Salvianolic acid B attenuates spinal cord ischemia-reperfusion-induced neuronal injury and oxidative stress by activating the extracellular signal-regulated kinase pathway in rats

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• 作者：Jun Fu ; PhD¹ ; Hong-bin Fan ; PhD¹ ; Zheng Guo ; PhD ; MD ; ^{fmmuguozheng@163.com" class="auth_mail} ; Zhen Wang ; PhD ; MD ; ^{fmmuwangzhen@163.com" class="auth_mail} ; Xiang-dong Li ; MD ; Jing Li ; MD ; Guo-xian Pei ; PhD ; MD
• 关键词：Salvianolic acid B ; Ischemia-reperfusion injury ; Neuroprotection ; Oxidative stress
• 刊名：Journal of Surgical Research
• 出版年：1 May, 2014
• 年：2014
• 卷：188
• 期：1
• 页码：222-230
• 全文大小：2121 K

文摘

Background

Salvianolic acid B (SalB), the main bioactive compound isolated from the traditional Chinese medicinal herb broad Radix Salviae Miltiorrhizae exerts a spectrum of pharmacologic activities. We investigated the effects of SalB treatment in a rat model of spinal cord ischemia and reperfusion (I/R) injury and the underlying mechanism.

Materials and methods

SalB was administered at 1, 10, or 50聽mg/kg after spinal cord ischemia. The potential protective effects on spinal cord injury were determined by spinal cord edema, infarct volume, and motor function assessment of the hind limbs.

Results

SalB treatment significantly decreased spinal cord edema and infarct volume and preserved motor function of the hind limbs in a dose-dependent manner. SalB administration ameliorated the generation of oxidative products and preserved antioxidant defense activities in the injured spinal cord at both 4 and 24聽h after I/R injury. Moreover, SalB prolonged the I/R injury-induced activation of extracellular signal-regulated kinase (ERK), and blocking ERK activation with PD98059 partially prevented the neuroprotective effects of SalB.

Conclusions

These findings demonstrate the neuroprotective effects of SalB in a spinal cord I/R injury model and suggest that SalB-induced neuroprotection was mediated by ERK activation.