Search

Your search keyword '"Zhan, Qiong"' showing total 491 results
Start Over Author "Zhan, Qiong"
491 results on '"Zhan, Qiong"'

105. Ligustilide alleviates neurotoxicity in SH-SY5Y cells induced by Aβ

Author

Li-Juan, Gao, Ping, Li, Tengyun, Ma, Zhan-Qiong, Zhong, and Shi-Jun, Xu

Subjects
Neuroprotective Agents, 4-Butyrolactone, Autophagy, Humans, Apoptosis, Neurotoxicity Syndromes, Endoplasmic Reticulum Stress, Transfection, Endoplasmic Reticulum Chaperone BiP, Signal Transduction
Abstract

Ligustilide is a phenolic compound isolated from Asian plants of Umbelliferae family. This study was aimed at exploring the neuroprotective effects of Ligustilide from the perspective of endoplasmic reticulum stress (ERS) and autophagy. The Alzheimer's disease (AD) cell models were constructed by SH-SY5Y cell line, which was exposed to 20 μM Aβ

Published
2020

112. Association of AMPK Pathway-Related Gene Polymorphisms with Symptomatic Intracranial Atherosclerotic Stenosis in a Chinese Han Population

Author

Liu, Zeyu, primary, Zhou, Xiaoqing, additional, Wang, Junyan, additional, Yu, Fang, additional, Feng, Xianjing, additional, Huang, Qin, additional, Liao, Di, additional, Li, Xi, additional, Zhan, Qiong, additional, Liu, Yunhai, additional, Yang, Qidong, additional, Jin, Xin, additional, and Xia, Jian, additional

Published
2020
Full Text
View/download PDF

113. Resolving an underrepresented circulating tumor cell population in lung cancer enabled by Hexokinase 2 analysis

Author

Yang, Liu, primary, Yan, Xiaowei, additional, Chen, Jie, additional, Zhan, Qiong, additional, Hua, Yingqi, additional, Xu, Shili, additional, Dong, Yu, additional, Li, Ziming, additional, Wang, Zhuo, additional, Zuo, Dongqing, additional, Xue, Min, additional, Tang, Yin, additional, Herschman, Harvey R., additional, Lu, Shun, additional, Shi, Qihui, additional, and Wei, Wei, additional

Published
2020
Full Text
View/download PDF

121. Lentivirus-mediated inhibition of AQP4 accelerates motor function recovery associated with NGF in spinal cord contusion rats

Author

Li-xin Zhang, Xiu-ya Zhou, Hongyu Xiang, Zhan-qiong Zhong, Jian-min Chen, Xi Zeng, Xi Hu, Xiao Zhang, Qingjie Xia, Ying Rao, Tinghua Wang, and Li Shengnan

Subjects
0301 basic medicine, medicine.medical_specialty, Genetic Vectors, Motor Activity, Biology, Severity of Illness Index, Rats, Sprague-Dawley, Random Allocation, 03 medical and health sciences, 0302 clinical medicine, Western blot, Internal medicine, Nerve Growth Factor, medicine, Animals, Molecular Biology, Spinal cord injury, Spinal Cord Injuries, Aquaporin 4, medicine.diagnostic_test, General Neuroscience, Lentivirus, Recovery of Function, Spinal cord, medicine.disease, Pathophysiology, Disease Models, Animal, RNAi Therapeutics, 030104 developmental biology, medicine.anatomical_structure, Nerve growth factor, Endocrinology, Spinal Cord, Immunohistochemistry, Female, sense organs, Neurology (clinical), Neuron, Neuroscience, 030217 neurology & neurosurgery, Developmental Biology
Abstract

Aquaporin-4 (AQP4) is a water channel protein in spinal cord and plays a critical role in the pathophysiological process of spinal cord injury (SCI). However, little is known about the molecular mechanism of AQP4 involved in SCI. The present study was performed to investigate the possible molecules regulated by AQP4 after SCI by use of lentivirus-mediated RNA interference (RNAi). First, the motor function was evaluated by Basso, Beattie, Bresnahan (BBB) scale and the expression of AQP4 was measured by western blot, immunohistochemical staining and immunofluorescence in rats after contusion spinal cord injury (cSCI). After cSCI, the rats exhibited a gradual motor function recovery from 3dpo to 28dpo. And the expression and localization of AQP4 changed with different post-injury stages. At 3d after SCI, AQP4 located mainly in vascular endothelial cells (VECs) in the anterior horn of spinal cord, which was similar to the sham rats. At 7d and 28d after SCI, AQP4 was expressed both in VECs and the position of neuron membranes. The protein level of AQP4 increased significantly at 12h, 1d and 3d after SCI, and decreased slightly at 7d after SCI. Then lentivirus-mediated AQP4 RNA interference (AQP4-RNAi) was constructed and used to inhibit AQP4 expression in cSCI rats. The results from real-time quantitative polymerase chain reactions (RT-qPCR) and immunohistochemical staining suggested that the expression of nerve growth factor (NGF) was up-regulated by lentivirus-mediated AQP4 inhibition in cSCI rats, while the motor function recovery was accelerated. The results suggested that the acceleration of motor function recovery by AQP4 inhibition was associated with NGF up-regulation. This is the first report on the relationship between AQP4 and NGF in SCI, which may shed light on illustrating the role of AQP4 in SCI. These findings may also provide strategies of the clinical treatment for SCI in the future.

