In:
Microcirculation, Wiley, Vol. 21, No. 7 ( 2014-10), p. 615-627
Kurzfassung:
TSI is a new drug derived from Chinese medicine for treatment of ischemic stroke in China. The aim of this study was to verify the therapeutic effect of TSI in a rat model of MCAO , and further explore the mechanism for its effect. Methods Male Sprague–Dawley rats were subjected to right MCAO for 60 minutes followed by reperfusion. TSI (1.67 mg/kg) was administrated before reperfusion via femoral vein injection. Twenty‐four hours after reperfusion, the fluorescence intensity of DHR 123 in, leukocyte adhesion to and albumin leakage from the cerebral venules were observed. Neurological scores, TTC staining, brain water content, Nissl staining, TUNEL staining, and MDA content were assessed. Bcl‐2/Bax, cleaved caspase‐3, NADPH oxidase subunits p47 phox /p67 phox /gp91 phox , and AMPK /Akt/ PKC were analyzed by Western blot. Results TSI attenuated I/R‐induced microcirculatory disturbance and neuron damage, activated AMPK , inhibited NADPH oxidase subunits membrane translocation, suppressed Akt phosphorylation, and PKC translocation. Conclusions TSI attenuates I/R‐induced brain injury in rats, supporting its clinic use for treatment of acute ischemic stroke. The role of TSI may benefit from its antioxidant activity, which is most likely implemented via inactivation of NADPH oxidase through a signaling pathway implicating AMPK /Akt/ PKC .
Materialart:
Online-Ressource
ISSN:
1073-9688
,
1549-8719
DOI:
10.1111/micc.2014.21.issue-7
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2014
ZDB Id:
2008083-9
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