研究报告

  • 梁刚,夏瑾,秦国华,桑楠.PM2.5暴露导致老年小鼠可逆性心肌肥大[J].环境科学学报,2018,38(8):3361-3366

  • PM2.5暴露导致老年小鼠可逆性心肌肥大
  • PM2.5 exposure induced reversible myocardial hypertrophy in aged mice
  • 基金项目:国家自然科学基金资助项目(No.21777091);广州市环境暴露与健康重点实验室开放基金资助项目(No.GZKLEEH201612);环境化学与生态毒理学国家重点实验室开放基金资助项目(No.KF2016-17)
  • 作者
  • 单位
  • 梁刚
  • 山西大学环境与资源学院, 环境与健康研究中心, 太原 030006
  • 夏瑾
  • 山西大学环境与资源学院, 环境与健康研究中心, 太原 030006
  • 秦国华
  • 1. 山西大学环境与资源学院, 环境与健康研究中心, 太原 030006;2. 暨南大学环境学院, 广州市环境暴露与健康重点实验室, 广州 510632
  • 桑楠
  • 山西大学环境与资源学院, 环境与健康研究中心, 太原 030006
  • 摘要:采用10月龄C57BL/6雌性小鼠作为实验模型,将小鼠分为对照和PM2.5染毒组两组.将染毒组小鼠采用3 mg·kg-1 PM2.5暴露4周后,分别在最后一次暴露后1 d、1周和2周处死小鼠.采用苏木素-伊红染色(H&E)对小鼠心脏组织进行观察;采用荧光定量PCR技术检测心肌肥大相关因子ANP和β-MHC及基质金属蛋白酶MMP2和MMP9的mRNA水平;并采用Western Blot技术检测TGFβ1和MMP2的蛋白表达水平.结果发现,与对照组相比,经PM2.5暴露4周后,小鼠心肌细胞核质比显著降低,心脏组织中ANP、β-MHC、MMP2和MMP9的mRNA表达水平及TGFβ1和MMP2的蛋白表达水平显著上升.停止暴露恢复1周后,小鼠心肌细胞核质比降低仍有显著差异,TGFβ1和MMP2蛋白表达水平仍显著上升,而各基因mRNA表达水平与对照组相比无显著变化.停止暴露恢复2周后,小鼠心肌细胞核质比、上述基因的mRNA和蛋白表达均无显著性差异.实验表明PM2.5暴露可导致小鼠可逆性心肌肥大,提示PM2.5所造成的心肌肥大损伤效应是可逆的,在暴露停止后机体可以通过自我修复等过程逐渐恢复正常.
  • Abstract:10-month-old C57Bl/6 female mice were divided into control and PM2.5 exposure groups. The mice in PM2.5 group were exposed to PM2.5 (3 mg·kg-1) for 4 weeks. Mice were sacrificed 24 h, one week, or two weeks after the final exposure, respectively. Histological assessments were detected by H&E stain. The mRNA levels of myocardial hypertrophy related factors (ANP and β-MHC) and matrix metalloproteinases (MMP2 and MMP9) were analysed by real-time PCR. And the protein levels of TGFβ1 and MMP2 were detected by Western Blot. The results showed that PM2.5 significantly decreased the nucleus/cytoplasm ratio, elevated the mRNA levels of ANP, β-MHC, MMP2, and MMP9 of mice hearts compared with the control group. And the protein levels of TGFβ1 and MMP2 in hearts increased significantly after PM2.5 exposure. After withdrawal from PM2.5 exposure for one week, the nucleus/cytoplasm ratio of myocardial cell in mice was significantly decreased. The protein levels of TGFβ1 and MMP2 increased significantly, while the mRNA levels were restored after withdrawal from exposure to PM2.5 for one week. All the above indexes were restored after withdrawal from exposure to PM2.5 for two weeks. The results proved that PM2.5 exposure caused a reversible myocardial hypertrophy in mice. It indicated that the myocardial hypertrophy by PM2.5 exposure is reversible. It could be recovered to normal by self-repair of organism.

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