Published
2017

140. Ligustilide alleviates neurotoxicity in SH‐SY5Y cells induced by Aβ25‐35 via regulating endoplasmic reticulum stress and autophagy.

Author

Gao, Li‐juan, Li, Ping, Ma, Tengyun, Zhong, Zhan‐qiong, and Xu, Shi‐jun

Abstract

Ligustilide is a phenolic compound isolated from Asian plants of Umbelliferae family. This study was aimed at exploring the neuroprotective effects of Ligustilide from the perspective of endoplasmic reticulum stress (ERS) and autophagy. The Alzheimer's disease (AD) cell models were constructed by SH‐SY5Y cell line, which was exposed to 20 μM Aβ25‐35. CCK‐8 was used to evaluate the cell viability of Ligustilide on AD cell model. Hoechst staining and LysoTracker Red were used to test the cell apoptosis and Lysosome function, respectively. ERS in living cells were detected by Thioflavin T. The expression of autophagy‐related proteins (LC3B‐II/I, P62/SQSTM1, Beclin1, and Atg5), ERS marker proteins (PERK, GRP78, and CHOH), and apoptosis proteins (Bax, Bcl‐2, and Caspase‐12) were analyzed by Western blot analyses. Aβ25‐35 could induce ERS and autophagy in a time‐dependent manner in SH‐SY5Y cells. We demonstrated that Ligustilide significantly decreased the rate of apoptosis, and improved the viability of cells. Simultaneously, Ligustilide effectively modulated ERS via inhibiting the over‐activation of GRP78/PERK/CHOP signaling pathway. In addition, Ligustilide alleviated the accumulation of autophagy vacuoles, reduced the ratio of LC3B‐II/I and the level of P62/SQSTM1. Ligustilide significantly up‐regulated lysosomal acidity and the expression of Cathepsin D (CTSD). Ligustilide could rescue lysosomal function to promote autophagy flux and inhibit the over‐activation of ERS. This finding may contribute to the development of new therapeutic strategies for AD. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

141. Formation and internal nucleosynthesis in massive rotating Wolf-Rayet stars

Author

Zhan Qiong, Peng Wei-Guo, Jing Jiang-Hong, Wu Xing-Hua, and Song HF(宋汉峰)

Subjects
Physics, Stars, Solar mass, Wolf–Rayet star, Stellar mass, Metallicity, General Physics and Astronomy, Roche lobe, Astrophysics, Orbital period, O-type star
Abstract

Wolf-Rayet stars (WR stars) were discovered by French astronomers Charles Wolf and Georges Rayet in 1867. The Wolf-Rayet (WR) stars are the evolved descents of the most massive, extremely hot (temperatures up to 200000 K) and very luminous (105\begin{document}$ L_{\odot} $\end{document}－106\begin{document}$L_{\odot}$\end{document}) O stars, with 25\begin{document}$ M_{\odot} $\end{document}－30\begin{document}$M_{\odot}$\end{document} solar mass for solar metallicity. The WR stars possess very strong stellar winds, which have velocities up to 3000 km/s and wind mass loss rate \begin{document}$10^{-5} M_{\odot}$\end{document} a year. These winds are observed in the broad emission line profiles (sometimes, even P-Cygni profiles) of WR spectra in the optical and UV range. Actually, these winds are so strong that they can peel the star and convert it into a nude nucleus without envelope. It has been found that three bright galactic stars located at Cygnus region have broad strong emission bands, rather than absorptions lines, superposed on the typical continuum of hot stars. In 1930 Beals correctly identified these features as emission lines produced by high ionized elements such as helium, carbon, nitrogen and oxygen. The physical factors which can affect the evolution of WR stars are explored in this paper. These physical factors include stellar mass, initial velocities, orbital periods, metallicities, etc. According to the equations for angular momentum transfer and chemical element diffusion, we can ascertainhow these physical factors influence the evolution of WR stars and the mixing of chemical elements in WR stars.The result indicates that massive stars with high initial velocities and metallicities have strong stellar winds and be prone to producing WR stars. In contrast with the counterpart with high metallicities,it is hard for the single star with low metallicity to generate WR star due to weak wind. However, the star with very high initial velocity and low metallicity can form chemical homogenious evolution. Thestar has an enlarged convective core and a very thin hydrogen envelope and it can also generate WR star. The component in the binary system with short orbital period can transfer mass to the companion star through Roche lobe overflow, and this physical process can produce WR star under the condition of low metallicity. Furthermore, mass removal due to Roche lobe overflow reduces the temperature of stellar convective core and rate of nuclear reaction. It is shown that mass metallicities of chemical elements including 4He, 12C, 19F, 22Ne, 23Na, 25Mg in the primary star are higher than those in the single stars, whereas mass metallicities of chemical elements including 1H, 14N, 16O, 20Ne, and 26Al are lower than those in the single counterparts. In a word, the conditions for massive stars with high initial velocities and metallicities in the binary system with short orbital period favor the formation of WR stars.

Published
2019

Catalog

Books, media, physical & digital resources
See catalog results