Acta Veterinaria et Zootechnica Sinica ›› 2022, Vol. 53 ›› Issue (12): 4429-4438.doi: 10.11843/j.issn.0366-6964.2022.12.028

• BASIC VETERINARY MEDICINE • Previous Articles     Next Articles

Effects of P7C3-A20 on Apoptosis and Oxidation of PC12 Cells in Traumatic Brain Injury

YANG Zhiqing1, ZHANG Haoquan1, XIAN Runxi1, LI Xinran1,2*   

  1. 1. College of Life Science and Engineering, Foshan University, Foshan 528225, China;
    2. Foshan University Veterinary Teaching Hospital, Foshan 528225, China
  • Received:2022-03-14 Online:2022-12-23 Published:2022-12-25

Abstract: The study was conducted to explore the repair effect of 3, 6-Dibromo-beta-fluoro-N-(3-methoxyphenyl)-9H-carbazole-9-propanamine (P7C3-A20) on traumatic brain injury (TBI) of rat adrenal medullary pheochromoma differentiated cell line (PC12 cells). The cells were divided into control group (group A), model group (group B) and 0.03 μmol·L-1 drug treatment group (Group C), 0.3 μmol·L-1 drug treatment group (Group D), 3 μmol·L-1 drug treatment group (Group E) and drug control group (Group F). TBI cell models were prepared by scribing straight lines 4 mm apart horizontally and vertically using a 10 μL gun tip. The cell viability was detected by CCK8 kit, the apoptosis and reactive oxygen (ROS) situation were observed by fluorescence microscope, and the relative mRNA expression of cysteine aspartate-specific protease-3 (Caspase-3), B-cell lymphoma/leukemia-2 (Bcl-2), Heme Oxygenase-1 (HO-1), NAD (P) H: quinone oxidoreductase 1 (NQO1) and glutamate-cysteine ligase catalytic subunit (GCLC) genes were detected by fluorescence quantitative PCR instrument. The results showed that the cell viability was extremely significantly decreased after TBI modeling (P<0.01). P7C3-A20 at concentrations of 0.03 μmol·L-1 could significantly increase the cell viability after TBI (P<0.05). P7C3-A20 at a concentration of 0.3 μmol·L-1 could extremely significantly increase the cell viability after TBI (P<0.01). After TBI modeling, the proportion of early and late apoptotic cells increased extremely significantly (P<0.01). P7C3-A20 at a concentration of 0.03 μmol·L-1 could significantly reduce the proportion of early apoptotic cells after TBI (P<0.05), and extremely significantly reduce the proportion of late apoptotic cells after TBI (P<0.01), P7C3-A20 at concentrations of 0.3 and 3 μmol·L-1 could extremely significantly reduce the proportion of early and late apoptotic cells after TBI (P<0.01). After TBI modeling, the proportion of reactive oxygen species increased extremely significantly (P<0.01). P7C3-A20 at concentrations of 0.03 and 3 μmol·L-1 could significantly reduce the proportion of reactive oxygen species after TBI (P<0.05), 0.3 μmol·L-1 concentration of P7C3-A20 can significantly reduce the proportion of reactive oxygen species after TBI (P<0.01). P7C3-A20 at a concentration of 0.3 μmol·L-1 can extremely significantly reduce the relative mRNA expression of Caspase-3 after TBI (P<0.01), and significantly increase the relative mRNA expression of Bcl-2, HO-1, NQO1 and GCLC genes expression level after TBI (P<0.05). P7C3-A20 has the repair effect of anti apoptosis and reducing oxidative stress on PC12 cells after traumatic brain injury.

Key words: P7C3-A20, PC12 cells, traumatic brain injury, apoptosis, oxidative stress

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