[Effect of clausenamide on the expression of Bcl-2 protein and apoptosis after focal cerebral ischemia/reperfusion in renovascular hypertensive rats].

Abstract

OBJECTIVE:

To observe the effect and mechanism of clausenamide on the expression of Bcl-2 and apoptosis after focal cerebral ischemia/reperfusion in renovascular hypertensive rats.

METHODS:

Seventy-five renovascular hypertensive rats were randomly divided into three groups (25 in each group): clausenamide intervention group, single ischemia/reperfusion model group and sham-operated group. Focal cerebral ischemia was reproduced by ligature for 2 hours and loosening of the ligature in the rats. No arterial ligature was applied in sham-operated group. Computerized pathological image analyzer was used to determine the number of cells positive for Bcl-2 by immunohistochemical staining, and also the counts of apoptotic cells after TdT-mediated dUTP nick end labeling (TUNEL) staining respectively in coronal sections of brain after reperfusion (6, 12, 24, 48 and 72 hours).

RESULTS:

(1) The expression of Bcl-2 protein was detected 6 hours after reperfusion, peaking at 24 hours, then declined gradually. The Bcl-2 protein positive cell counts at every time point in clausenamide intervention group were significantly higher than simple ischemia/reperfusion model group (all P<0.01). (2) The number of apoptotic cells was increased with reperfusion, reaching its peak at 72 hours. The apoptosis counts in clausenamide intervention group were significantly lower than single ischemia/reperfusion model group (all P<0.01). At all time points, except at 48 hours after reperfusion, as there was no significant difference (all P>0.05). No Bcl-2 positive cells and only 0-2 apoptotic cells could be discernible in brain sections from sham-operated animals or in the contralateral side of ischemia in animals of the other groups.

CONCLUSION:

Expression of Bcl-2 protein is enhanced and apoptosis appears after focal cerebral ischemia/reperfusion in rat brain. Clausenamide can enhance the expression of Bcl-2 protein and inhibit apoptosis remarkably. Clausenamide may coordinate with Bcl-2 in inhibiting apoptosis. This may be the mechanism of protection of brain cells from ischemic damage of clausenamide treatment.

• Authors: Zhu-chang Jiang, Gui-nan Bi, Sheng-liang Shi
• Journal: Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue (Zhongguo Wei Zhong Bing Ji Jiu Yi Xue) Vol. 17 Issue 5 Pg. 289-92 (May 2005) ISSN: 1003-0603 [Print] China
• PMID: 15877958 (Publication Type: English Abstract, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Lactams
• Lignans
• Proto-Oncogene Proteins c-bcl-2
• clausenamide

Topics

• Animals
• Apoptosis (drug effects)
• Brain Ischemia (complications, metabolism, pathology)
• Disease Models, Animal
• Hypertension (complications)
• Lactams (pharmacology)
• Lignans (pharmacology)
• Male
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• Random Allocation
• Rats
• Rats, Wistar
• Reperfusion Injury (complications, metabolism, pathology)