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[孕酮对新生大鼠缺氧缺血性脑损伤后基质金属蛋白酶-3表达的影响]

[Effect of progesterone on MMP-3 expression in neonatal rat brain after hypoxic-ischemia].

作者信息

Xu Chun-Yang, Li Shuang, Li Xin-Qiang, Li Dong-Liang

机构信息

Department of Physiology, Xinxiang Medical College, Xinxiang 453003, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2010 Aug;26(3):370-3.

Abstract

OBJECTIVE

To study the effect of progesterone on matrix metalloproteinase-3 (MMP-3) expression in neonatal rat brain after hypoxic-ischemia.

METHODS

Followed the hypoxic-ischemia of neonatal rat brain, Evans blue (EB) staining and transmission electron microscopy were used to detect the blood-brain barrier pathological changes on permeability. MMP-3 protein expression in cerebral cortex was measured with Western blot.

RESULTS

Transmission electron microscopy results showed that the blood brain barrier in hypoxic-ischemic group changed significantly compare to progesterone group. EB staining results suggested that the blood-brain barrier permeability of hypoxic-ischemic group was significantly increased compared to sham-operated group (P < 0.01). The blood-brain barrier permeability in progesterone group was also decreased in comparison to that of hypoxic-ischemic group (P < 0.05). Western blot image analysis results indicated that MMP-3 protein expression in the hypoxic-ischemic group increased significantly than that in sham-operated group (P < 0.01), and the progesterone group was decreased significantly than that in hypoxic-ischemic group (P < 0.05).

CONCLUSION

Progesterone may reduce the blood-brain barrier damage by reducing MMP-3 expression. This might be one of the protective mechanisms in the hypoxic-ischemic brain injury.

摘要

目的

研究孕酮对新生大鼠缺氧缺血后脑组织基质金属蛋白酶-3(MMP-3)表达的影响。

方法

新生大鼠脑缺氧缺血后,采用伊文思蓝(EB)染色和透射电镜检测血脑屏障通透性的病理变化。用蛋白质免疫印迹法检测大脑皮质中MMP-3蛋白的表达。

结果

透射电镜结果显示,与孕酮组相比,缺氧缺血组血脑屏障变化显著。EB染色结果表明,与假手术组相比,缺氧缺血组血脑屏障通透性显著增加(P<0.01)。与缺氧缺血组相比,孕酮组血脑屏障通透性也降低(P<0.05)。蛋白质免疫印迹图像分析结果表明,缺氧缺血组MMP-3蛋白表达显著高于假手术组(P<0.01),孕酮组显著低于缺氧缺血组(P<0.05)。

结论

孕酮可能通过降低MMP-3表达减轻血脑屏障损伤。这可能是缺氧缺血性脑损伤的保护机制之一。

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