| 肉桂醛对烟草疫霉菌的体外抑制作用 |
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| 引用本文： | 凌天孝,陈健,薛延丰,周涵君,张晓帆,付仲毅,秦燚鹤,马静,韩秋静,叶协锋.肉桂醛对烟草疫霉菌的体外抑制作用[J].中国烟草学报,2017,23(4):70-76. |
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| 作者姓名： | 凌天孝 陈健 薛延丰 周涵君 张晓帆 付仲毅 秦燚鹤 马静 韩秋静 叶协锋 |
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| 作者单位： | 1 河南农业大学烟草学院, 国家烟草栽培生理生化研究基地, 烟草行业烟草栽培重点实验室, 郑州 450002; |
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| 基金项目： | 烟草行业烟草栽培重点实验室资助项目（30800665），重庆市烟草公司“云烟品牌导向型生态优质烟叶生产技术模式构建研究与推广”（NY20140401070010） |
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| 摘 要： | 目的]为探讨肉桂醛对烟草疫霉菌的体外抑制作用。方法]以烟草疫霉菌为研究对象，研究肉桂醛作用下烟草疫霉菌菌丝的径向生长和细胞膜透性，通过菌丝ROS和PI荧光染色，进一步测定菌丝丙二醛和甘油含量。结果]（1）肉桂醛能够有效地抑制烟草疫霉菌菌丝的径向生长和破坏菌丝形态，抑制菌丝径向生长的EC50值约为0.93 mmol/L；（2）烟草疫霉菌菌丝ROS和PI荧光染色结果显示，经肉桂醛处理的菌丝，其活性氧含量增加并出现细胞死亡现象，并表现出浓度效应；（3）随着肉桂醛处理浓度的升高，烟草疫霉菌菌丝MDA和甘油含量以及细胞膜透性均呈现逐渐升高的趋势。结论]肉桂醛可能通过增加烟草疫霉菌胞内ROS含量，引发脂质过氧化反应，刺激丙二醛产生，从而使细胞膜受损，进一步导致细胞死亡，达到抑菌效果。
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| 关 键 词： | 肉桂醛 烟草疫霉菌 活性氧 细胞膜 抑菌 |
| 收稿时间： | 2017-01-05 |
Inhibition effect of cinnamaldehyde against Phytophthora nicotiance in vitro |
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| Affiliation: | 1 Tobacco Science College, Henan Agricultural University, National Tobacco Cultivation and Physiology and Biochemistry Research Centre, Key Laboratory for Tobacco Cultivation of Tobacco Industry, Zhengzhou 450002, China;2 Institute of Food Quality and Safety, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China |
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| Abstract: | Purpose] The aim of current study was to explore the inhibitory effects of Cinnamaldehyde (CA) on Phytophthora nicotiance in vitro.Methods] P. nicotiance was used in this study. The effects of CA were investigated by measuring mycelial radial growth, mycelia membrane permeability, reactive oxygen species (ROS) and propidium (PI) fluorescence staining, malondialdehyde (MDA) and glycerol content.Results] (1) CA efficiently inhibited the P. nicotiance mycelial radial growth and destroyed mycelial morphology, with an EC50 value of 0.93mmol/L. (2) CA increased mycelial ROS level and cell death incidence in a dose-dependent manner, according to ROS and PI staining results. (3) The concentration increase in CA treatment led to the increment of mycelia membrane permeability and the content of mycelial MDA and glycerol.Conclusion] CA may exhibit an antifungal effect on P. nicotiance through increasing ROS level, inducing lipid peroxidation, stimulating MDA production, damaging the mycelia membrane, and leading to cell death. |
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