Abstract
Painful cervical radiculopathy is characterized by chronic neuroinflammation that lowers endogenous antioxidant responses leading to the development of oxidative stress and pain after neural trauma. Therefore, antioxidants such as secoisolariciresinol diglucoside (SDG), that promote antioxidant signaling and reduce oxidative damage may also provide pain relief. This study investigated if repeated systemic administration of synthetic SDG after a painful root compression reduces the established pain, oxidative stress and spinal glial activation that are typically evident. SDG was administered on days 1–3 after compression and the extent of oxidative damage in the dorsal root ganglia (DRG) and spinal cord was measured at day 7 using the oxidative stress markers 8-hydroxguanosine (8-OHG) and nitrotyrosine. Spinal microglial and astrocytic activation were also separately evaluated at day 7 after compression. In addition to reducing pain, SDG treatment reduced both spinal 8-OHG and nitrotyrosine, as well as peripheral 8-OHG in the DRG. Moreover, SDG selectively reduced glial activation by decreasing the extent of astrocytic but not microglial activation. These findings suggest that synthetic SDG may attenuate existing radicular pain by suppressing the oxidative stress and astrocytic activation that develop after painful injury, possibly identifying it as a potent therapeutic for painful radiculopathies.
Highlights
Chronic neck pain remains a major concern for the aging population, with up to two-thirds of adults in the United States experiencing neck pain in their lifetime [1]
Animal models of radiculopathy from nerve root compression suggest that in addition to the local axonal injury and disruption in neurotransmitter release in the spinal cord [2,3,4], there is widespread inflammation that contributes to the initiation and maintenance of chronic pain [5,6,7]
In addition to reactive oxygen species (ROS) accumulation, neural injury is accompanied by a decrease in the endogenous antioxidant enzymes that are activated in an effort to reduce cellular oxidative stress [9,11,12]
Summary
Chronic neck pain remains a major concern for the aging population, with up to two-thirds of adults in the United States experiencing neck pain in their lifetime [1]. Animal models of radiculopathy from nerve root compression suggest that in addition to the local axonal injury and disruption in neurotransmitter release in the spinal cord [2,3,4], there is widespread inflammation that contributes to the initiation and maintenance of chronic pain [5,6,7]. In addition to ROS accumulation, neural injury is accompanied by a decrease in the endogenous antioxidant enzymes that are activated in an effort to reduce cellular oxidative stress [9,11,12]. Mounting evidence points to the contribution of oxidative and nitrosative stress in chronic radicular pain [11,13], few antioxidant therapies are effective in both addressing the generation of ROS and in reactivating endogenous antioxidant enzymes after neural injury
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