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Ligusticum chuanxiong as a potential neuroprotectant for preventing serum deprivation-induced apoptosis in rat pheochromocytoma cells: Functional roles of mitogen-activated protein kinases

Authors Lin, Yun-Lian; Wang, Guei-Jane; Huang, Chuen-Lin; Lee, Yi-Chao; Liao, Wei-Chen; Lai, Wen-Lin; Lin, Yen-Ju; Huang, Nai-Kuei

Journal JOURNAL OF ETHNOPHARMACOLOGY , APR 21 2009,3:122

DOI 10.1016/j.jep.2009.02.011 PubMed 19429305

Abstract Ethnopharmacological relevance: Ligusticum chuanxiong (LC) as a common component in many traditional Chinese medicinal formulas and decoctions has been used to treat different central nervous diseases, suggesting a neuroprotective function.Aim of the study: To investigate the functional roles of mitogen-activated protein kinases (MAPKs) in mediating the neuroprotection of LC.Materials and methods: Different extractions of LC were applied with or without MAPK inhibitor to test their protection against serum deprivation-induced apoptosis in rat neuronal-like pheochromocytoma (PC12) cells as revealed by an MTT assay or Hoechst staining. Western blot was used to identify the activations of MAPKs.Results: The most effective butanol extraction (LC-BuOH) was used in the following experiments. LC-BuOH reversed serum deprivation-induced decreased phosphorylation of extracellular signal-regulated kinase (ERK) and increased phosphorylation of c-Jun NH2-terminal kinase (JNK) and p38, the family of MAPKs. A PKA inhibitor, blocked the protection of LC-BuOH and partially blocked LC-BuOH-induced alterations in MAPKs, suggesting that the LC-BuOH regulates MAPKs through both PKA-dependent and -independent pathways. Although PD 98059, an inhibitor of MEK which activates ERK, blocked LC-BuOH-induced ERK phosphorylation, it did not block the protection of LC-BuOH.Conclusions: LC-BuOH mediates protection by suppressing JNK/p38 instead of activating ERK activity. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

Species covered 川芎 Ligusticum chuanxiong