The aim is to study the neuroprotective effect and
optimize the therapeutic dose and time window of picrosede II by orthogonal
test in cerebral ischemic injury in rats. The forebrain ischemia models of rats
were established by bilateral common carotid artery occlusion (BCCAO) methods.
The successful models were randomly grouped according to orthogonal experimental
design and treated by injecting picroside II intraperitonenally with different
therapeutic dose at different ischemic time. The contents of aquaporins 4
(AQP4), matrix metalloproteinases 9 (MMP 9) and cyclooxygenase 2 (COX2) in
brain tissue were determined by enzyme linked immunosorbent assay to evaluate
the therapeutic effect of picroside II on cerebral ischemic injury. The results
indicated that the best therapeutic time window and dose of picroside II in
cerebral ischemic injury should be 1) ischemia 1.5 h with 20 mg/kg body weight
according to the content of AQP4; 2) ischemia 2.0 h with 20 mg/kg according to
the content of MMP9; and 3) ischemia 1.5 h with 20 mg/kg according to the
content of COX2 inbrain tissue. It is concluded that the optimized therapeutic dose and time
window is injecting picroside II peritonenally with 10 - 20 mg/kg body weight
at ischemia 1.5 - 2.0 h in cerebral ischemic injury according to the
principle of lowest therapeutic dose with longest time window.

/pdf/the-effect-of-picroside-ii-on-the-expressions-of-aqp4-mmp9-46q8e0iqmo.pdf

The effect of picroside II on the expressions of AQP4, MMP9 and COX2 in cerebral ischemic injury in rats

Objective To observe the expressions of Kir4.1 and aquaporin-4 (AQP4) in rats with focal brain ischemia-reperfusion (IR) injury and clarify the role of Kir4.1 and AQP4 in IR injury. Methods Male Wistar rats were randomized into 5 groups, including a sham-operated group and 4 IR groups with focal brain IR injury induced by middle cerebral artery occlusion (MCAO). In the 4 IR groups, the rats were subjected to a 2-hour ischemia and sacrificed atter reperfusion for 3, 12, 24 or 72 h. Immunohistochemistry and RT-PCR were used to detect the expressions of Kir4.1 and AQP4 proteins and mRNAs in the brain tissues, respectively. Results Compared with the sham-operated group, the IR groups showed significantly increased expressions of Kir4.1 and AQP4 in the peri-infarct cortex surrounding the primary infarct area (P<0.05), which began at 3 h after the reperfusion and reached the peak level at 24 h, subsiding at 72 h. The mRNA levels of Kir4.1 (represented as the absorbance) were 0.343±0.02, 0.47±0.06, 0.61±0.08, 0.83±0.10 and 0.68±0.09 in the sham-operated group and the 4 IR groups with reperfusion for 3, 12, 24 and 72 h, respectively. The mRNA levels of AQP4 were 0.49±0.05, 0.66±0.09, 0.91±0.09, 1.12±0.11 and 0.94±0.08 in the 5 groups, respectively. Kir4.1 expression was positively correlated to AQP4 expression at the mRNA level (r=0.780, P=0.000). Conclusion Kir4.1 and AQP4 react with each other in the course of focal brain ischemia-reperfusion, both playing roles in the mechanism of brain IR injury.

Key words: 
Brain ischemia; Reperfusion injury; Kir4.1; Aquaporin-4

Role of Kit4.1 and aquaporin--4 in focal brain ischemia-reperfusion injury in rats

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Role of Kit4.1 and aquaporin--4 in focal brain ischemia-reperfusion injury in rats