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| Effect of amiodarone on oxidative stress of fibroblasts and the intervention effect of panax notoginseng saponin R1 |
| TU Mengyun1,2, WANG Zhiyi3, WAN Xinlong4, WENG Jie3, XIE Mengying5, ZHENG Xiaoqun1,2 |
| 1.Department of Clinical Laboratory, the Second Affiliated Hospital & Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, 325027; 2.School of Laboratory Medical and Life Science, Wenzhou Medical University, the Key Laboratory of Laboratory Medicine of Ministry of Education, Wenzhou, 325035; 3.Department of General Practice, the Second Affiliated Hospital & Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, 325027; 4.Institute of Health & Environmental Ecology, Wenzhou Medical University, Wenzhou, 325035; 5.Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325015 |
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| Cite this article: |
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TU Mengyun,WANG Zhiyi,WAN Xinlong, et al. Effect of amiodarone on oxidative stress of fibroblasts and the intervention effect of panax notoginseng saponin R1[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2018, 48(11): 786-790.
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Abstract Objective: To study the effects of different concentrations of Notoginsenoside R1 on amiodarone-induced damage to human embryonic lung fibroblasts (HELFs). Methods: The HELFs were exposed to amiodarone in vitro. The experiment was divided into control group, amiodarone group, Notoginsenoside R1 intervention group and Notoginsenoside R1 control group. The morphological changes of cells were observed by inverted phase contrast microscope, CCK8 kit was used to observe cell proliferation activity, the level of reactive oxygen species (ROS) was measured by fluorescence microscope and fluorescence cytometry, enzyme bioassay was used to detect superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. Results: When amiodarone was exposed to cells, the morphology of the cells was changed. After the intervention of Notoginsenoside R1, the cells showed no obvious morphological changes. Compared with the control group, amiodarone caused increased cell proliferation activity, increased intracellular ROS activity, decreased SOD activity and increased MDA content (P<0.05). Compared with amiodarone group, a certain concentration of Notoginsenoside R1 inhibited cell proliferation, reduced ROS activity and MDA levels and increased SOD activity (P<0.05). Conclusion: Amiodarone can induce cell proliferation and oxidative stress in HELFs, and Notoginsenoside R1 has a protective effect on it.
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Received: 01 August 2018
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