Jun Fu1, Hong-bin Fan1, Zheng Guo2, Zhen Wang3, Xiang-dong Li1, Jing Li1, Guo-xian Pei1. 1. Department of Orthopaedic Oncology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. 2. Department of Orthopaedic Oncology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. Electronic address: fmmuguozheng@163.com. 3. Department of Orthopaedic Oncology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China. Electronic address: fmmuwangzhen@163.com.
Abstract
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 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 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.
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 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 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.
Authors: Ovidiu Horea Bedreag; Alexandru Florin Rogobete; Mirela Sărăndan; Alina Cradigati; Marius Păpurică; Oana Maria Roşu; Corina Maria Dumbuleu; Dorel Săndesc Journal: Rom J Anaesth Intensive Care Date: 2014-10