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Effects of miR-301a-3p on the apoptosis and proliferation of astrocytes in rats / 中华行为医学与脑科学杂志
Chinese Journal of Behavioral Medicine and Brain Science ; (12): 303-307, 2020.
Article in Chinese | WPRIM | ID: wpr-867059
ABSTRACT

Objective:

To explore the effects of miR-301a-3p on proliferation and apoptosis of astrocytes in rats.

Methods:

miR-301a-3p agomir and miR-301a-3p antagomir were synthetized and transfected into astrocytes. The cells were divided into Blank group, miR-NC group, miR-301a agomir group and antagomir group.Each group has 3 multiple pores, 2×10 5 cells per pore. CCK8 method was used to detect proliferation and growth ability of astrocytes in each group. Anncxin V-FITC/PI cytometry and Caspase-3 were used to test apoptosis of cells in each group.

Results:

Compared with Blank group (48 h 0.83±0.09; 72 h 1.20±0.21; 96 h 1.65±0.17) and miR-NC group (48 h 0.79±0.10; 72 h 1.12±0.25; 96 h 1.60±0.15), the proliferation ability of miR-301a group (48 h 1.16±0.07; 72 h 1.56±0.11; 96 h 2.13±0.14) was significantly improved ( P<0.05), and the apoptosis rate of miR-301a group decreased significantly (Blank group 10.44±1.33, miR-NC group 9.84±1.40, miR-301a group 4.32±0.51, P<0.05). Compared with Blank group and miR-NC group, the proliferation ability of the cells in antagomir group (48 h 0.52±0.12; 72 h 0.72±0.09; 96 h 1.01±0.15) decreased significantly ( P<0.05), and the apoptotic rate was significantly increased in the antiagor group (Blank group 10.44±1.33, miR-NC group 9.84±1.40, antiagor group 21.41±2.57, P<0.05).

Conclusion:

miRNA-301a-3p hyperexpression can promote the proliferation of astrocytes and inhibit the apoptosis pathway, thereby regulating the biological function of rat astrocytes.
Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Behavioral Medicine and Brain Science Year: 2020 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Behavioral Medicine and Brain Science Year: 2020 Type: Article