The Rat Offspring Hippocampus Of Pregnancy Hyperthyroidism

Posted on:2013-02-27Degree:MasterType:Thesis
Country:ChinaCandidate:Z H LiuFull Text:PDF
GTID:2214330374459066Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective: Pregnancy hyperthyroidism is a common endocrine systemdiseases, prevalence rate is0.1%~0.2%.Women of reproductive age areliable to thyroid disease. Excess thyroid hormones can cause the bodymetabolic disorders and affect the function of each system. Pregnancyhyperthyroidism can cause premature birth, neonatal hyperthyroidism andhypothyroidism, etc. By regulating many structure proteins and signal proteinexpression, thyroid hormones affect brain nerve cell proliferation andmigration,differentiation. Simultaneously thyroid hormones affect theformation of a developing brain function and behavior in the process ofabnormal by influencing the development of synapses and myelin sheath, etc.Nitric oxide(NO) participates in synaptic plasticity and long-term potentiationby retrograde pass way, excess NO can produce neurotoxic by free radicals orother ways aggravating neuron damage. Neuronal nitric oxide synthase is thethe rate-limiting enzyme in the synthesis of nitric oxide. Synaptophysin(Syn)is a kind of specific glycoprotein distributing in most presynaptic vesicles ofcentral nervous system. Expression of synaptophysin can reflect the synapticnumber and size. This study observed the development of rat offspring brainof pregnancy hyperthyroidism by investigating expression of ratshippocampus synaptophysin and neuronal nitric oxide synthase, providedtheory basis to further research the influence of the thyroid hormone onintelligence and preventive measures.Methods:Randomly divided female SD rats into normal control group (N group),mild hyperthyroidism group (A group), severe hyperthyroidism group (Bgroup). To establish the rat's hyperthyroidism model with levothyroxinesodium, then made female rats and male SD rats in one cage by2:1ratio. After conception,continued giving levothyroxine sodium to A and B group,Ngroup to the same amount of saline. Observed each group rat general conditionas well as their postnatal rats. Tested21days and60days thyroid function ofrats offing. Observed the0day,21days,60days histopathologicalhippocampus by HE staining and the expression of synaptophysin andneuronal nitric oxide synthase by western blotting technology.Results:1General situation of pregnancy rats: compared with the normal controlgroup, mild hyperthyroidism rats'drinking water quantity increased slightly,the activity increased, wears increased and daily mental state were a littleexcited. Severe hyperthyroidism rats showed high metabolic signs,eatingwater quantity significantly increased and are more irritability, reaction to theoutside world irritability, wears increased (bowel movements were paste).2General situation of postnatal rats: normal control group growth weregood, gradually sprouted, with good color and luster; mild hyperthyroidismgroup and severe hyperthyroidism group weight loss, with slow growth, dull,especially in the severe hyperthyroidism.3The thyroid function examination of pregnant rats: The level of FT3and FT4of the mild hyperthyroidism group and the severe hyperthyroidismgroup was more significantly increased than normal control group (P<0.05).The level of FT3and FT4of severe hyperthyroidism group was increasedsignificantly contrasting the mild hyperthyroidism group (P<0.05). The levelof TSH of mild hyperthyroidism group and severe hyperthyroidism group wasdecreased significantly than normal control group (P<0.05).The level of TSHsevere hyperthyroidism group was decreased significantly contrasting the mildhyperthyroidism group (P<0.05).4The thyroid function examination of postnatal rats: The level of FT3and FT4in21days mild hyperthyroidism group and sever hyperthyroidismgroup was higher than normal control group (P<0.01), TSH was lower thannormal control group (P<0.01). The level of FT3and FT4in21days severhyperthyroidism group was higher than mild hyperthyroidism group (P<0.01), TSH was lower than mild hyperthyroidism group (P<0.01). The level of FT3and FT4in60days mild hyperthyroidism group was higher than normalcontrol group, TSH was lower than normal control group but both were notstatistically significant (P>0.05), The level of FT3and FT4in60days severhyperthyroidism group was higher than normal control group (P<0.01), TSHwas lower than normal control group (P<0.01). The level of FT3and FT4in60days sever hyperthyroidism group was higher than mild hyperthyroidismgroup (P<0.05), TSH was lower than mild hyperthyroidism group (P<0.05).The level of FT3and FT4in60days of mild hyperthyroidism group and severhyperthyroidism group was higher than in21days, but was not statisticallysignificant(P>0.05).The level of FT3and FT4in60days of severhyperthyroidism group was lower than in21days, but was not statisticallysignificant(P>0.05).The level of TSH in60days of mild hyperthyroidismgroup and sever hyperthyroidism group was higher than in21days (P<0.01).5The mother rats and rats offing21days,60days TSH had positivecorrelation (R=0.966,P=0.00085;R=0.619,P=0.006), all have statisticallysignificant (P<0.05); mother rats and rats offing21days,60days FT3had thepositive correlation(R=0.835,P=0.00016;R=0.404,P=0.02),all have statisticallysignificant (P<0.05); mother rats and rats offing21days,60days FT3had thepositive correlation (R=0.898,P=0.00043;R=0.871,P=0.00025),all havestatistically significant (P<0.05).6Histopathologic change of postnatal rats hippocampal: Normal controlgroup hippocampal tissue cells each period in order, even the size of the cells.Mild hyperthyroidism group hippocampal organization cells were arranged alittle disorder, cell size not consistent, severe hyperthyroidism grouphippocampal organization cells were arranged disorder with a celldegeneration phenomenon.7Rats offing hippocampal tissue protein expression:0day21days60days of mild hyperthyroidism group Syn was decreased than normal controlgroup, a statistically significant(P<0.05);0day21days60days severehyperthyroidism group Syn was decreased than normal control group, a statistically significant (P<0.05),0day21days60days severehyperthyroidism group was statistically significant decreased than mildhyperthyroidism group (P<0.05).0day21days60days of mildhyperthyroidism group nNOS was increased than normal control group, astatistically significant (P<0.05);0day21days60days of severehyperthyroidism group nNOS was increased than normal control group, astatistically significant (P<0.05);0day21days60days of severehyperthyroidism nNOS was increased than mild hyperthyroidism group, astatistically significant (P<0.05). The expression of nNOS and Syn increasedwith time,21days highest (P<0.05); The expression of nNOS and Syn in60days had rising trend than0days, not statistically significant (P>0.05).Twoproteins with negative correlation between (R=-0.433, P<0.05)Conclusion:1Thyroid hormone can through the placenta into the fetal bloodcirculation, resulting in neonatal rat hyperthyroidism.2The more serious degree matrix hyperthyroidism, the more obviousdegree hyperthyroidism of rat offspring.3Hyperthyroidism can reduce synaptophysin expression in the hippoca-mpus of rat offspring.4Hyperthyroidism can increase neuronal nitric oxide synthase expressionin the hippocampus of rat offspring...
Keywords/Search Tags:Hippocampus, Neuronal nitric oxide synthase, Thyroidhormone, Synaptophysin, Western blotting
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