Mechanism of Non-receptor Tyrosine Kinase Src Regulating Neuroinflammation Through Phosphatase and Tensin Homology Protein in Microglia.
10.3881/j.issn.1000-503X.2017.04.012
- Author:
Sheng-Nan CAO
1
;
Wen-Wen YU
1
;
Cai-Xia ZANG
1
;
Xiu-Qi BAO
1
;
Hua SUN
1
;
Dan ZHANG
1
Author Information
1. State Key Laboratory of Natural Products and Functions,Institute of Materia Medica,CAMS and PUMC,Beijing 100050,China.
- Publication Type:Journal Article
- From:
Acta Academiae Medicinae Sinicae
2017;39(4):534-538
- CountryChina
- Language:English
-
Abstract:
Objective To investigate the mechanism of non-receptor tyrosine kinase Src regulating neuroinflammation through phosphatase and tensin homology protein(PTEN)in microglia. Methods BV2 cells were incubated with PTEN inhibitor bpv(HOpic)for 2 hours,and then added with lipopolysaccharide(LPS)to induce neuroinflammation,Western blot was performed to determine the expression of phosphorylated protein kinase B(Akt)to investigate the activity of PTEN. Enzyme-linked immunosorben assay(ELISA)was used to determine the release of tumor necrosis factor α(TNF-α)to assess neuroinflammation.After PTEN inhibitor or Src specific small interfering RNA was added,the change of neuroinflammation was evaluated to study the mechanism of Src regulating neuroinflammation. Results LPS induced significant neuroinflammation in BV2 cells,as indicated by significantly increased expression of p-Akt and release of TNF-α(P<0.001).The PTEN inhibitor signficantly increased Akt phosphorylation(P<0.05)and TNF-α release(P<0.001)in LPS-induced BV2 cells compared to simply LPS-induced cells.The Src small interfering RNA significantly decreased the release of TNF-α(P<0.001)and inhibited PTEN(P<0.001)and Akt(P<0.001)phosphorylation. Conclusion Src kinase may regulate neuroinflammtion response in BV2 cells by regulating the phosphorylation of PTEN.
