Abstract
Inflammation is one of the crucial mechanisms mediating spinal cord injury (SCI) progress. Sesamol, a component of sesame oil, has anti-inflammatory activity, but its mechanism in SCI remains unclear. We investigated if the AMPK/SIRT1/NF-κB pathway participated in anti-inflammation of sesamol in SCI. Sesamol could inhibit neuronal apoptosis, reduce neuroinflammation, enhance M2 phenotype microglial polarization, and improved motor function recovery in mice after SCI. Furthermore, sesamol increased SIRT1 protein expression and p-AMPK/AMPK ratio, while it downregulated the p-p65/p65 ratio, indicating that sesamol treatment upregulated the AMPK/SIRT1 pathway and inhibited NF-κB activation. However, these effects were blocked by compound C which is a specific AMPK inhibitor. Together, the study suggests that sesamol is a potential drug for antineuroinflammation and improving locomotor functional recovery through regulation of the AMPK/SIRT1/NF-κB pathway in SCI.
Highlights
Spinal cord injury (SCI) is severe central nervous system (CNS) damage, and more than 250000 patients suffer from it every year [1]
The primary insult makes a direct crash to the spinal cord and damages cells, which leads to a series of complex secondary injury molecular events, including toxic oxidative stress, excessive microglial activation, continuous inflammation, and rampant apoptosis [2, 5]
The resident microglia are activated after SCI, and a lot of inflammatory cytokines produced in the early stage of SCI, which will cause neuronal apoptosis, aggravate the injury and make recovery more difficult [10,11,12]
Summary
Spinal cord injury (SCI) is severe central nervous system (CNS) damage, and more than 250000 patients suffer from it every year [1]. The primary insult makes a direct crash to the spinal cord and damages cells, which leads to a series of complex secondary injury molecular events, including toxic oxidative stress, excessive microglial activation, continuous inflammation, and rampant apoptosis [2, 5]. The resident microglia are activated after SCI, and a lot of inflammatory cytokines produced in the early stage of SCI, which will cause neuronal apoptosis, aggravate the injury and make recovery more difficult [10,11,12]. The previous studies have proven that sesamol plays roles in anti-inflammation by suppressing NF-κB activation and upregulating AMPK signaling [26, 27] and attenuating oxidative stress via activation of SIRT1 [28].
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