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KMID : 0624620110440100647
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BMB Reports
2011 Volume.44 No. 10 p.647 ~ p.652
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Imipramine enhances neuroprotective effect of PEP-1-Catalase against ischemic neuronal damage
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Kim Dae-Won
Kim Duk-Soo
Kim Mi-Jin
Kwon Soon-Won
Ahn Eun-Hee
Jeong Hoon-Jae
Sohn Eun-Jeong
Dutta Suman
Lim Soon-Sung
Cho Sung-Woo
Lee Kil-Soo
Park Jin-Seu
Eum Won-Sik
Hwang Hyun-Sook
Choi Soo-Young
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Abstract
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The protein transduction domains have been reported to have potential to deliver the exogenous molecules, including proteins, to living cells. However, poor transduction of proteins limits therapeutic application. In this study, we examined whether imipramine could stimulate the transduction efficiency of PEP-1 fused proteins into astrocytes. PEP-1-catalase (PEP-1- CAT) was transduced into astrocytes in a time- and dose-dependent manner, reducing cellular toxicity induced by H(2)O(2). Additionally, the group of PEP-1-CAT (+) imipramine showed enhancement of transduction efficiency and therefore increased cellular viability than that of PEP-1-CAT alone. In the gerbil ischemia models, PEP-1-CAT displayed significant neuroprotection in the CA1 region of the hippocampus. Interestingly, PEP-1-CAT (+) imipramine prevented neuronal cell death and lipid peroxidation more markedly than PEP-1-CAT alone. Therefore, our results suggest that imipramine can be used as a drug to enhance the transduction of PEP-1 fusion proteins to cells or animals and their efficacies against various disorders.
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KEYWORD
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Imipramine, Ischemic damage, PEP-1-CAT, Protein transduction
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