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Aims To explore risk factors for stroke independent of hypertension and the relationship between riboflavin kinase ( RFK) and stroke. Methods Gene expression profiling in the brains of spontaneously hypertensive rats ( SHR) and stroke-prone spontaneously hypertensive rats ( SHRSP) was comparatively analyzed by gene chips. The differentially expressed gene RFK was further verified by q- PCR and Western blot. The protective role of RFK-regulated flavins (including riboflavin, flavin mononucleotide, and flavin adenine dinucleotide) in stroke was observed in middle cerebral artery occlusion ( MCAO) mice. Influence of flavins on apoptosis and death in oxygen and glucose deprivation ( OGD)-treated neurons was examined by flow cytometry. Bax and Bcl-2 proteins were detected by Western blot. Results Of the 76 differentially expressed genes, 41 genes were upregulated, and 35 genes were downregulated in SHRSP as compared with SHR. RFK was significantly downregulated in SHRSP. Flavins markedly decreased infarct area in MCAO mice, inhibited apoptosis and death in OGD-treated neurons, and decreased Bax protein expression. Conclusions Physiological downregulation of RFK may be a new potential risk factor for stroke, which probably affects the absorbance and utility of riboflavin and further destroys the protective effect of flavins on stroke. RFK might act as a therapeutic target for stroke. [ABSTRACT FROM AUTHOR]

J Oral Pathol Med (2012) 41: 322-331 Background: To clarify the efficacy of grape seed procyanidin (GSP) on antiproliferative effects related to p53 functional status of oral squamous cell carcinoma (OSCC) for its chemoadjuvant potential. Methods: We used GSP to investigate SCC-25 cells with wild-type p53 gene and OEC-M1 cells with mutant p53 gene for the assessment of antiproliferative effects including cell viability, cell cycle, apoptosis, migration and invasion potential, and alterations of associated oncoproteins involved in cellular and molecular events. Results: The findings suggest that GSP on OEC-M1 cells leads to cell cycle arrest by increasing the expression of p21Cip1/p27Kip1 protein without functioning mitochondria-mediated apoptosis, whereas GSP on SCC-25 cells inhibits cell proliferation via both G1-phase arrest and mitochondria-mediated apoptosis in a dose-dependent manner as a result of alterations of Bcl-2. GSP also inhibits the migration and invasion of both cells, which are associated with the suppression of matrix metalloproteinases (MMPs), MMP-2 and MMP-9. Conclusion: Antiproliferative effectiveness of GSP is closely associated with the p53 status of OSCC cells. GSP displays chemoadjuvant potential via cell cycle blockage and apoptotic induction. Our findings clearly suggest that GSP may play a role as a novel chemopreventive or therapeutic agent for OSCC. [ABSTRACT FROM AUTHOR]