Photocatalytic discoloration kinetics of Reactive Black 5 (RB5), a vinylsulfone dye, has been studied spectrophotometrically by following the decrease in dye concentration with time at ambient conditions using a flow ...Photocatalytic discoloration kinetics of Reactive Black 5 (RB5), a vinylsulfone dye, has been studied spectrophotometrically by following the decrease in dye concentration with time at ambient conditions using a flow loop reactor. UV lump, Black Light Blue (BLB) emitting at maximum wavelength of 365 nm and Ahlstrom Research Service paper consistent of TiO2 P500 coated on non woven paper was used respectively as source of UV light and photocatalyst. At natural pH, the result shows that photolysis of RB5 and its adsorption in the presence of photocatalyst was negligible while the photocatalytic oxidation (PCO) permits 30.8% of RB5 degradation. The degradation of dye was studied under a variety of conditions such as volumetric flow rate, initial pH, photocatalyst reuse, and in the presence of electron acceptor such as sodium persulphate ((Na)2S2O8). The degradation rates were found to be strongly influenced by all the above parameters. The circulation flow rate of 108 L/h was the best. The rate constant calculated when the initial pH was varied shows that pH 3 was more favorable for RB5 removal. Peroxydisulphate ions have the strong effect on RB5 discoloration even in dark without and with photocatalyst. When UV light was used in the presence of photocatalyst, 50 min was enough for quasi-total removal of RB5 with (0.2 M).展开更多
Baicalin, a type of flavonoid extracted from the dried root of Scutellaria baicalensis georgi, has been shown to effectively inhibit cell apoptosis. Therefore, we assumed that baicalin would suppress colistin sulfate-...Baicalin, a type of flavonoid extracted from the dried root of Scutellaria baicalensis georgi, has been shown to effectively inhibit cell apoptosis. Therefore, we assumed that baicalin would suppress colistin sulfate-induced neuronal apoptosis. PC12 cells exposed to colistin sulfate （62.5-500 μg/mL） for 24 hours resulted in PCl2 cell apoptosis. In addition, caspase-3 activity, lactate dehydrogenase level and free radical content increased in a dose-dependent manner. Subsequently, PC12 cells were pretreated with baicalin （25, 50 and 100 pg/mL）, and exposed to 125 pg/mL colistin sulfate. Cell morphology markedly changed, and cell viability increased. Moreover, caspase-3 activity, lac- tate dehydrogenase level and free radical content decreased. Results indicated that baicalin inhib- ited colistin sulfate-induced PC12 cell apoptosis by suppressing free radical injury, and reducing caspase-3 activity and lactate dehydrogenase activity.展开更多
In this study, poly（L-lactic acid）/ammonium persulfate doped-polypyrrole composite fibrous scaffolds with moderate conductivity were produced by combining electrospinning with in situ polymerization. PC12 cells were...In this study, poly（L-lactic acid）/ammonium persulfate doped-polypyrrole composite fibrous scaffolds with moderate conductivity were produced by combining electrospinning with in situ polymerization. PC12 cells were cultured on these fibrous scaffolds and their growth following electrical stimulation （0-20.0 μA stimulus intensity, for 1-4 days） was observed using inverted light microscopy, and scanning electron microscopy coupled with the MTT cell viability test. The results demonstrated that the poly（L-lactic acid）/ammonium persulfate doped-polypyrrole fibrous scaffold was a dual multi-porous micro/nano fibrous scaffold. An electrical stimulation with a current intensity 5.0- 10.0 μAfor about 2 days enhanced neuronal growth and neurite outgrowth, while a high current intensity （over 15.0 μA） suppressed them. These results indicate that electrical stimulation with a moderate current intensity for an optimum time frame can promote neuronal growth and neurite outgrowth in an intensity- and time-dependent manner.展开更多
