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BACKGROUND: More and more evidences show that ROCK signaling pathway is involved in inflammation and oxidative stress. Fasudil is an effective Rho kinase inhibitor. Our previous series of studies have proved that fasudil has neuroprotective effects. However, it is still unclear that whether fasudil has protective effect on oxidative damage to astrocytes and its possible mechanisms. OBJECTIVE: To explore the protective effect and mechanism of fasudil on lipopolysaccharide-induced oxidative injury in astrocytes. METHODS: Primary C57BL/6 mouse astrocytes were cultured and divided into PBS control group, lipopolysaccharide stimulation group (1 mg/L), lipopolysaccharide (1 mg/L) combined with fasudil (15 mg/L) treatment group. After 24 hours of treatment, MTT assay was used to detect the viability of astrocytes. The content of malondialdehyde and the activity of superoxide dismutase in astrocytes were measured using the kit to evaluate the level of oxidative stress. Immunofluorescence staining was used to detect the expression of cleaved-caspase-3, the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and the expression of heme oxygenase-1 (HO-1) in astrocytes. Western blot assay was used to detect the total Nrf2, nuclear Nrf2 and HO-1 protein levels. RESULTS AND CONCLUSION: (1) Compared with the PBS control group, the astrocyte viability in the lipopolysaccharide stimulation group was reduced, and fasudil treatment improved the cell damage induced by lipopolysaccharide. (2) Compared with the PBS control group, lipopolysaccharide resulted in a significant decrease in the activity of superoxide dismutase and a significant increase in the level of malondialdehyde in astrocytes (P < 0.01). Fasudil significantly increased the activity of superoxide dismutase (P < 0.01) and reduced the level of malondialdehyde (P < 0.01). (3) Compared with the PBS control group, the expression of cleaved-caspase-3 was significantly increased in the lipopolysaccharide stimulation group. Compared with the lipopolysaccharide stimulation group, the expression of cleaved-caspase-3 was decreased in the lipopolysaccharide combined with fasudil treatment group. (4) Fasudil could promote the nuclear translocation of Nrf2 and significantly increase the expression of total Nrf2, nucleus Nrf2 and HO-1 after lipopolysaccharide stimulation. (5) The results indicate that fasudil can inhibit lipopolysaccharide-induced astrocytic injury by regulating the Nrf2/HO-1 signaling pathway. [ABSTRACT FROM AUTHOR]

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In order to lessen the effect of La-doped on the gas-sensing response of SnO2 powders, different La-doped SnO2 powders were prepared by sol-gel method, and the prepared SnO2 and La-doped SnO2 powders were characterized and analyzed by Fourier transform infrared spectroscopy (FT-IR), transmission electron microscopy (TEM), scanning electron microscope (SEM), specific surface area and pore size tester ( BET) and X-ray diffractometer (XRD). The gas-sensing response of the samples were tested. The results show that La doping reduces the grain size of SnO2. With the increase of La doping, the gas-sensing response of La-doped SnO2 powders to ethanol increases first and then decreases. When the molar ratio of La/Sn is 0.25, the gas-sensing response of La-doped SnO2 powder to ethanol is the highest, 43. 5 % higher than that of pure SnO2 to ethanol. [ABSTRACT FROM AUTHOR]

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目的探讨脂蛋白相关磷脂酶A2(Lp-PLA2)、嗜铬粒蛋白(CgA)与慢性心力衰竭患者心室重构的关系。方法选择慢性心力衰竭患者97例(心衰组),按照美国纽约心脏病协会(NYHA)心功能分级,NYHAⅡ级35例,NYHAⅢ级29例,NYHAⅣ级33例。同期体检健康者40例作为对照组。心衰组于入院次日,对照组于体检日采集清晨空腹肘静脉血,采用ELISA法检测血清Lp-PLA2、CgA水平;同日,采用超声心动图检测左心房内径(LAD)、右心室内径(RVD)、左心室舒张末内径(LVEDD)、左心室射血分数(LVEF),并计算左心室质量指数(LVMI)。结果心衰组血清Lp-PLA2、CgA水平均高于对照组(P均<0.05);心衰组随着心功能分级增加,血清Lp-PLA2、CgA水平逐渐升高(P均<0.05)。心衰组LAD、RVD、LVEDD、LVMI均高于对照组,LVEF低于对照组(P均<0.05);心衰组随着心功能分级增加,LAD、RVD、LVEDD、LVMI、LVEF变化越明显(P均<0.05)。慢性心力衰竭患者血清Lp-PLA2、CgA与LAD、RVD、LVEDD、LVMI均呈正相关关系,与LVEF均呈负相关关系(P均<0.05)。结论血清Lp-PLA2、CgA水平升高与慢性心力衰竭患者心室重构有关。血清Lp-PLA2、CgA水平可作为临床辅助诊断慢性心力衰竭及评估患者病情程度的指标。 [ABSTRACT FROM AUTHOR]