目的:研究富氢水对糖尿病小鼠肾脏的保护作用,并探讨其可能的作用机制。方法:60只健康ICR雄性小鼠,随机分成空白对照组(A组)、糖尿病组(B组)和糖尿病富氢水干预组(C组)。链脲佐菌素(STZ)150 mg/kg腹腔注射诱发糖尿病,造模成功后,C组每日腹腔注射富氢水5 m L/kg,B组腹腔注射等量0.9%氯化钠溶液,连续8周。尾静脉取血测定小鼠血糖,HE染色观察肾脏组织学变化,免疫组织化学染色观察NADPH氧化酶4(Nox4)和血红素加氧酶-1(HO-1)蛋白的表达。结果:C组Nox4表达水平明显低于B组,而HO-1表达明显高于B组;B组与C组的空腹血糖均明显高于A组(P<0.01),B组与C组之间差异无统计学意义(P>0.05);3组肾脏组织病理HE染色未显示明显病变。结论:富氢水可减轻糖尿病小鼠肾脏组织的氧化应激水平。
Objective To study the dynamic characteristics of norepinephrine(NE)release in hypothalamus followed by electrical stimulation in locus coeruleus in the rat model of stress-inducedhypertension(SIH)and explore the role...
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Objective To study the dynamic characteristics of norepinephrine(NE)release in hypothalamus followed by electrical stimulation in locus coeruleus in the rat model of stress-inducedhypertension(SIH)and explore the role of angiotensin type 2 receptor in the pathogenesis of *** 44 rats were randomly divided into control(n=20)and stress groups(n=24).The hypertension model was established by combining noise and foot-shock *** the end of modeling,NE release in the hypothalamus by electrical stimulation in locus coeruleus was studied and NE signal was recorded by carbon fiber *** peak value,the time to peak and half-life period of NE signal in both group rats were *** The peak value of NE signal in the hypothalamic followed by electrical stimulation in locus coeruleus in SIH rats were more than in controls(P<0.01).Intraperitoneal injection of PD123,319(AT2 receptor antagonist)potentiated electrical stimulation in locus coeruleus induced NE release in the hypothalamus in SIH rats and elevated blood pressure(P<0.05),whereas intracerebroventricular injection of CGP42112(AT2 receptor agonist)inhibited the NE release and reduced the heart rate(P<0.05).Conclusions Combining noise and foot-shock stresses increased the secretion of NE in the hypothalamus followed by electrical stimulation in locus coeruleus in *** type 2 receptor plays an inhibition effect on NE release in hypothalamus in SIH *** findings suggest that angiotensin type 2 receptor can be a pharmacology target for treatment of SIH.
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