Protective effects of physcion on cerebral ischemia-reperfusion injury in rats

Ping ZHANG; Likai SU; Dechao WANG; Yangchen ZHAO; Xiaofang LI; Zhangqun YANG; Xiuyan CUI

ABSTRACT

BACKGROUND:

Interleukin-1 (IL-1β) and intercellular adhesion molecule-1 (ICAM-1 ) can mediate neutrophilic infiltration, which is closely relevant to cerebral ischemia-reperfusion injury.

OBJECTIVE:

To investigate the effect of physcion on cerebral inflammatory reaction after ischemia-reperfusion injury.

DESIGN:

A completely randomized study based on animals.

SETTING:

Neurological department in a university hospital.MATERIALS From September to December 2003, the study was conducted in the Animal Laboratory, Hebei Staff and Workers Medical College. Totally 91 healthy male SD rats, supplied by Laboratory Animal Center of Hebei Medical University, were used in the experiments. They were divided into sham operation (SO) group, ischemia-reperfusion group, normal control group, 20 mg/kg physcion group and 40 mg/kg physcion group.Each of the former two groups would be divided into 4 subgroups named as the 6th-hour-after-reperfusion group, the 12th-hour-after-reperfusion group, the 24th-hour-after-reperfusion group and the 48th-hour-after-reperfusion group. Each of the latter two groups were divided into 2 subgroups named as the 12thhour-after-reperfusion group and the 24th-hour-after-reperfusion group. Each subgroup contained 7 rats.

INTERVENTIONS:

Middle cerebral artery occlusion model (MCAO model) was applied, and IL-1β was measured by radioimmunoassay and ICAM-1 was detected by immunohistochemical staining.MAIN OUTCOME MEASUREMENTS The IL-1 β level and the positive expression of ICAM-1 in the rats' cerebella were observed.

RESULTS:

Cerebral ischemia-reperfusion injury in the rats reached its peak 6 hours after reperfusion, and then it decreased gradually. In the 12-hour-after-reperfusion subgroup amd the 24-hour-after-reperfusion subgroup of the 40 mg/kg physcion group, and the 12-hour-after-reperfusion subgroup of the 20 mg/kg physcion group, IL-1β in the injured parts of the cerebella decreased dramatically, compared with MCAO model controls ( P＜ 0.01 ). In the normal control group and SO group, a small quantity of ICAM-1 was detected in rat' s cerebral cortex, and some fulvous staining substance was observed in the plasma and membrane of cerebral vascular endothelium cells. In the cerebral ischemia-reperfusion injury group, positive staining substance could be observed 24 hours after the reperfusion, then darkened gradually (integral absorbency value 31.89 ± 4.38, area density value 0. 018 5 ± 0. 003 1). In the 12-hour-after-reperfusion subgroup of the 40 mg/kg physcion group (integral absorbency value 13.33 ±6. 12, area density value 0. 007 6 ± 0. 002 2) and the 24-hour-after-reperfusion subgroup of the 40 mg/kg physcion group (integral absorbency value 20.04 ±4.65,area density value 0. 012 9 ±0. 003 6), and in the 24-hour-after-reperfusion subgroup of the 20 mg/kg physcion group (integral absorbency value23.73 ±4.51 area density value 0. 014 1 ±0. 003 8), expressions of ICAM-1 around the infarctions significantly decreased as compared with those in the MCAO model controls respectively ( P ＜ 0.01 or P ＜ 0.05).

CONCLUSION:

Physcion tends to decrease the expressing of IL-1β and ICAM-1 in a cerebellum after ischemia-reperfusion injury, thus, it may help alleviate the ischemia-reperfusion injury.