Salvianolic acid B alleviate the disruption of blood-brain barrier in rats after cerebral ischemia-reperfusion by inhibiting MAPK pathway.
- Author:
Qin LI
1
;
Li-pei HAN
;
Ze-hui LI
;
Jun-tian ZHANG
;
Min-ke TANG
Author Information
1. Beijing University of Chinese Medicine, Beijing 100102, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Benzofurans;
isolation & purification;
pharmacology;
Blood-Brain Barrier;
drug effects;
metabolism;
Brain Ischemia;
etiology;
metabolism;
pathology;
Drugs, Chinese Herbal;
isolation & purification;
pharmacology;
Infarction, Middle Cerebral Artery;
complications;
MAP Kinase Kinase Kinase 1;
metabolism;
MAP Kinase Signaling System;
drug effects;
Male;
Matrix Metalloproteinase 9;
metabolism;
Nitric Oxide Synthase Type II;
metabolism;
Phosphorylation;
Plants, Medicinal;
chemistry;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Reperfusion Injury;
metabolism;
pathology;
Salvia miltiorrhiza;
chemistry;
p38 Mitogen-Activated Protein Kinases;
metabolism
- From:
Acta Pharmaceutica Sinica
2010;45(12):1485-1490
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the study is to investigate the effect of salvianolic acid B (SalB) on blood-brain barrier (BBB) in rats after cerebral ischemia-reperfusion, and to illustrate its possible mechanisms. Cerebral ischemia-reperfusion was induced by middle cerebral artery occlusion in rats. The break-down of BBB was indicated by extravasations of immunoglobulin (IgG) monitored with immunohistochemistry. The expression of MMP-9 and NOS2 in the brain was determined by immunohistochemistry, and the expression of p-p38 and p-ERK1/2 was detected by Western blotting. It was shown that on day 2 after ischemia-reperfusion the IgG accumulated around the vascular boundary zone, suggesting the break-down of BBB, and the expression of MMP-9 and NOS2 up-regulated at the same time. The result of Western blotting suggested that the expression of p-p38 and p-ERK1/2 increased. On day 7 after ischemia-reperfusion the. expression of MMP-9 and NOS2 was about the same level as day 2, the expression of p-p38 was higher than that on day 2 and the expression of p-ERK1/2 was slightly lower than that on day 2. SalB (1 and 10 mg x kg(-1)) significantly alleviated the extravasations of immunoglobulin induced by cerebral ischemia-reperfusion (P < 0.05). On day 2 and day 7 SalB attenuated the expression of MMP-9 and NOS2 (P < 0.05). SalB (10 mg x kg(-1)) reduced the expression of p-p38 and p-ERK1/2 apparently on day 2 and 7 after ischemia-reperfusion (P < 0.05). SalB (1 mg x kg(-1)) inhibited the expression of p-p38 on day 7 after ischemia-reperfusion (P < 0.05). The results indicate that SalB protects blood-brain barrier in rats after cerebral ischemia-reperfusion by inhibiting the MAPK pathway.
