Baicalein reduces Aβ25-35-induced PC12 cell damage by inhibiting the JAK2/STAT1 pathway
10.16438/j.0513-4870.2020-1270
- VernacularTitle:黄芩素通过抑制JAK2/STAT1通路减轻Aβ25-35诱导的PC12细胞损伤
- Author:
Wen-ge ZHENG
1
,
2
;
Feng ZHOU
1
,
2
;
Li GAO
1
;
Xue-mei QIN
1
Author Information
1. Modern Research Center for Traditional Chinese Medicine, Shanxi University, Taiyuan 030006, China
2. College of Chemistry and Chemical Engineering, Shanxi University, Taiyuan 030006, China
- Publication Type:Research Article
- Keywords:
baicalein;
PC12 cell;
JAK2/STAT1 pathway;
inflammation
- From:
Acta Pharmaceutica Sinica
2021;56(3):771-777
- CountryChina
- Language:Chinese
-
Abstract:
This study investigated the mechanism by which baicalein protected PC12 cells from Aβ25-35-induced injury. PC12 cells were treated with Aβ25-35 (20 μmol·L-1) and the ability of baicalein to prevent apoptosis was investigated by monitoring changes in cell morphology, Hoechst 33342 staining, and measurement of inflammatory factors. Western blotting was used to detect the expression of the apoptosis-related proteins cysteinyl aspartate specific proteinase-3 (caspase-3), cleaved cysteinyl aspartate specific proteinase-3 (cleaved caspase-3), proteins involved in the Janus kinase 2/signal transducer and activator of transcription 1 (JAK2/STAT1) pathway, and downstream inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). The results show that baicalein (80 μmol·L-1) can significantly inhibit apoptosis and the release of inflammatory factor IL-8 and TNF-α in Aβ25-35-treated PC12 cells. Western blotting results showed that baicalein can inhibit the phosphorylation of JAK2 and STAT1 and decrease the expression of downstream iNOS and COX-2, thereby inhibiting the JAK2/STAT1 signaling pathway and preventing Aβ25-35-induced PC12 cell damage.
