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RISS 인기검색어
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- 저자 : Yongshan Nan (검색결과 3 건)
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High Omega-3 Polyunsaturated Fatty Acids in fat-1 Mice Reduce Inflammatory Pain
장은지,김좌진,신나라,Yuhua Yin,Yongshan Nan,Yinshi Xu,홍진표,Tzung Min Hsu,정우석,고영권,이원형,임규,김동운,이선열 한국식품영양과학회 2017 Journal of medicinal food Vol.20 No.6
Omega-3 and omega-6 polyunsaturated fatty acids (PUFAs), such as α-linolenic and linoleic acids, are essential fatty acids in mammals, because they cannot be synthesized de novo. However, fat-1 transgenic mice can synthesize omega-3 PUFAs from omega-6 PUFAs without dietary supplementation of omega-3, leading to abundant omega-3 PUFA accumulation in various tissues. In this study, we used fat-1 transgenic mice to investigate the role of omega-3 PUFAs in response to inflammatory pain. A high omega-3 PUFA tissue content attenuated formalin-induced pain sensitivity, microglial activation, inducible nitric oxide synthase expression, and the phosphorylation of NR2B, a subunit of the N-methyl-d-aspartate (NMDA) receptor. Our findings suggest that elevated omega-3 PUFA levels inhibit NMDA receptor activity in the spinal dorsal horn and modulate inflammatory pain transmission by regulating signal transmission at the spinal dorsal horn, leading to the attenuation of chemically induced inflammatory pain.
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Zhang, Enji,Lee, Sunyeul,Yi, Min-Hee,Nan, Yongshan,Xu, Yinshi,Shin, Nara,Ko, Youngkwon,Lee, Young Ho,Lee, Wonhyung,Kim, Dong Woon SPANDIDOS PUBLICATIONS 2017 MOLECULAR MEDICINE REPORTS Vol.16 No.2
<P>In previous studies that have profiled gene expression in patients with complex regional pain syndrome (CRPS), the expression of granulocyte colony-stimulating factor 3 receptor (G-CSFR) was elevated, as were a number of pain-associated genes. The present study determined the expression of G-CSFR and the mechanisms by which it may affect hypersensitivity, focusing on the signal transducer and activator of transcription 3 (STAT3)/transient receptor potential cation channel subfamily V 1 (TRPV1) signaling pathway in particular, which is an important mediator of pain. Following L5 spinal nerve ligation (SNL) surgery, the protein and mRNA levels of G-CSFR increased in the ipsilateral spinal dorsal horn when compared with the sham and/or contralateral control. Double immunofluorescence further demonstrated that G-CSFR colocalized with TRPV1 and phosphorylated STAT in the neurons of the spinal dorsal horn. G-CSF treatment led to an increase in G-CSFR and TRPV1 expression and phosphorylation of STAT3. These results indicate that G-CSF-induced G-CSFR expression may activate TRPV1 by promoting phosphorylation of STAT3. Collectively, the results suggest, for the first time, that the expression of G-CSFR in neurons following peripheral nerve injury may be involved in the induction and maintenance of neuropathic pain through the STAT3 and TRPV1 signaling pathway.</P>
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Increased Serum Cathepsin K in Patients with Coronary Artery Disease
Xiang Li,Lan Cui,Yuzi Li,Jiyong Jin,Dehao Jin,Xiangshan Li,Yanna Rei,Haiying Jiang,Guangxian Zhao,Guang Yang,Enbo Zhu,Yongshan Nan,Xianwu Cheng 연세대학교의과대학 2014 Yonsei medical journal Vol.55 No.4
Purpose: Cathepsin K is a potent collagenase implicated in human and animal atherosclerosis-based vascular remodeling. This study examined the hypothesis that serum CatK is associated with the prevalence of coronary artery disease (CAD). Materials and Methods: Between January 2011 and December 2012, 256 consecutive subjects were enrolled from among patients who underwent coronary angiography and percutaneous coronary intervention treatment. A total of 129 age-matched subjects served as controls. Results: The subjects’ serum cathepsin K and high sensitive C-reactive protein (hs-CRP) and high-density lipoprotein cholesterolwere measured. The patients with CAD had significantly higher serum cathepsinK levels compared to the controls (130.8±25.5 ng/mL vs. 86.9±25.5 ng/mL, p<0.001), and the patients with acute coronary syndrome had significantly higher serum cathepsin K levels compared to those with stable angina pectoris (137.1± 26.9 ng/mL vs. 102.6±12.9 ng/mL, p<0.001). A linear regression analysis showed that overall, the cathepsin K levels were inversely correlated with the high-density lipoprotein levels (r=-0.29, p<0.01) and positively with hs-CRP levels (r=0.32, p<0.01). Multiple logistic regression analyses shows that cathepsin K levels were independent predictors of CAD (odds ratio, 1.76; 95% confidence interval, 1.12 to 1.56; p<0.01). Conclusion: These data indicated that elevated levels of cathepsin K are closely associated with the presence of CAD and that circulating cathepsin K serves a useful biomarker for CAD.
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