COX2-PGI2/TXA2 signal pathway involved in protective mechanism of PDTC pretreatment against global cerebral ischemia reperfusion rat hippocampus injury
10.3969/j.issn.1001-1978.2014.06.010
- VernacularTitle:NF-κB抑制剂PDTC保护全脑缺血/再灌注大鼠海马损伤机制涉及COX2-PGI2/TXA2通路的初探
- Author:
Jia WANG
;
Junqing YANG
;
Lijuan YU
;
Bin YANG
;
Lei ZHAO
;
Qingsong JIANG
- Publication Type:Journal Article
- Keywords:
global cerebral ischemia reperfusion;
hip-pocampus;
NF-κB;
COX2;
PDTC;
prostacyclin;
thromboxane A2
- From:
Chinese Pharmacological Bulletin
2014;(6):782-786
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effects and mecha-nism of nuclear factor-κ B inhibitor, PDTC, on global cerebral ischemia reperfusion ( GCIR ) rat hippocam-pus. Methods Forty-eight adult male Sprague-Daw-ley rats were randomly divided into one control group receiving sham operation and three experimental groups all receiving global cerebral ischemia for 20 min. In PDTC 100 mg·kg-1 group ( P100 ) and PDTC 200 mg ·kg-1 group ( P200 ) , PDTC 100 mg · kg-1 or PDTC 200 mg·kg-1 was injected ip one hour before ischemi-a respectively. Spatial learning and memory function of rats were tested using Morris water maze. HE staining was employed to observe pathological changes of hipp-ocampal neurons. Expression of COX2 was measured by Western blot, and the content of PGI2 and TXA2 in
rat hippocampus was detected by enzyme-linked immu-nosorbent assay. Results A significant increase of es-cape latency was observed in GCIR group compared to the sham operation group(P<0.05). PDTC 100 mg· kg-1 and PDTC 200 mg · kg-1 significantly reduced escape latency ( P <0.05 ) and histopathological injury in CA1 region of hippocampus. PDTC 100 mg · kg-1 and PDTC 200 mg · kg-1 also reduced COX2 expres-sion, PGI2 content, TXA2 content and PGI2/TXA2 . Conclusion Pretreatment with PDTC can protect hip-pocampus from GCIR injury through inhibition of COX2 expression and PGI2/TXA2 .
