Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10415 (Bcl-2)
 33,771 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fraxetin belongs to an extensive group of natural phenolic anti-oxidants. In the present study, using a human neuroblastoma SH-SY5Y cells, we have investigated the protective effects of this compound on modifications in endogenous reduced glutathione (GSH), intracellular oxygen species (ROS) and apoptotic death on rotenone-mediated cytoxicity. Incubation of cells with the fraxetin led to a significant elevation dose-dependent of cellular GSH and this was accompanied by a marked protection against rotenone-mediated toxicity, which was also significantly reversed in the cells with buthionine sulfoximine (BSO) co-treatment. Taken together, this study suggested that intracellular GSH appeared to be an important factor in fraxetin-mediated cytoprotection against rotenone-toxicity in SH-SY5Y cells. Fraxetin at 10-100 muM inhibited the formation of ROS, cytochrome c release, activation of caspase-3 and 9, and suppressed the up-regulation of Bax, whereas no significant change occurred in Bcl-2 levels. Our results indicated that the anti-oxidative and anti-apoptotic properties render this natural compound potentially protective against rotenone-induced cytotoxicity.
 ...
PMID:Fraxetin prevents rotenone-induced apoptosis by induction of endogenous glutathione in human neuroblastoma cells. 1599 79

The aim of the present study was to examine the effect of fraxetin on proliferation and apoptosis in the MCF-7 breast cancer cell line. Cell proliferation was measused using an MTT assay and 4',6-diamidino-2-phenylindole (DAPI) staining was used to determine shrinkage and condensation. RT-PCR was used to examine the expression of factor-associated suicide (Fas) and Fas ligand (FasL) mRNA, and western blot analysis was used to examine Bax and Bcl-2 protein. MTT showed that the proliferation of MCF-7 cells was significantly inhibited by fraxetin in a dose-dependent manner. Fraxetin also induced significant morphological changes of MCF-7 cells, suggestive of apoptosis, whereas DAPI staining showed that fraxetin caused cell shrinkage and chromatin condensation. RT-PCR showed that the expression of Fas and FasL mRNA was upregulated by fraxetin and the western blot analysis revealed that Bax was upregulated and Bcl-2 was downregulated. In conclusion, fraxetin can inhibit the proliferation of MCF-7 cells, induce apoptosis, upregulate Fas, FasL and Bax, and downregulate Bcl-2 to induce apoptosis. These results support the potential therapeutic role for fraxetin in breast cancer.
 ...
PMID:Effect of fraxetin on proliferation and apoptosis in breast cancer cells. 2934 76