In this study, we treated PC12 cells with 0-20 μM amyloid-β peptide （25-35） for 24 hours to induce cytotoxicity, and found that 5-20 μM amyloid-β peptide （25-35） decreased PC12 cell viability, but adenosine tr...In this study, we treated PC12 cells with 0-20 μM amyloid-β peptide （25-35） for 24 hours to induce cytotoxicity, and found that 5-20 μM amyloid-β peptide （25-35） decreased PC12 cell viability, but adenosine triphosphate-sensitive potassium channel activator diazoxide suppressed the decrease in PC12 cell viability induced by amyloid-β peptide （25-35）. Diazoxide protected PC12 cells against amyloid-β peptide （25-35）-induced increases in mitochondrial membrane potential and intracellular reactive oxygen species levels. These protective effects were reversed by the selective mitochondrial adenosine triphosphate-sensitive potassium channel blocker 5-hydroxydecanoate. An inducible nitric oxide synthase inhibitor, Nw-nitro-L-arginine, also protected PC12 cells from amyloid-β peptide （25-35）-induced increases in both mitochondrial membrane potential and intracellular reactive oxygen species levels. However, the H202-degrading enzyme catalase could not reverse the amyloid-β peptide （25-35）-induced increase in intracellular reactive oxygen species. A 24-hour exposure to amyloid-13 peptide （25-35） did not result in apoptosis or necrosis, suggesting that the increases in both mitochondrial membrane potential and reactive oxygen species levels preceded cell death. The data suggest that amyloid-β peptide （25-35） cytotoxicity is associated with adenosine triphosphate-sensitive potassium channels and nitric oxide. Regulation of adenosine triphosphate-sensitive potassium channels suppresses PC12 cell cytotoxicity induced by amyloid-β peptide （25-35）.展开更多
Iron overload can lead to cytotoxicity, and it is a risk factor for diabetic peripheral neuropathy. However, the underlying mechanism remains unclear. We conjectured that iron overload-induced neurotoxicity might be a...Iron overload can lead to cytotoxicity, and it is a risk factor for diabetic peripheral neuropathy. However, the underlying mechanism remains unclear. We conjectured that iron overload-induced neurotoxicity might be associated with oxidative stress and the NF-E2-related factor 2 （Nrf2）/ARE signaling pathway. As an in vitro cellular model of diabetic peripheral neuropathy, PC12 cells ex- posed to high glucose concentration were used in this study. PC12 cells were cultured with ferric ammonium citrate at different concentrations to create iron overload. PC12 cells cultured in ferric ammonium citrate under high glucose concentration had significantly low cell viability, a high rate of apoptosis, and elevated reactive oxygen species and malondialdehyde levels. These changes were dependent on ferric ammonium citrate concentration. Nrf2 mRNA and protein expression in the ferric ammonium citrate groups were inhibited markedly in a dose-dependent manner. All changes could be inhibited by addition of deferoxamine. These results indicate that iron overload aggravates oxidative stress injury in neural cells under high glucose concentration and that the Nrf2/ARE sigfnaling pathway might play an important role in this process.展开更多
文摘Photocatalytic discoloration kinetics of Reactive Black 5 (RB5), a vinylsulfone dye, has been studied spectrophotometrically by following the decrease in dye concentration with time at ambient conditions using a flow loop reactor. UV lump, Black Light Blue (BLB) emitting at maximum wavelength of 365 nm and Ahlstrom Research Service paper consistent of TiO2 P500 coated on non woven paper was used respectively as source of UV light and photocatalyst. At natural pH, the result shows that photolysis of RB5 and its adsorption in the presence of photocatalyst was negligible while the photocatalytic oxidation (PCO) permits 30.8% of RB5 degradation. The degradation of dye was studied under a variety of conditions such as volumetric flow rate, initial pH, photocatalyst reuse, and in the presence of electron acceptor such as sodium persulphate ((Na)2S2O8). The degradation rates were found to be strongly influenced by all the above parameters. The circulation flow rate of 108 L/h was the best. The rate constant calculated when the initial pH was varied shows that pH 3 was more favorable for RB5 removal. Peroxydisulphate ions have the strong effect on RB5 discoloration even in dark without and with photocatalyst. When UV light was used in the presence of photocatalyst, 50 min was enough for quasi-total removal of RB5 with (0.2 M).
