http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 저자 : Yingchun Zhou (검색결과 3 건)
- 무료
- 기관 내 무료
- 유료
-
Xiangdong Zhou,Yufa Sun,Yingchun Chen,Bing Sun 한국고분자학회 2018 폴리머 Vol.42 No.2
Monomer of polyamide (PA66) and flame-retardant intermediate product (FR) were firstly synthesized, and the flame-retardant (PA-FR) was further gained by polymerization of PA66 and FR. The structure of PA-FR was confirmed by Fourier transform infrared spectroscopy (FTIR), nuclear magnetic resonance spectroscopy (NMR), X-ray photoelectron spectroscopy (XPS), and gel permeation chromatography (GPC). The thermal properties of PA-FR and the finished fabric were evaluated by thermal gravity analysis (TGA) and differential scanning calorimetry (DSC). Moreover, X-ray diffraction analysis (XRD) showed that melting eutectic reaction occurred between PA-FR and nylon fabric. The experimental results showed that the limiting oxygen index (LOI) value of PA-FR treated fabric and PA-FR treated fabric after 10 laundries were improved to 28.8% and 26.4%, respectively. It implied that PA-FR had a good and durable function of imparting fire-resistance to nylon fabric.
-
( Tao Li ),( Yingchun Wan ),( Lijuan Sun ),( Shoujun Tao ),( Peng Chen ),( Caihua Liu ),( Ke Wang ),( Changyu Zhou ),( Guoqing Zhao ) 한국응용약물학회 2019 Biomolecules & Therapeutics(구 응용약물학회지) Vol.27 No.4
There is accumulating evidence that microRNAs are emerging as pivotal regulators in the development and progression of neuropathic pain. MicroRNA-15a/16 (miR-15a/16) have been reported to play an important role in various diseases and inflammation response processes. However, whether miR-15a/16 participates in the regulation of neuroinflammation and neuropathic pain development remains unknown. In this study, we established a mouse model of neuropathic pain by chronic constriction injury (CCI) of the sciatic nerves. Our results showed that both miR-15a and miR-16 expression was significantly upregulated in the spinal cord of CCI rats. Downregulation of the expression of miR-15a and miR-16 by intrathecal injection of a specific inhibitor significantly attenuated the mechanical allodynia and thermal hyperalgesia of CCI rats. Furthermore, inhibition of miR-15a and miR-16 downregulated the expression of interleukin-1β and tumor-necrosis factor-αin the spinal cord of CCI rats. Bioinformatic analysis predicted that G protein-coupled receptor kinase 2 (GRK2), an important regulator in neuropathic pain and inflammation, was a potential target gene of miR-15a and miR-16. Inhibition of miR-15a and miR-16 markedly increased the expression of GRK2 while downregulating the activation of p38 mitogen-activated protein kinase and NF-κB in CCI rats. Notably, the silencing of GRK2 significantly reversed the inhibitory effects of miR-15a/16 inhibition in neuropathic pain. In conclusion, our results suggest that inhibition of miR-15a/16 expression alleviates neuropathic pain development by targeting GRK2. These findings provide novel insights into the molecular pathogenesis of neuropathic pain and suggest potential therapeutic targets for preventing neuropathic pain development.
-
Honglin Xu,Haifeng Miao,Guanghong Chen,Guoyong Zhang,Yue Hua,Yuting Wu,Tong Xu,Changlei Hu,Mingjie Pang,Leyi Tan,Xin Han,Bin Liu,Yingchun Zhou 고려인삼학회 2023 Journal of Ginseng Research Vol.47 No.6
Background: Myocardial fibrosis post-myocardial infarction (MI) can induce maladaptive cardiacremodeling as well as heart failure. Although 20(S)-ginsenoside Rg3 (Rg3) has been applied to cardiovasculardiseases, its efficacy and specific molecular mechanism in myocardial fibrosis are largely unknown. Herein, we aimed to explore whether TGFBR1 signaling was involved in Rg3's anti-fibrotic effectpost-MI. Methods: Left anterior descending (LAD) coronary artery ligation-induced MI mice and TGF-b1-stimulated primary cardiac fibroblasts (CFs) were adopted. Echocardiography, hematoxlin-eosin andMasson staining, Western-blot and immunohistochemistry, CCK8 and Edu were used to study the effectsof Rg3 on myocardial fibrosis and TGFBR1 signaling. The combination mechanism of Rg3 and TGFBR1 wasexplored by surface plasmon resonance imaging (SPRi). Moreover, myocardial Tgfbr1-deficient mice andTGFBR1 adenovirus were adopted to confirm the pharmacological mechanism of Rg3. Results: In vivo experiments, Rg3 ameliorated myocardial fibrosis and hypertrophy and enhanced cardiacfunction. Rg3-TGFBR1 had the 1.78 10 7 M equilibrium dissociation constant based on SPRi analysis,and Rg3 inhibited the activation of TGFBR1/Smads signaling dose-dependently. Cardiac-specific Tgfbr1knockdown abolished Rg3's protection against myocardial fibrosis post-MI. In addition, Rg3 downregulatedthe TGF-b1-mediated CFs growth together with collagen production in vitro through TGFBR1signaling. Moreover, TGFBR1 adenovirus partially blocked the inhibitory effect of Rg3. Conclusion: Rg3 improves myocardial fibrosis and cardiac function through suppressing CFs proliferationalong with collagen deposition by inactivation of TGFBR1 pathway.
ScienceON
DBpia연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
