P38MAPK pathway regulates COX-2 and caspase-3 expression in a mouse model of Parkinson disease.
- Author:
Zi-feng WEI
1
;
Yong-sheng WANG
;
Li-ren MA
;
Qian WANG
;
Zuo-feng ZHANG
;
Yu-xin ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Caspase 3; genetics; metabolism; Cyclooxygenase 2; genetics; metabolism; Male; Mice; Mice, Inbred C57BL; Parkinson Disease; metabolism; Signal Transduction; Substantia Nigra; metabolism; p38 Mitogen-Activated Protein Kinases; metabolism
- From: Journal of Southern Medical University 2009;29(10):2010-2017
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of p38 mitogen-activated protein kinase (p38MAPK) on the expression of COX-2 and caspase-3 in the substania nigra (SN) of mice with MPTP-induced Parkinson disease (PD).
METHODSC57BL/CN mice were treated with MPTP to prepare a subacute PD model, and their behavioral changes following the treatment were observed. Immunohistochemistry and Western blotting were performed to detect the expression of tyrosine hydroxylase (TH), COX-2 and phosphorylation of P38MAPK in the SN and their changes following treatment with SB203580, a specific inhibitor of P38MAPK.
RESULTSThe 7-day model group showed typical symptoms of PD with decrements of TH-positive neurons and TH protein level in the SN of the midbrain by about 65% and 75%, respectively (P<0.01). In the 3-day model group, the COX-2-, caspase-3- and phosphorylated P38MAPK-immunoreactive cells and their protein levels in the SN increased markedly with obvious loss of TH-positive neurons. Administration of SB203580 obviously lessened the above changes (P<0.01).
CONCLUSIONP38MAPK regulates the inflammation and apoptosis in the SN of the mouse model of subacute PD, and SB203580 may provide some neuroprotective effect.