Abstract
α-asarone, a bioactive compound found in Acorus plant species, has been shown to exhibit neuroprotective, anti-oxidative, anti-inflammatory, and cognitive-enhancing effects. However, the effects of α-asarone on spinal cord injury (SCI) have not yet been elucidated. The present study investigated the effects of α-asarone on the mRNA of pro-inflammatory cytokines, macrophage polarization toward an anti-inflammatory M2 phenotype, and angiogenesis in rats with compressive SCI. α-Asarone was orally administered (10 mg/kg) once per day for 14 days following moderate static compression SCI. Compared to controls, α-asarone treatment significantly improved locomotor score, prevented neuroinflammation, and facilitated angiogenesis in the spinal cord at 14 days after SCI. Furthermore, α-asarone significantly reduced the TNF-α, IL-1β, IL-6, monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 2 (MIP-2), and inducible nitric oxide synthase (iNOS) levels but increased the IL-4, IL-10, and arginase 1 levels at 24 h after SCI. At 7 and 14 days after SCI, immunohistochemistry showed reduced reactive gliosis and neuroinflammation and an increased expression of M2 macrophage markers and angiogenesis. The results suggest that the inhibition of pro-inflammatory cytokines, macrophage polarization toward an anti-inflammatory M2 phenotype, and angiogenesis by α-asarone may be some of the mechanisms underlying the α-asarone-mediated neuroprotective effects on an injured spinal cord.
Highlights
Spinal cord injury (SCI) is a two-step process that includes a primary mechanical injury and a subsequent secondary injury mediated by multiple injury processes, including inflammation, apoptosis, free radical-induced cell death, and glutamate excitotoxicity (Bharne et al, 2013; Cheng et al, 2014; Losey et al, 2014)
The present study investigated the effects of α-asarone on the mRNA of pro-inflammatory cytokines, macrophage polarization toward an anti-inflammatory M2 phenotype, and angiogenesis in rats with compressive SCI. α-Asarone was orally administered (10 mg/kg) once per day for 14 days following moderate static compression SCI
The results suggest that the inhibition of pro-inflammatory cytokines, macrophage polarization toward an anti-inflammatory M2 phenotype, and angiogenesis by α-asarone may be some of the mechanisms underlying the α-asarone-mediated neuroprotective effects on an injured spinal cord
Summary
Spinal cord injury (SCI) is a two-step process that includes a primary mechanical injury and a subsequent secondary injury mediated by multiple injury processes, including inflammation, apoptosis, free radical-induced cell death, and glutamate excitotoxicity (Bharne et al, 2013; Cheng et al, 2014; Losey et al, 2014). Inflammatory responses following SCI are initiated by peripherally derived immune cells and activated glial cells that proliferate or migrate into the lesion site This influx of inflammatory cells induces the apoptosis of neurons and oligodendrocytes and the formation of glial scars, and results in the reduction of neuronal function (Zhou et al, 2014; Shultz and Zhong, 2017). This inflammatory process deteriorates macrophage responses and changes the polarization state of macrophages, which is thought to depend in large part on cytokines and other immune cells in SCI neurons, but it retards the recovery process (Hu et al, 2015). Developing a compound with potent therapeutic efficacy and fewer side effects has been an unmet clinical need for SCI treatment
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