Effect of saw palmetto extract on PI3K cell signaling transduction in human glioma.

Saw palmetto extract can induce the apoptosis of prostate cancer cells. The aim of the present study was to investigate the effect of saw palmetto extract on the phosphatidylinositol 3-kinase (PI3K)/Akt signaling transduction pathway in human glioma U87 and U251 cell lines. Suspensions of U87 and U251 cells in a logarithmic growth phase were seeded into six-well plates at a density of 104 cells/well. In the experimental group, 1 µl/ml saw palmetto extract was added, while the control group was cultured without a drug for 24 h. The expression levels of PI3K, B-cell lymphoma-extra large (Bcl-xL) and p53 were evaluated through western blot analysis. In the experimental group, the U87 and U251 cells exhibited a lower expression level of PI3K protein as compared with the control group (t=6.849; P<0.001). In addition, the two cell lines had a higher expression level of p53 protein in the experimental group as compared with the control group (t=40.810; P<0.001). Protein expression levels of Bcl-xL decreased significantly in the experimental group as compared with the control group (t=19.640; P=0.000). Therefore, saw palmetto extract induces glioma cell growth arrest and apoptosis via decreasing PI3K/Akt signal transduction.

Occlusion of middle cerebral artery induces apoptosis of cerebellar cortex neural cells via caspase-3 in rats.

AIM: Occlusion of the middle ferebral artery in rats may cause secondary injury that is not associated with middle ferebral artery feeding zone. This entity has been investigated very rarely. MATERIAL AND METHODS: HE staining method observed the changes of cerebellar cortex after MCAO operation. Electron Microscopy and TUNEL methods observed the apoptosis of neural cells of cerebellar cortex after MCAO in rats. Immunohistochemical analyses method observed the caspase-3 in neural cells of cerebellar cortex. RESULTS: The results of HE staining indicated that no ischemia-necrosis changes of cerebellar cortex tissue were observed after MCAO operation by HE staining. Further experiments by Electron Microscopy and TUNEL assay revealed that the apoptosis of neural cells of cerebellar cortex were induced after MCAO in rats. Furthermore, immunohistochemical analyses showed that caspase-3 played an important role on MCAO-induced apoptosis of neural cells of cerebellar cortex. CONCLUSION: These data showed for the first time that the role of caspase-3 in the mechanism of secondary injury of separated infarction in cerebellar cortex after middle cerebral artery occlusion in rats and it might give a new treatment strategy for individuals with human ischemic stroke.