AI Article Synopsis
- Icariin helps protect brain cells from damage caused by a lack of oxygen and glucose.
- It works by increasing the levels of a special protein called SIRT1, which supports cell survival.
- The way icariin activates SIRT1 is through a pathway called MAPK/P38, making it a potential treatment for brain injuries related to poor blood flow.
Article Abstract
It has been reported that icariin protects neurons against ischemia/reperfusion injury. In this study, we found that icariin could enhance neuronal viability and suppress neuronal death after oxygen and glucose deprivation (OGD). Further study showed that neuroprotection by icariin was through the induction of Sirtuin type 1 (SIRT1), an effect that was reversed by SIRT1 inhibitor III and P38 inhibitor SB203580. SIRT1 is an endogenous gene of longevity, which increased neuronal viability and could be activated by stimulating the mitogen-activated protein kinase (MAPK) pathway. However, this study found that icariin activated the MAPK/P38 pathway, not the extracellular signal-regulated kinase (MAPK/ERK) or c-Jun N-terminal protein kinase (MAPK/JNK) to regulate SIRT1 expression. The results suggest that icariin may be developed into a neuroprotectant for ischemia-related brain injury.
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| http://dx.doi.org/10.1016/j.ejphar.2009.03.033 | DOI Listing |
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