Estrogen alleviates neuropathic pain induced after spinal cord injury by inhibiting microglia and astrocyte activation |
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Authors: | Jee Youn Lee Hae Young Choi Bong-Gun Ju Tae Young Yune |
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Institution: | 1. Age-Related and Brain Diseases Research Center, Kyung Hee University, Seoul 02447, Republic of Korea;2. Department of Life Science, Sogang University, Seoul 04107, Republic of Korea;3. Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul 02447, Republic of Korea;4. KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 130-701, Republic of Korea |
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Abstract: | Neuropathic pain after spinal cord injury (SCI) is developed in about 80% of SCI patients and there is no efficient therapeutic drug to alleviate SCI-induced neuropathic pain. Here we examined the effect of estrogen on SCI-induced neuropathic pain at below-level and its effect on neuroinflammation as underlying mechanisms. Neuropathic pain is developed at late phase after SCI and a single dose of 17β-estradiol (100, 300?μg/kg) were administered to rats with neuropathic pain after SCI through intravenous injection. As results, both mechanical allodynia and thermal hyperalgesia were significantly reduced by 17β-estradiol compared to vehicle control. Both microglia and astrocyte activation in the lamina I and II of L4-5 dorsal horn was also inhibited by 17β-estradiol. In addition, the levels of p-p38MAPK and p-ERK known to be activated in microglia and p-JNK known to be activated in astrocyte were significantly decreased by 17β-estradiol. Furthermore, the mRNA expression of inflammatory mediators such as Il-1β, Il-6, iNos, and Cox-2 was more attenuated in 17β-estradiol-treated group than in vehicle-treated group. Particularly, we found that the analgesic effect by 17β-estradiol was mediated via estrogen receptors, which are expressed in dorsal horn neurons. These results suggest that 17β-estradiol may attenuate SCI-induced neuropathic pain by inhibiting microglia and astrocyte activation followed inflammation. |
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Keywords: | Spinal cord injury Estrogen receptor Neuropathic pain Microglia Astrocyte |
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