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2024, Vol. 28 ›› Issue (28): 4547-4552

Neuroprotective mechanism by which fenofibrate regulates superoxide dismutase 2 expression in transgenic C57BL/6J mice

Ma Jianglei1, Zhang Huijie2, Zhang Chenfang3, Yang Xitong1, 4, Cheng Jianjie1, Wang Guangming1, 4   

  1. 1School of Clinical Medicine, Dali University, Dali 671000, Yunnan Province, China; 2Department of Obstetrics, 3Department of Neurology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai 264000, Shandong Province, China; 4Center of Genetic Testing, The First Affiliated Hospital of Dali University, Dali 671000, Yunnan Province, China

  • Received:2023-07-24 Accepted:2023-08-18 Online:2024-10-08 Published:2023-11-27

  • Contact: Wang Guangming, MD, Professor, Doctoral supervisor, School of Clinical Medicine, Dali University, Dali 671000, Yunnan Province, China; Center of Genetic Testing, The First Affiliated Hospital of Dali University, Dali 671000, Yunnan Province, China

  • About author:Ma Jianglei, Master candidate, Attending physician, School of Clinical Medicine, Dali University, Dali 671000, Yunnan Province, China

  • Supported by:

    National Natural Science Foundation of China, No. 82160244 (to WGM); Joint Project of Local Colleges and Universities in Yunnan Province, No. 202001BA070001-156 (to CJJ); Medical Discipline Leader Program of Yunnan Provincial Health Planning Commission, No. D-2017057 (to WGM); Yunnan Provincial Department of Education Science Research Fund Project, No. 2023Y0989 (to MJL); Key Construction Disciplines of the First Affiliated Hospital of Dali University, No. (2021)34 (to WGM)


Abstract: BACKGROUND: Oxidative injury is considered to be one of the important factors of cerebral ischemia-reperfusion injury. Superoxide dismutase 2 (SOD2) is a key mitochondrial antioxidant molecule, and fenofibrate can regulate the expression of SOD2 by activating peroxisome proliferator-activated receptor α.
OBJECTIVE: To explore whether the mechanism of fenofibrate in the treatment of cerebral ischemia-reperfusion injury depends on the expression of SOD2.
METHODS: The TALENs system was used to construct SOD2 transgenic mice. The transgenic mice were genotyped by PCR and DNA sequencing techniques. The expression of SOD2 protein in transgenic mice was detected by western blot assay. Wild-type and SOD2 transgenic mice were randomly divided into four groups: wild-type control group (n=6), wild-type fenofibrate group (n=6), SOD2 transgenic control group (n=5) and SOD2 transgenic fenofibrate group (n=5). A mouse model of middle cerebral artery occlusion was prepared using the suture-occlusion method. After 90 minutes of ischemia, the thread was removed to reperfuse cerebral blood flow for 30 minutes. A cerebral blood flow monitor was used to monitor local cerebral blood flow. Brain tissue slices were taken for 2,3,5-triphenyltetrazolium chloride staining to analyze the situation of cerebral infarction in each group.
RESULTS AND CONCLUSION: After PCR and DNA sequencing analysis, nine SOD2+/+ transgenic mice were successfully constructed. After cerebral ischemia-reperfusion, the wild-type fenofibrate group showed partial recovery of cerebral blood flow and significantly reduced cerebral infarction volume compared with the wild-type control group (P < 0.001). There was no significant difference in cerebral blood flow and cerebral infarction volume between the SOD2 transgenic fenofibrate group and the SOD2 transgenic control group. The SOD2 transgenic control was superior to the wild-type control group in terms of improving cerebral blood flow and cerebral infarction (P < 0.001). There were also no significant differences in cerebral blood flow and cerebral infarction volume between the wild-type fenofibrate group and the SOD2 transgenic control group and between the wild-type fenofibrate group and the SOD2 transgenic fenofibrate group. To conclude, the expression of SOD2 is one of the mechanisms of fenofibrate in the treatment of cerebral ischemia-reperfusion injury.

Key words: cerebral ischemia-reperfusion injury, fenofibrate, superoxide dismutase 2, oxidative stress, cerebral infarction, neuroprotection


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