[Effect of Brucea Javanica Oil Emulsion on the Invasiveness of Glioma Cells and Its Possible Mechanism].

OBJECTIVE: To investigate the effect of brucea javanica oil emulsion on the invasiveness of glioma cells and hosphatidylinositol 3 kinase/protein kinase B (PI3K/AKT) signaling pathway. METHODS: C6 glioma cells were treated by brucea javanica oil emulsion. The inhibition rate of glioma cells was detected by MTT, Western blot was used to detect protein expression levels of PI3K, AKT, and nuclear factor (NF)-κB in glioma cells. The number of the glioma cells migrated through polycarbonate membrane was detected by crystal violet staining method. RESULTS: Brucea javanica oil emulsion inhibited PI3K, AKT, and NF-κB protein expression which reached the highest inhibition at 30 min, 60 min, and 120 min after brucea javanica oil emulsion, respectively. Maximum suppression on the proliferation of C6 glioma cells reached at 180 min after brucea javanica oil emulsion, while the number of glioma cells migrated through polycarbonate membrane was the least. CONCLUSION: Brucea javanica oil emulsion inhibit the proliferation and invasiveness of glioma cells, which may be related to the inhibition of PI3K/AKT signal pathway.

Local hypothermia and optimal temperature for stroke therapy in rats.

BACKGROUND: Local hypothermia induced by intravascular infusion of cold saline solution effectively reduces brain damage in stroke. We further determined the optimal temperature of local hypothermia in our study. METHODS: Seventy-eight adult male Sprague Dawley rats (260 - 300 g) were randomly divided into 3 groups: group A, ischemia/reperfusion without cold saline infusion (n = 26) (control group); group B, infusion with 20 degrees C saline before reperfusion (n = 26); group C: infusion with 10 degrees C saline before reperfusion (n = 26). In each group, we chose 15 rats for monitoring physical indexes and the temperature of the brain (cortex and striatum) and body (anus), measurement of brain infarction volume, assessment of neurological deficits and the survival rate of reperfusion at 48 hours. Another 8 rats from each group was chosen for examining brain edema, another 3 from each group for histological observation by electron microscopy (EM) and light microscopy (LM) at 48 hours after reperfusion. RESULTS: There was no significant difference among the 3 groups for physical indexes during the examination (F((2, 45)) = 0.577, P = 0.568; F((2, 45)) = 0.42, P = 0.78 for blood pressure and blood gas analysis, respectively). The brain temperature was significantly reduced in the group C compared to the other groups (F((2, 45)) = 37.074, P = 0.000; F((2, 45)) = 32.983, P = 0.000, for cortex and striatum temperature respectively), while the difference in rectal temperature between group A and B or C after reperfusion was not significant (F((2, 45)) = 0.17115, P = 0.637). And the brain infarct volume was significantly reduced in group C (from 40% +/- 10% in group A, 26% +/- 8% in group B, to 12% +/- 6% in group C, F((2, 45)) = 43.465, P = 0.000) with the neurological deficits improving in group C (chi(2) = 27.626, P = 0.000). The survival rate at 48 hours after 10 degrees C and 20 degrees C saline reperfusion was increased by 132.5% and 150%, respectively, as compared to the control group (chi(2) = 10.489, P = 0.005). The extent of the brain edema showed no significant difference (F((2, 21)) = 0.547, P = 0.587) after cold saline infusion compared to the control group. No obvious vascular injury was found by electron or light microscopy in either infusion group. CONCLUSIONS: Regional hypothermia with 10 degrees C cold saline infusion can significantly decrease the infarction volume, improve the neurological deficits, and 10 degrees C seems to be the optimal temperature in inducing a cerebral protection effect during stroke. This procedure could be adopted as a further treatment for acute stroke patients.