The Journal of Practical Medicine ›› 2022, Vol. 38 ›› Issue (19): 2419-2423.doi: 10.3969/j.issn.1006⁃5725.2022.19.008

• Basic Research • Previous Articles     Next Articles

Effect of calycosin on proliferation and apoptosis of H2O2 ⁃ induced oxidative damaged astrocytes

XU Yang*,WU Chenglin,GUO Dehua,ZHANG Guofu.   

  1. Graduate SchoolJiangxi University of Traditional Chinese MedicineNanchang 330004China

  • Online:2022-10-10 Published:2022-10-10
  • Contact: ZHANG Guofu E⁃mail:zgf8613@163.com

Abstract:

Objective To investigate the effect of rissoflavones on proliferation and apoptosis of H2O2 ⁃ induced oxidative damage⁃induced astrocyte. Methods Astrocytes of SD neonatal rat were isolatedafter treating astrocytes with 51020 μmol/L isoflavones for 12 hand adding H2O2 for 24 h to induce oxidative damage modelthe cell proliferation in each group was detected by CCK8 method. In order to screen the appropriate treatment concentration of mulleinthe experiment was divided into control groupH2O2100 μmol/Lmodel groupH2O2 100 μmol/L+ Calycosin20 μmol/Lintervention groupCCK8 method was used to detect the effect on the proliferation of astrocytesFlow cytometry was used to detect astrocyte apoptosisimmunofluorescence was used to detect the level of Brdu in each group of cell samplesWestern blot was used to detect the protein expression of p⁃AKTGP130 and IL⁃6 in each group of cells. Results Compared with the control groupthe proliferation activity of astrocytes in the H2O2 group was decreasedthe degree of apoptosis was aggravatedand the protein expressions of p⁃AKTGP130 and IL⁃6 were significantly increasedP < 0.05. After treatmentthe proliferation activity of astrocytes was significantly increasedand the apoptosis was effectively inhibitedand the protein expressions of p⁃AKTGP130 and IL⁃6 were down⁃regulatedP < 0.05. Conclusion Calycosin could promote the proliferation of H2O2 ⁃ induced oxidatively damaged astrocytes and inhibit their apoptosis by inhibiting the PI3K/Akt signaling pathway.

Key words: calycosin,  , oxidative damage,  , astrocytes,  , pi3k/akt signaling pathway