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Icariin Enhances Neuronal Survival After Oxygen and Glucose Deprivation by Increasing SIRT1

Lin Wang, Ling Zhang, Zhi-Bin Chen, Jia-Yong Wu, Xin Zhang, Yun Xu

Eur J Pharmacol. 2009 May 1;609(1-3):40-4.

PMID: 19303870

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.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
AP251456607-A Histone Deacetylase Inhibitor III Histone Deacetylase Inhibitor III 251456-60-7 Price
AP49843983-B SIRT1 Inhibitor III SIRT1 Inhibitor III 49843-98-3 Price
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