Monday, October 28, 2013

Salvianolate increases heat shock protein expression in a cerebral ischemia-reperfusion injury model

Researchers still haven't figured out that you measure objective results rather than the nebulous(were significantly better) crap these ones are doing.
http://d.wanfangdata.com.cn/periodical_zgsjzsyj-e201325003.aspx
Abstract:
Stroke remains a worldwide health problem. Salvianolate exerts a protective effect in various microcirculatory disturbance-related diseases, but studies of the mechanisms underlying its protective action have mainly focused on the myocardium, whereas little research has been carried out in brain tissue following ischemia-reperfusion. We assessed the neuroprotective effects of salvianolate in a rat model of cerebral ischemia-reperfusion injury induced using the suture method. At onset and 24 and 48 hours after reperfusion, rats were intraperitoneal y injected with salvianolate (18 mg/kg) or saline. Neurological deficit scores at 72 hours showed that the neurological functions of rats that had received salvianolate were significantly better than those of the rats that had received saline. 2,3,5-Triphenyltetrazolium chloride was used to stain cerebral tissue to determine the extent of the infarct area. A significantly smaller infarct area and a significantly lower number of apoptotic cel s were observed after treatment with salvianolate compared with the saline treatment. Expression of heat shock protein 22 and phosphorylated protein kinase B in ischemic brain tissue was significantly greater in rats treated with salvianolate compared with rats treated with saline. Our findings suggest that salvianolate provides neuroprotective effects against cerebral ischemia-reperfusion injury by upregulating heat shock protein 22 and phosphorylated protein kinase B expression.
Author: Jinnan Zhang    Wei Lu    Qiang Lei    Xi Tao    Hong You    Pinghui Xie

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