目的探讨α-突触核蛋白(α-synuc le in)在鱼藤酮处理的人类多巴胺能SH-SY5Y细胞内的作用。方法用脂质体转染的方法将-αsynuc le in基因转染入SH-SY5Y细胞内,并筛选稳定表达-αsynuc le in的细胞。经过不同浓度的鱼藤酮处理后,测定细胞活力、细胞内氧化应激和抗氧化能力。结果经鱼藤酮处理后,所有的细胞均表现为细胞活力下降和细胞内氧化应激增强。与正常SH-SY5Y细胞相比,过表达-αsynuc le in的细胞表现为较高的细胞活力和抗氧化能力(P<0.01)。结论α-synuc le in过表达可能通过增强SH-SY5Y细胞活力和抗氧化能力,来部分对抗鱼藤酮的毒性作用。 相似文献
Summary: The wavelength‐dependent vacuum ultraviolet (VUV) photolysis of several polymers, low density polyethylene (LDPE), biaxially oriented poly(propylene) (BOPP), atactic polystyrene (PS), and poly(methyl methacrylate) (PMMA), was studied by irradiation in vacuum with the well‐characterized emissions from four different resonant or excimer VUV sources. These lamps comprise radiofrequency (r.f.) discharges in different noble gases, such as krypton, xenon (at low pressures, producing near‐monochromatic resonant line radiations), xenon excimer (at “high” pressure), and a deuterium/argon mixture (producing a broad‐band emission). VUV‐induced mass loss (ablation or etching) was monitored in situ by quartz crystal microbalance measurements. Following irradiation, samples were analysed by ATR‐FTIR and XPS, to evaluate near‐surface structural changes (e.g., creation of unsaturation, cross‐linking) resulting from the VUV‐initiated bond scissions and radical‐creation reactions. PMMA was the most readily ablatable polymer, whereas the mass loss of BOPP was higher than that of LDPE, regardless of the irradiation wavelength, λ. All polymers were found to form double bonds, with the exception of PS, which is rather stable, probably due to energy dissipation by fluorescence.
Formation of double bonds in a) vinyl‐, b) vinylidene‐, and c) vinylene‐like unsaturated groups, as a function of the radiation dose, D, for KrL (?), XeL (?), and D2Ar‐irradiated (?) PMMA. 相似文献
Aim: AQP4 in the brain is involved in the occurrence and development of a variety of encephalopathy. AQPs family changes in kidney were accompanied by altered UTs family. The aim of this study was to observe AQP4 and UT-A3 expression in CNS and to explore their role in the pathogenesis of endotoxemia encephalopathy following peripheral LPS injection in mice. Methods: Endotoxemia was induced in C57Bl/6 mice by intraperitoneal injection of LPS. The expression of UT-A3 and AQP4 in brain were detected by Western blot and immunohistochemistry, the level of cytokines were detected by ELISA, and the content of LDH, AST/ALT, BUN and CREA were detected by colorimetric method. Results: As compared with the control group, in model group, the brain weight/ body weight ratio increased by 13%. Meanwhile, a 2.5 fold increase in LDH and a 1.2 fold increase in AST/ALT were found in peripheral serum (P < 0.05), and also, BUN and CREA increased 2.5 fold (P < 0.01). In addition to severe CNS injury in response to lipopolysaccharide, the contents of cytokines and the expression of AQP4 protein in hippocampal is increased (P < 0.05), while the expression of UT-A3 protein in the hippocampus and cortical astrocytes decreased (P < 0.05). And, in part, Dexa pretreatment attenuated those effects. Conclusions: In endotoxemia encephalopathy, AQPs and UTs which regulate the functions of cell membrane are both altered. We suggested that the molecular mechanisms of regulation in endotoxemia may provide a new strategy for clinical treatment of the disease and drug binding sites. 相似文献
