AI Article Synopsis
- Icariin (ICA), derived from Epimedium brevicornum Maxim, shows neuroprotective effects, particularly against apoptosis in neurons subjected to oxygen-glucose deprivation and reperfusion (OGD/R).
- The study found that ICA significantly improves cell survival and increases Bcl-2 levels while decreasing pro-apoptotic and autophagy markers like Bax and Beclin-1 in affected PC12 cells.
- These findings indicate that ICA's protective effects involve Bcl-2's regulation of both apoptosis and autophagy, suggesting a complex interplay in neuroprotection.
Article Abstract
Icariin (ICA), an active component of Epimedium brevicornum Maxim, exerts a variety of neuroprotective effects such as antiapoptosis. However, the mechanisms underlying antiapoptosis of ICA in neurons exposed to oxygen-glucose deprivation and reperfusion (OGD/R) are unclear. The B-cell lymphoma-2 (Bcl-2) protein family plays an important role in the regulation of apoptosis and autophagy through Bcl-2-dependent cross talk. Bcl-2 suppresses apoptosis by binding to Bax and inhibits autophagy by binding to Beclin-1 which is an autophagy related protein. In the present study, MTT result showed that ICA increased cell viability significantly in OGD/R treated PC12 cells (P < 0.01). Results of western blotting analysis showed that ICA increased Bcl-2 expression significantly and decreased expressions of Bax, cleaved Caspase-3, Beclin-1, and LC3-II significantly in OGD/R treated PC12 cells (P < 0.01). These results suggest that ICA protects PC12 cells from OGD/R induced autophagy via Bcl-2-dependent cross talk between apoptosis and autophagy.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5004044 | PMC |
| http://dx.doi.org/10.1155/2016/4343084 | DOI Listing |
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