标题：Effects of Baicalin on Protease-Activated Receptor-1 Expression and Brain Injury in a Rat Model of Intracerebral Hemorrhage
作者：Zhou, Qing-Bo; Jia, Qing; Zhang, Yuan; Li, Lu-Yang; Chi, Zhao-Fu; Liu, Ping
作者机构：[Zhou, Qing-Bo; Zhang, Yuan] Shandong Univ, Hosp 2, Dept Neurol, Jinan 250033, Shandong, Peoples R China.; [Jia, Qing] Shangdong Acad Med Sci, Inst 更多
通讯作者地址：[Zhou, QB]Shandong Univ, Hosp 2, Dept Neurol, 247 Beiyuan St, Jinan 250033, Shandong, Peoples R China.
来源：CHINESE JOURNAL OF PHYSIOLOGY
关键词：baicalin; intracerebral hemorrhage; protease-activated receptor;; neuroprotection
摘要：Baicalin, a major flavonoid compound isolated from the dry roots of Scutellaria baicalensis Georgi, has been shown to be neuroprotective after ischemic brain injury. However, little is known about its effects on brain injury following intracerebral hemorrhage (ICH). In this study, we evaluated the effects of baicalin on ICH-induced brain injury in an ICH rat model. Male Wistar rats were injected intracerebrally with 0.5 U collagenaseVII to induce ICH, while control rats were injected with an equal volume of saline. After ICH induction, the rats were randomly divided into four groups and treated with baicalin at different doses (0, 25, 50 or 100 mg/kg) through peritoneal injection. The control rats were injected with an equal volume of vehicle. Brain tissues around the hemorrhage areas were collected on day 1, 3, 5 and 10 after treatment. Brain water content was analyzed by desiccation method; mRNA and protein levels of brain protease-activated receptor-1 (PAR-1) were determined by RT-PCR and Western blot, respectively; cell apoptosis was evaluated by terminal transferase dUTP nick end labeling staining. The results showed that baicalin effectively attenuated brain edema and inhibited cell apoptosis following ICH in a dose- and time-dependent manner, with concomitant suppression of PAR-1 expression at both the mRNA and protein levels. These findings indicate that baicalin has protective effects on ICH-induced brain injury. The effects of baicalin may involve a mechanism of inhibition of PAR-1 expression.