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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2004, Vol. 9 ›› Issue (9): 1045-1049.

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Effects of progesterone on apoptosis and neuroprotective in rats during focal cerebral ischemia/reperfusion injury

LI Chao, DONG Liang-Li1, LU-Na1, ZHANG Jian-Kai2   

  1. Department of Ophthalmology, the Third Affiliated Hospital,1Department of Physiology, Xingxiang Medical College, Xingxiang 453003, Henan, China;
    2Department of anatomy, Zhanjiang Medical College, Zhanjiang 524000, Guangdong,China
  • Received:2004-06-12 Revised:2004-07-20 Online:2004-09-26 Published:2020-11-23

Abstract: AIM: To study the effects of neuroprotective and molecular mechanism of progesterone on ischemia reperfusion injury.METHODS: The rats with transient middle cerebral artery occlusion (MACO) were treated by Zea-Longa for 2 h and reperfused for 24 h. 48 male rats were divided into 6 group randomly. There were the sham group, ischmia/reperfusion (I/R), dimethl sulfoxide (DMSO), and pretreatment, posttreatment, pre +posttreament with PROG. The score of neurological deficit was measured by Zea-Longa method and insitu end labeling (ISEL) was used to investigate apoptosis in the brain tissues.RESULTS: The score of neurological deficit was 0 in the sham operation after reperfusion 24 h, 1. 38±0. 92 in the I/R group, 1. 0±0. 53 in the DMSO group, 0. 35±0. 51 in the pretreatment group, 0. 62±0. 52 in the posttreatment group, and 0. 25±0. 46 in the pre +posttreament group. The number of apoptosic cells was 1. 88±0. 25 in the sham group, 41. 38±3. 85 in the I/R group, 38. 13±5. 69 in the DMSO group, 22. 88±2. 70 in the pretreatment group, 25. 63±2. 93 in the posttreatment group, and 20. 88±2. 30 in the pre + posttreament group. There were significant differences in pretreament, posttreament, pre +posttreament and control groups(I/R or DMSO) (P<0. 05).CONCLUSION: PROG may protect the focal ischemia brain on reperfusion injury and reduce the expression of apoptosis and the neurological deficit.

Key words: progesterone, ischemia, reperfusion injury, neurological defici, apoptosis

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