Effects of Silencing RND3 Expression on the Inflammatory Response and Apoptosis of Hippocampal Neurons Injured by Oxygen Glucose Deprivation/Reoxygenation

Jun-jie LI; Hai-yan JIANG; Wen-ya BAI; Si-ying HUO; Zhi-sheng SUN; Jian-lin SHAO

doi:10.12259/j.issn.2095-610X.S20211012

Volume 42 Issue 10

Oct. 2021

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Jun-jie LI, Hai-yan JIANG, Wen-ya BAI, Si-ying HUO, Zhi-sheng SUN, Jian-lin SHAO. Effects of Silencing RND3 Expression on the Inflammatory Response and Apoptosis of Hippocampal Neurons Injured by Oxygen Glucose Deprivation/Reoxygenation[J]. Journal of Kunming Medical University, 2021, 42(10): 14-21. doi: 10.12259/j.issn.2095-610X.S20211012

Citation:

Jun-jie LI, Hai-yan JIANG, Wen-ya BAI, Si-ying HUO, Zhi-sheng SUN, Jian-lin SHAO. Effects of Silencing RND3 Expression on the Inflammatory Response and Apoptosis of Hippocampal Neurons Injured by Oxygen Glucose Deprivation/Reoxygenation[J]. Journal of Kunming Medical University, 2021, 42(10): 14-21. doi: 10.12259/j.issn.2095-610X.S20211012

Citation:

Jun-jie LI, Hai-yan JIANG, Wen-ya BAI, Si-ying HUO, Zhi-sheng SUN, Jian-lin SHAO. Effects of Silencing RND3 Expression on the Inflammatory Response and Apoptosis of Hippocampal Neurons Injured by Oxygen Glucose Deprivation/Reoxygenation[J]. Journal of Kunming Medical University, 2021, 42(10): 14-21. doi: 10.12259/j.issn.2095-610X.S20211012

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Effects of Silencing RND3 Expression on the Inflammatory Response and Apoptosis of Hippocampal Neurons Injured by Oxygen Glucose Deprivation/Reoxygenation

doi: 10.12259/j.issn.2095-610X.S20211012

1.
Dept. of Anesthesiology, The 1st Affiliated Hospital of Kunming Medical University, Kunming Yunnan 650032
2.
Dept. of Anesthesiology, Mengzi People’s Hospital, Mengzi Yunnan 661100, China

Received Date: 2021-07-26
Available Online: 2021-10-29
Publish Date: 2021-10-30

Abstract

Abstract

Objective To investigate the protective effect of silencing Rho family GTPase3 （RND3） expression against oxygen glucose deprivation/reoxygenation （OGD/R） injury in hippocampal neurons via inhibiting inflammation and apoptosis and its mechanism. Methods The OGD/R model was established after transfecting cells with lentiviral vectors containing the short hairpin RNA of silencing RND3 gene expression （shRND3） and its negative control （shRND3-NC） sequence. CCK-8 assay was used to detect cell viability. RT-qPCR was used to detect the gene expression of RND3 and inflammation-related and apoptotic molecules. ELISA was used to detect the protein concentration of inflammatory factors in the supernatant of cell culture. Western blot was used to detect the protein expression of RND3, apoptotic proteins and NF-κB of cell nucleus.Cell apoptosis rate was determined by Annexin V-FITC/PI staining and flow cytometry. Results Compared with normal cells, the cell viability was decreased after OGD/R injury, the expression of inflammatory factors and NF-κB was increased, the expression of pro-apoptotic proteins was increased, the expression of anti-apoptotic proteins was decreased, and the apoptosis rate of cells was increased. While compared with the negative RND3 silencing group, the cell viability was increased, the expression of inflammatory factors and NF-κB were decreased, the expression of pro-apoptotic protein was decreased, the expression of anti-apoptotic protein was increased, and the apoptosis rate of cells was decreased. Conclusion Silencing RND3 alleviates OGD/R injury in hippocampal neurons via inhibiting inflammatory response and apoptosis and the mechanism of inhibiting the inflammatory response by silencing RND3 may be related to the inhibition of NF-κB pathway.
- Rho family GTPase 3,
- Oxygen glucose deprivation/reoxygenation,
- Inflammation,
- Apoptosis,
- NF-κB pathway

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References(23)

References

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