摘要
【目的】研究内源性一氧化碳(carbon monoxide,CO)、内源性糖皮质激素(glucocorticoid,GC)、环磷鸟苷(cGMP)在新生鼠缺氧缺血性脑损伤中的作用及锡原卟啉(SnPP)对其的治疗前景。【方法】制备缺氧缺血性脑损伤(hypoxia-ischemic brain damage,HIBD)新生鼠模型和锡原卟啉治疗模型。利用分光光度法测定新生大鼠HIBD后血一氧化碳血红蛋白(COHb)和GC含量,放免法检测脑cGMP水平,并观察脑组织形态学变化。【结果】HIBD组在2、12、24 h GC含量、COHb及cGMP水平与对照组相比显著增高(P<0.01);SnPP组COHb含量及cGMP水平明显低于HIBD组(P<0.01),但仍显著高于对照组(P<0.01)。脑组织病理改变显示HIBD组呈重度改变,SnPP组的病理改变明显减轻。【结论】HIBD后GC、CO和cGMP明显增高;而SnPP可抑制CO活性,使CO和cGMP水平下降,减轻脑损伤,表明GC、CO、cGMP系统在缺氧缺血的病理生理过程起着重要作用。
[Objectives] To study the role of endogenous glucocorticoid（GC） and carbon monoxide（CO） and cyclic GMP in newborn rats with hypoxia-ischemic brain damage（HIBD） and therapeutic effect of the Sn-protoporphyrin（SnPP） on HIBD. [Methods] Models of HIBD in newborn rats were established. SnPP was injected into the abdominal cavity of rats in SnPP group before hypoxia-ischemic. CO, GC level in the blood and cGMP level in the brain were determined respectively at 2,12 h after HIBD by spectrophotometry etc. [Results] CO,GC and cGMP level of HIBD group were significant higher than those of control groups at 2,12 h（P〈0. 01 ）;In HIBD, neurons were damaged severely. SnPP could effectively antagonize the pathological changes mentioned above. [Conclusion] In HIBD,the increased GC activity resulted in increase of endogenous CO that could enhance cGMP; SnPP may protect nerve cells from damage by preventing GC level resulted in a decrease of endogenous CO. HO-CO-cGMP system may play an important role in the pathogenesis of HIBD.
出处
《中国儿童保健杂志》
CAS
2006年第2期166-168,共3页
Chinese Journal of Child Health Care
基金
浙江省教育厅基金资助(SJY03027)
温州市科技局基金项目(Y2005A024)
关键词
内源性糖皮质澈素
一氧化碳
脑缺氧
脑缺血
大鼠
锡原卟啉
glucocorticoid
carbon monoxide
cerebral anoxia
cerebral ischemia
rat
Sn-protoporphyrin
