Abstract Title:

Icariin enhances neuronal survival after oxygen and glucose deprivation by increasing SIRT1.

Abstract Source:

Eur J Pharmacol. 2009 May 1;609(1-3):40-4. Epub 2009 Mar 20. PMID: 19303870

Abstract Author(s):

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

Article Affiliation:

Department of Neurology, Affiliated Drum Tower Hospital of Nanjing University Medical School, PR China.


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.

Study Type : In Vitro Study

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