Inhibitory effect of Sophora subprosrate polysaccharide on mitochondria oxidative stress induced by PCV-2 infection in RAW264.7 cells.
Inhibitory effect of Sophora subprosrate polysaccharide on mitochondria oxidative stress induced by PCV-2 infection in RAW264.7 cells.
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DOI：
10.1016/j.ijbiomac.2016.11.101
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发表时间：
2017-02
影响因子：
8.2
通讯作者：
Z. Su;Jian Yang;W. Luo;Ying-Yi Wei;Xue-hong Shuai;Ting‐Jun Hu
中科院分区：
文献类型：
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作者：
Z. Su;Jian Yang;W. Luo;Ying-Yi Wei;Xue-hong Shuai;Ting‐Jun Hu
本研究首次研究了苦参亚prosate多糖（sophorassubprosate多糖，SSP）对pcv -2诱导的RAW264.7细胞线粒体呼吸爆发的抑制作用。结果表明，PCV-2感染后RAW264.7细胞SOD活性和抗超氧阴离子自由基活性显著降低，MnSOD mRNA水平显著降低，NOX2 mRNA水平和蛋白表达升高。同时，O2•−水平和线粒体膜电位显著升高。经SSP处理后，PCV-2感染细胞中SOD活性、抗超氧阴离子自由基活性和MnSOD mRNA水平均显著升高。同时，NOX2 mRNA水平和蛋白表达、O2•−水平和线粒体膜电位均显著升高。结果表明，PCV2感染引起RAW264.7细胞线粒体氧化应激，表现为线粒体膜电位升高，而SSP抑制了线粒体膜电位的升高。综上所述，SSP对RAW264.7细胞的线粒体损伤可能是通过抑制线粒体膜电位介导的。
In the present study, the inhibitory effect ofSophorasubprosratepolysaccharide (SSP) on PCV-2-induced mitochondrial respiratory burst in RAW264.7 cells was first investigated. The findings suggested that SOD activity and the anti-superoxide anion radical activity of the RAW264.7 cells were significantly decreased after PCV-2 infection, and MnSOD mRNA levels were significantly decreased, while NOX2 mRNA levels and protein expression were increased. Meanwhile, the O2•−levels and mitochondrial membrane potentials were significantly increased. After treatment with SSP, significant increases in the activities of SOD, anti-superoxide anion radical activities, and MnSOD mRNA levels in the PCV-2 infected cells were observed. Meanwhile, significant increases in NOX2 mRNA levels and protein expression, O2•−levels and mitochondrial membrane potentials were also observed. The results showed that PCV2 infection resulted in the mitochondria oxidative stress of RAW264.7 cells as indicated by an increasing mitochondrial membrane potential, which was then inhibited by SSP. It was concluded that RAW264.7 cells treated with SSP could suffer from mitochondrial damage, which may be mediated by the inhibition of the mitochondrial membrane potential.