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- 검색키워드
- 저자 : Sheu-Ran Choi (검색결과 6 건)
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Choi, Hoon-Seong,Lee, Mi-Ji,Choi, Sheu-Ran,Smeester, Branden A.,Beitz, Alvin J.,Lee, Jang-Hern Elsevier 2018 NEUROSCIENCE Vol.372 No.-
<P><B>Abstract</B></P> <P>Aromatase is a key enzyme responsible for the biosynthesis of estrogen from testosterone. Although recent evidence indicates that spinal cord aromatase participates in nociceptive processing, the mechanisms underlying its regulation and its involvement in nociception remain unclear. The present study focuses on the potential role of astrocyte aromatase in formalin-induced acute pain and begins to uncover one mechanism by which spinal aromatase activation is controlled. Following intraplantar formalin injection, nociceptive responses were quantified and immunohistochemistry/co-immunoprecipitation assays were used to investigate the changes in spinal Fos expression and the phospho-serine levels of spinal aromatase. Intrathecal (i.t.) injection of letrozole (an aromatase inhibitor) mitigated both the late phase formalin-induced nociceptive responses and formalin-induced spinal Fos expression. Furthermore, formalin-injected mice showed significantly reduced phospho-serine levels of aromatase, which is associated with the rapid activation of this enzyme. However, sigma-1 receptor inhibition with i.t. BD1047 blocked the dephosphorylation of aromatase and potentiated the pharmacological effect of letrozole on formalin-induced nociceptive responses. In addition, i.t. administration of a sub-effective dose of BD1047 potentiated the pharmacological effect of cyclosporin A (a calcineurin inhibitor) on both the formalin-induced reduction in phospho-serine levels of aromatase and nociceptive behavior. These results suggest that dephosphorylation is an important regulatory mechanism involved in the rapid activation of aromatase and that spinal sigma-1 receptors mediate this dephosphorylation of aromatase through an intrinsic calcineurin pathway.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Dephosphorylated aromatase in astrocyte is involved in the process of formalin-induced acute nociception. </LI> <LI> Activation of astrocyte sigma-1 receptors is associated with the dephosphorylation of aromatase. </LI> <LI> Calcineurin signaling pathway is involved in the sigma-1 receptor-mediated dephosphorylation of aromatase. </LI> </UL> </P>
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Choi, Sheu-Ran,Beitz, Alvin J.,Lee, Jang-Hern Elsevier 2019 BIOMEDICINE AND PHARMACOTHERAPY Vol.118 No.-
<P><B>Abstract</B></P> <P>We have recently demonstrated that the neurosteroid-metabolizing enzyme, cytochrome P450c17 is increased in spinal astrocytes contributing to the development of mechanical allodynia in chronic constriction injury (CCI)-induced neuropathic mice. However, the mechanisms by which spinal P450c17 modulates pathological changes in astrocytes remain unclear. In this study we investigated whether P450c17 modulates astrocyte activation and whether this process is mediated by spinal p38 mitogen-activated protein kinase phosphorylation ultimately leading to the development of mechanical allodynia in CCI mice. Sciatic nerve injury induced a significant increase in glial fibrillary acidic protein (GFAP) expression in the superficial dorsal horn (SDH, laminae I-II) and nucleus proprius (NP, laminae III-IV) regions of the spinal cord dorsal horn. Repeated daily (from days 0–3 post-surgery) intrathecal administration of the P450c17 inhibitor, ketoconazole (10 nmol) significantly inhibited the CCI-induced increase in GFAP-immunoreactivity, but had no effect on the CCI-induced increase in Iba-1-immunoreactivity. In addition, intrathecal administration of ketoconazole significantly inhibited the CCI-induced increase in p38 phosphorylation, while the levels of ERK and JNK phosphorylation remained unchanged. The CCI-induced development of mechanical allodynia was attenuated by administration of either ketoconazole (10 nmol) or the p38 MAPK inhibitor, SB203580 (5 nmol). Administration of a sub-effective dose of SB203580 (0.5 nmol) potentiated the pharmacological effect of ketoconazole (1 nmol) on spinal GFAP-immunostaining, as well as, the development of mechanical allodynia following CCI. Collectively these data suggest that spinal P450c17 activates astrocytes via p38 phosphorylation, ultimately leading to the development of mechanical allodynia in a model of peripheral neuropathy.</P> <P><B>Highlights</B></P> <P> <UL> <LI> P450c17 inhibition suppresses the activation of spinal astrocytes in CCI mice. </LI> <LI> P450c17 inhibition has no effect on the activation of spinal microglial cells in CCI mice. </LI> <LI> Spinal P450c17 increases p38 MAPK phosphorylation in the spinal cord of CCI mice. </LI> <LI> SB203580 potentiates the pharmacological effects of ketoconazole on neuropathic pain and astrocyte activation. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
