Aim To study the mechanism and inhibitory effect of aspirin on U251 cells in vitro.Methods The effects of aspirin on proliferation of U251 cells were assessed using the MTT assay.Cell cycle analysis was done by flow cytometry.AnnexinⅤ-FITC Apoptosis Detection Kit was used to detect apoptosis of cells.Western blot was employed to analyze expression of apoptosis-related protein Bcl-2 and Caspase-3.Results The growth inhibiton of U251 cells by aspirin was in a time-and-dose-dependent manner.After treatment with 8 mmol?L-1,cell cycle was arrested at G2/M phase.Aspirin also significantly enhanced apoptosis of U251 cells with down-regulated anti-apoptotic protein Bcl-2,and activation of Caspase-3.Conclusions Aspirin can significantly inhibit the growth of U251 cells through inducing cell apoptosis in vitro.

Abnormal aggregation of α-synuclein(α-Syn) is thought to be a key event in the pathogenesis of Parkinson disease (PD). In recent years, it was shown that above 90% of α-Syn deposited in Lewy bodies in brain tissues from patients with PD is phosphorylated, which suggested that α-Syn phosphorylation be connected with the occurrence of PD. Several kinds of phosphokinases can make α-Syn phosphorylated, however the precise roles of these phosphokinases in PD are less clear.

Aim To investigate the effects of curcumin on the adherence between isolated rat brain microvascular endothelial cells(BMECs)and leukocytes induced by TNF-? in vitro.Methods The adherence ofleukocytes to BMECs and the effects of curcumin were determined by myeloperoxidase.The expression of ICAM-1 was detected by RT-PCR and immunoblotting.Results Curcumin inhibited the TNF-? stimulated adherence of leukocytes to BMECs.Pretreament of curcumin also inhibited TNF-?-induced increases in the mRNA and protein levels of ICAM-1 in BMECs.Conclusions Curcumin could protect the endothelial cells against damage caused by TNF-?.The protective effects of curcumin may be mediated through downregulation of the expression of ICAM-1.

AIM To observe the effect of aspirin on a model of Alzheimers disease in rats and its molecular mechanism. METHODS The AD pathological model was made by hippocampal CA 1 lesions with stereotaxic mini-injection of quinolinic acid;the rats learning and memory was observed by Y-maze; the apoptosis of hippocampal cells were detected by using flow cytometry and electronic microscope; the content of calcium in AD rats hippocampus was determined by atomic absortion spectrophotometer. RESULTS Aspirin was shown to improve learning and memory deficiency in rats with bilateral hippocampal lesions induced by quinolinc acid, to decrease apoptosis rate in hippocampal cells significantly and to reduce the concentration of calcium in hippocampus. CONCLUSION The protective effects of aspirin on a model of AD in rats may be involved in antagonism of calcium and inhibition of apoptosis in hippocampal cells induced by quinolinic acid.

Valproate (VPA) has long been used for the treatment of bipolar mood disorder. VPA is effective in control of mania and depression. Recent studies have demonstrated that VPA has profound neuroprotective effects in against various apoptotic stimuli. Moreover, VPA can promote neurogenesis, neuronal proliferation and differentiation. Although intensive research has been dedicated to VPA′s neuroprotection, the molecular mechanisms by which VPA protects neurons are still not fully understood. In this paper, recent progresses in the study of VPA′s neuroprotection and underlying mechanism are reviewed.

Objective:To study the action of Xinnaotong on adhesion molecule expression by cultured endothelial cells and platelets. Methods: Tumor necrosis factor ?(TNF ?) stimulated ICAM I expression on the cell surface was studied with human umbilical vein endothelial cells(HUVEC).Thrombin stimulated expression of platelet P selectin was studied with human blood platelets. Adhesion molecule expression was measured by flow cytometry. Results: ICAM I molecule expression on HUVEC was significantly stimulated by TNF ?. The stimulatory effect of TNF ? on HUVEC was inhibited by Xinnaotong(0.25～2g/L) in a concentration dependent manner. The same dose of Xinnaotong can inhibit the p selectin expression on human blood platelets stimulated by thrombin. Conclusion: Xinnaotong inhibites expression of adhesion molecues(ICAM I, p selectin) in HUVEC and in human blood platelets.

Aim To study the effects of Quercetin on the angioge ne sis and cultured human vascular endothelial cells (HUVEC).Methods In vivo, the effects of Quercetin on angiogenesis induced by vascular en dothelial growth factor (VEGF) and basic fibroblast growth factor(bFGF), were observ ed by chorioallantioic membrane (CAM) test. The effects of quercetin on proliferation of human vascular endothelial cells (HUVEC) were assessed by MTT assay. The effects of Quercetin on cell cycle of HUCEC were observed by flow cytometer (FCM ).Results The angiogenesis induced by VEGF in CAM was strongly inhibited by Quercetin with 0.1, 0.05 and 0.025 mmol?L -1; The angiogen esis induced by bFGF in CAM. was strongly inhibited by Quercetin with 0.1 and 0 .05 mmol?L -1. Quercetin markedly inhibited the proliferation of HUVEC with 240,120,60 and 30 ?mol?L -1. The inhibition rate was 67.0%,58.1% ,39.7% and 20.7% respectively. Quercetin at the concentration of 240 ?mol? L -1 and 120 ?mol?L -1 resulted in S,G 2 arrest of HUVEC. Conclusion Quercetin has substantial inhibitory effects on angiogenesi s induced by VEGF and bFGF, and on proliferation of HUVEC.