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2篇 您的检索式:作者名="Qiushi Kong"
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1Photocatalytic activity of Lu^(3+)/TiO_2 prepared by ball milling method显示文摘Ball milling method was applied to prepare Lu^(3+)/TiO_2 photocatalysts. The catalysts were characterized with X-ray powder diffraction(XRD), X-ray photoelectron spectroscopy(XPS), UV-visible diffuse reflectance spectra(UV-vis DRS), energy dispersive X-ray spectrometer(EDS), transmission electron microscopy(TEM) and Brunauer-Emmett-Teller(BET) method. The photocatalytic activities were determined by the degradation of methylene blue(MB) equipped with a 300 W medium pressure mercury lamp. Results show that the first order reaction rate constants of Lu^(3+)/TiO_2 and pure TiO_2 are0.0565 and 0.0263 min-1, respectively, which both were evaluated under the condition of catalysts loading of 0.2 g/L,initial concentration of 25 mg/L for MB, mole ratio of Lu^(3+)/TiO_2 of 1.5% and milling time of 4 h. The average crystal sizes of 1.5 mol% Lu^(3+)/TiO_2 and pure TiO_2 are 18.7 and 19.3 nm, respectively.Di Wu Chen Li Qiushi Kong Zaifeng Shi Dashuai Zhang Lili Wang Lizhi Han Xiaopeng Zhang Qiang Lin 2018Journal of Rare Earths2018,36,8:3
2PXR activation impairs hepatic glucose metabolism partly via inhibiting the HNF4α-GLUT2 pathway显示文摘Drug-induced hyperglycemia/diabetes is a global issue. Some drugs induce hyperglycemia by activating the pregnane X receptor(PXR), but the mechanism is unclear. Here, we report that PXR activation induces hyperglycemia by impairing hepatic glucose metabolism due to inhibition of the hepatocyte nuclear factor 4-alpha(HNF4 a)-glucose transporter 2(GLUT2) pathway. The PXR agonists atorvastatin and rifampicin significantly downregulated GLUT2 and HNF4 a expression, and impaired glucose uptake and utilization in HepG2 cells. Overexpression of PXR downregulated GLUT2 and HNF4 a expression, while silencing PXR upregulated HNF4 a and GLUT2 expression.Silencing HNF4 a decreased GLUT2 expression, while overexpressing HNF4 a increased GLUT2 expression and glucose uptake. Silencing PXR or overexpressing HNF4 a reversed the atorvastatininduced decrease in GLUT2 expression and glucose uptake. In human primary hepatocytes, atorvastatin downregulated GLUT2 and HNF4 a mRNA expression, which could be attenuated by silencing PXR. Silencing HNF4 a downregulated GLUT2 mRNA expression. These findings were reproduced with mouse primary hepatocytes. Hnf4 a plasmid increased Slc2 a2 promoter activity. Hnf4 a silencing or pregnenolone-16 a-carbonitrile(PCN) suppressed the Slc2 a2 promoter activity by decreasing HNF4 a recruitment to the Slc2 a2 promoter. Liver-specific Hnf4 a deletion and PCN impaired glucose tolerance and hepatic glucose uptake, and decreased the expression of hepatic HNF4 a and GLUT2. In conclusion, PXR activation impaired hepatic glucose metabolism partly by inhibiting the HNF4 aGLUT2 pathway. These results highlight the molecular mechanisms by which PXR activators induce hyperglycemia/diabetes.Peihua Liu Ling Jiang Weimin Kong Qiushi Xie Ping Li Xiaonan Liu Jiayi Zhang Ming Liu Zhongjian Wang Liang Zhu Hanyu Yang Ying Zhou Jianjun Zou Xiaodong Liu Li Liu 2022Acta Pharmaceutica Sinica B2022,12,5:1
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