Parthenolide inhibits neuroinflammation and promotes neurogenesis in the ischemic striatum following transient middle cerebral artery occlusion in the adult rat brain
10.3321/j.issn:1007-8738.2009.11.009
- VernacularTitle:Parthenolide抑制脑缺血后神经炎症并促进纹状体内神经发生
- Author:
Zhinian LEI
;
Shuilin ZENG
;
Lei WANG
;
Jianbao ZHU
;
Tao LI
- Publication Type:Journal Article
- Keywords:
stroke;
neuroinflammation;
parthenolide;
neurogenesis;
TNF-α
- From:
Journal of Cellular and Molecular Immunology
2009;25(11):994-997
- CountryChina
- Language:Chinese
-
Abstract:
AIM: The objective of this study was to test the hypothesis that parthenolide suppresses ischemia-induced neuroinflammation in the MCAO model of adult rat. METHODS: MCAO rats were treated i.p. with parthenolide (500 μg/kg). Brain sections were analyzed for BrdU, BrdU-DCX, BrdU-Tuj-1, BrdU-MAP-2 and BrdU-GFAP staining. Total protein was extracted from ischemic striatum, and Western blot was used to determine TNF-α expression. RESULTS: Cerebral ischemia increases expression of TNF-α in the ischemic striatum. Parthenolide suppressed the expression of TNF-α and enhances the proliferation of newborn cells in the ischemic striatum. The cell number of BrdU~+-DCX~+, BrdU~+-Tuj-1~+, and BrdU~+-MAP-2~+ is increased in the ischemic striatum after parthenolide treatment at 3 d, 7 d or 28 d after MCAO. Furthermore, parthenolide depressed the cell number of BrdU~+-GFAP~+ in the ischemic striatum at 3 d, 7 d and 28 d after MCAO. CONCLUSION: Parthenolide inhibits neuroinflammation induced by cerebral ischemia and promotes neurogenesis in the ischemic striatum. Further study of the effects of parthenolide on inflammatory gene expression using model animal systems as described here are critical to elucidating their mechanisms of action.