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Choi, Sheu-Ran,Roh, Dae-Hyun,Yoon, Seo-Yeon,Choi, Hoon-Seong,Kang, Suk-Yun,Han, Ho-Jae,Beitz, Alvin J.,Lee, Jang-Hern Elsevier 2019 NEUROPHARMACOLOGY - Vol.149 No.-
<P><B>Abstract</B></P> <P>While evidence indicates that sigma-1 receptors (Sig-1Rs) play an important role in the induction of peripheral neuropathic pain, there is limited understanding of the role that the neurosteroidogenic enzymes, which produce Sig-1R endogenous ligands, play during the development of neuropathic pain. We examined whether sciatic nerve injury upregulates the neurosteroidogenic enzymes, cytochrome P450c17 and 3β-hydroxysteroid dehydrogenase (3β-HSD), which modulate the expression and/or activation of Sig-1Rs leading to the development of peripheral neuropathic pain. Chronic constriction injury (CCI) of the sciatic nerve induced a significant increase in the expression of P450c17, but not 3β-HSD, in the ipsilateral lumbar spinal cord dorsal horn at postoperative day 3. Intrathecal administration of the P450c17 inhibitor, ketoconazole during the induction phase of neuropathic pain (day 0 to day 3 post-surgery) significantly reduced the development of mechanical allodynia and thermal hyperalgesia in the ipsilateral hind paw. However, administration of the 3β-HSD inhibitor, trilostane had no effect on the development of neuropathic pain. Sciatic nerve injury increased astrocyte Sig-1R expression as well as dissociation of Sig-1Rs from BiP in the spinal cord. These increases were suppressed by administration of ketoconazole, but not by administration of trilostane. Co-administration of the Sig-1R agonist, PRE084 restored the development of mechanical allodynia originally suppressed by the ketoconazole administration. However, ketoconazole-induced inhibition of thermal hyperalgesia was not affected by co-administration of PRE084. Collectively these results demonstrate that early activation of P450c17 modulates the expression and activation of astrocyte Sig-1Rs, ultimately contributing to the development of mechanical allodynia induced by peripheral nerve injury.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Sciatic nerve injury increases P450c17 expression in astrocytes of the ipsilateral lumbar spinal cord dorsal horn. </LI> <LI> Spinal P450c17 contributes to the CCI-induced development of neuropathic pain. </LI> <LI> Spinal P450c17 modulates the CCI-induced increase in astrocyte Sig-1R expression. </LI> <LI> P450c17 increases the dissociation of Sig-1Rs from BiP in the spinal cord dorsal horn of CCI mice. </LI> <LI> Sig-1R plays an important role in the P450c17-induced development of mechanical allodynia in neuropathic mice. </LI> </UL> </P>
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Hoon-Seong Choi,Suk-Yun Kang,노대현,Sheu-Ran Choi,Yeonhee Ryu,Jang-Hern Lee 대한수의학회 2018 Journal of Veterinary Science Vol.19 No.5
Respiratory inflammation is a frequent and fatal pathologic state encountered in veterinary medicine. Although diluted bee venom (dBV) has potent anti-inflammatory effects, the clinical use of dBV is limited to several chronic inflammatory diseases. The present study was designed to propose an acupoint dBV treatment as a novel therapeutic strategy for respiratory inflammatory disease. Experimental pleurisy was induced by injection of carrageenan into the left pleural space in mouse. The dBV was injected into a specific lung meridian acupoint (LU-5) or into an arbitrary non-acupoint located near the midline of the back in mouse. The inflammatory responses were evaluated by analyzing inflammatory indicators in pleural exudate. The dBV injection into the LU-5 acupoint significantly suppressed the carrageenan-induced increase of pleural exudate volume, leukocyte accumulation, and myeloperoxidase activity. Moreover, dBV acupoint treatment effectively inhibited the production of interleukin 1 beta, but not tumor necrosis factor alpha in the pleural exudate. On the other hand, dBV treatment at non-acupoint did not inhibit the inflammatory responses in carrageenan-induced pleurisy. The present results demonstrate that dBV stimulation in the LU-5 lung meridian acupoint can produce significant anti-inflammatory effects on carrageenan-induced pleurisy suggesting that dBV acupuncture may be a promising alternative medicine therapy for respiratory inflammatory diseases.
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