Tanshinone IIA increases levels of NeuN, protein disulfide isomerase, and Na+/K+-ATPase and decreases evidence of microglial activation after cerebral ischemic injury.

Abstract:

:This study was designed to clarify the neuroprotective effects of tanshinone IIA (TSA) following cerebral ischemic insult. Adult Sprague-Dawley rats were operated upon to achieve a middle cerebral artery occlusion to cause transient focal cerebral ischemia, which were then randomly divided into the sham-operated control group and cerebral ischemia/reperfusion (I/R) groups receiving a 2 h occlusion. The treatment groups received daily intraperitoneal injections of high or low doses of TSA, for 7 or 15 days. NeuN immunostaining revealed neuronal loss following I/R, which was partially prevented with subsequent TSA dosing. Protein disulfide isomerase and adenosine triphosphatase (Na(+)/K(+)-ATPase) levels were all depressed by means of I/R. TSA treatment markedly reversed the depression of all indices examined. The intensity of microglial activation, as evidenced with CD11b staining, was increased by means of cerebral artery occlusion, but this was partially reversed with subsequent TSA treatment. TSA may affect neuroprotection by way of minimizing deficits in energy metabolism and reduction of the extent of cell death within affected regions.

journal_name

Neuroreport

journal_title

Neuroreport

authors

Wen PY,Li J,Lu BL,Liu J,Yang FZ,Zhou L,Luo H,Li WW,Zhou J

doi

10.1097/WNR.0000000000000559

subject

Has Abstract

pub_date

2016-04-13 00:00:00

pages

435-44

issue

6

eissn

0959-4965

issn

1473-558X

journal_volume

27

pub_type

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