The neuroprotective effects of an extract of Gastrodia elata

被引:53
作者
Tsai, Chung-Fen [2 ]
Huang, Chuen-Lin [3 ,4 ]
Lin, Yun-Lian [1 ]
Lee, Yi-Chao [5 ]
Yang, Ying-Chen [6 ]
Huang, Nai-Kuei [1 ,7 ]
机构
[1] Natl Res Inst Chinese Med, Taipei 112, Taiwan
[2] Cardinal Tien Hosp, Dept Neurol, New Taipei City, Taiwan
[3] Cardinal Tien Hosp, Med Res Ctr, Hsintien, New Taipei Coun, Taiwan
[4] Natl Def Med Ctr, Dept Physiol & Biophys, Grad Inst Physiol, Taipei, Taiwan
[5] Natl Cheng Kung Univ, Coll Med, Dept Pharmacol, Ctr Gene Regulat & Signal Transduct Res, Tainan 70101, Taiwan
[6] Natl Ilan Univ, Dept Anim Sci, Ilan, Taiwan
[7] Natl Yang Ming Univ, Inst Biophoton, Taipei 112, Taiwan
关键词
Gastrodia elata; Pheochromocytoma cells; A(2A)-R; cAMP; PKA; CREB; Apoptosis; BINDING PROTEIN CREB; PC12; CELLS; ADENOSINE RECEPTORS; SERUM DEPRIVATION; TRANSCRIPTION; APOPTOSIS; BRAIN; DISEASE; GROWTH; BL;
D O I
10.1016/j.jep.2011.08.064
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Ethnopharmacological relevance: Gastrodia elata (GE) Blume (family Orchidaceae) is a traditional Chinese herbal medicine for treating headaches, dizziness, tetanus, and epilepsy, indicating neuronal protective functions. Aim of the study: To evaluate the neuroprotection of GE and its molecular mechanism in preventing serum deprivation-induced PC12 cell apoptosis. Materials and methods: An MIT assay and Hoechst staining were used to respectively validate serum deprivation-induced cell death and apoptosis. Cyclic (c)AMP formation and protein kinase (PK)A activity were also measured after GE treatment. Western blotting was used to detect the phosphorylation of the cAMP response element-binding (CREB) protein. Transient transfection of a dominant negative CREB was used to validate the importance of CREB. Results: GE targeted the adenosine A(2A) receptor (A(2A)-R). GE increased cAMP formation, PKA activity, and phosphorylation of the CREB protein. GE-induced CREB protein phosphorylation and protection was blocked by a PKA inhibitor and overexpression of the dominant negative CREB, respectively. Conclusions: These results support the neuroprotective effects of GE. The protective mechanism might be mediated through an A(2A)-R/cAMP/PKA/CREB-dependent pathway. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:119 / 125
页数:7
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