Yan Lu, Mahady Gail, Qian Yiyun, Song Pingping, Jian Tunyu, Ding Xiaoqin, Guan Fuqin, Shan Yu, Wei Min
Institute of Botany, Jiangsu Province and Chinese Academy of Sciences, Nanjing 210014, China.
Jiangsu Key Laboratory for Research and Utilization of Plant Resources, Nanjing 210014, China.
Evid Based Complement Alternat Med. 2020 Mar 9;2020:4845028. doi: 10.1155/2020/4845028. eCollection 2020.
Acori Tatarinowii Rhizome (ATR, the dried rhizome of Schott), a well-recognized traditional Chinese herbal medicine, is prescribed to treat neurological disorders. The essential oil is considered as the active fraction of ATR, and the neuroprotection of ATR essential oil (ATEO) is proven, including the protection against oxidative stress. However, the cellular mechanism of ATEO against oxidative stress has not been fully illustrated. In this study, to investigate the cellular mechanism of ATEO, the cytoprotective effect of ATEO against HO-induced injury was revealed in PC12 cells. ATEO treatment increased the viability of cells affected by HO-mediated injury, inhibited reactive oxygen species (ROS) accumulation, and induced the expression of several antioxidant proteins (SODs, GPx, and UCPs). The cytoprotective effect of ATEO was related to upregulation of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1) expression, which was counteracted by PGC-1 specific knockdown. Using inhibitor of protein kinase A (PKA), we found that cAMP-response element binding protein (CREB) activation was involved in ATEO-induced PGC-1 expression. Taken together, we suggest that ATEO effectively prevents HO-induced cell injury possibly through the activation of CREB/PGC-1 signaling in PC12 cells. The results provide a molecular insight into the effect of ATEO on cytoprotection against oxidative stress.
石菖蒲根茎(ATR,石菖蒲干燥根茎)是一种公认的传统中药,常用于治疗神经系统疾病。精油被认为是ATR的活性成分,且已证实ATR精油(ATEO)具有神经保护作用,包括对抗氧化应激。然而,ATEO对抗氧化应激的细胞机制尚未完全阐明。在本研究中,为了探究ATEO的细胞机制,揭示了ATEO对PC12细胞中过氧化氢(HO)诱导损伤的细胞保护作用。ATEO处理提高了受HO介导损伤影响的细胞活力,抑制了活性氧(ROS)积累,并诱导了几种抗氧化蛋白(超氧化物歧化酶、谷胱甘肽过氧化物酶和解偶联蛋白)的表达。ATEO的细胞保护作用与过氧化物酶体增殖物激活受体γ共激活因子1α(PGC-1)表达上调有关,PGC-1特异性敲低可抵消这种作用。使用蛋白激酶A(PKA)抑制剂,我们发现环磷酸腺苷反应元件结合蛋白(CREB)激活参与了ATEO诱导的PGC-1表达。综上所述,我们认为ATEO可能通过激活PC12细胞中的CREB/PGC-1信号通路有效预防HO诱导的细胞损伤。这些结果为ATEO对抗氧化应激的细胞保护作用提供了分子层面的见解。