基金supported by the National Natural Science Foundation of China,No.31201951 and 31272613the Scientific and Technological Innovation Talent Scientific Research Foundation for the Returned Overseas Chinese Scholars by State Education Ministry and Heilongjiang Province in China,No.2012RFLXN005 and LC201018+1 种基金the Youth Science and Technology Foundation of Liaoning Medical University in China,No.Y2012Z023the Science and Technology Department of Liaoning Provincial Foundation Programs,No.2011214001
文摘Baicalin, a type of flavonoid extracted from the dried root of Scutellaria baicalensis georgi, has been shown to effectively inhibit cell apoptosis. Therefore, we assumed that baicalin would suppress colistin sulfate-induced neuronal apoptosis. PC12 cells exposed to colistin sulfate （62.5-500 μg/mL） for 24 hours resulted in PCl2 cell apoptosis. In addition, caspase-3 activity, lactate dehydrogenase level and free radical content increased in a dose-dependent manner. Subsequently, PC12 cells were pretreated with baicalin （25, 50 and 100 pg/mL）, and exposed to 125 pg/mL colistin sulfate. Cell morphology markedly changed, and cell viability increased. Moreover, caspase-3 activity, lac- tate dehydrogenase level and free radical content decreased. Results indicated that baicalin inhib- ited colistin sulfate-induced PC12 cell apoptosis by suppressing free radical injury, and reducing caspase-3 activity and lactate dehydrogenase activity.
基金supported by the National Natural Science Foundation of China,No.51073072the Natural Science Foundation of Zhejiang Province in China,No.Y4100745+1 种基金the Key Laboratory Open Foundation of Advanced Textile Materials&Manufacturing Technology of Zhejiang Sci-Tech University from Ministry of Education of China,No.2009007the Science and Technology Commission of Jiaxing Municipality Program,No.2010AY1089
文摘In this study, poly（L-lactic acid）/ammonium persulfate doped-polypyrrole composite fibrous scaffolds with moderate conductivity were produced by combining electrospinning with in situ polymerization. PC12 cells were cultured on these fibrous scaffolds and their growth following electrical stimulation （0-20.0 μA stimulus intensity, for 1-4 days） was observed using inverted light microscopy, and scanning electron microscopy coupled with the MTT cell viability test. The results demonstrated that the poly（L-lactic acid）/ammonium persulfate doped-polypyrrole fibrous scaffold was a dual multi-porous micro/nano fibrous scaffold. An electrical stimulation with a current intensity 5.0- 10.0 μAfor about 2 days enhanced neuronal growth and neurite outgrowth, while a high current intensity （over 15.0 μA） suppressed them. These results indicate that electrical stimulation with a moderate current intensity for an optimum time frame can promote neuronal growth and neurite outgrowth in an intensity- and time-dependent manner.
基金supported by the Project Sponsored by Yantai Science and Technology Bureau,China,No.2010232
文摘In this study, we treated PC12 cells with 0-20 μM amyloid-β peptide （25-35） for 24 hours to induce cytotoxicity, and found that 5-20 μM amyloid-β peptide （25-35） decreased PC12 cell viability, but adenosine triphosphate-sensitive potassium channel activator diazoxide suppressed the decrease in PC12 cell viability induced by amyloid-β peptide （25-35）. Diazoxide protected PC12 cells against amyloid-β peptide （25-35）-induced increases in mitochondrial membrane potential and intracellular reactive oxygen species levels. These protective effects were reversed by the selective mitochondrial adenosine triphosphate-sensitive potassium channel blocker 5-hydroxydecanoate. An inducible nitric oxide synthase inhibitor, Nw-nitro-L-arginine, also protected PC12 cells from amyloid-β peptide （25-35）-induced increases in both mitochondrial membrane potential and intracellular reactive oxygen species levels. However, the H202-degrading enzyme catalase could not reverse the amyloid-β peptide （25-35）-induced increase in intracellular reactive oxygen species. A 24-hour exposure to amyloid-13 peptide （25-35） did not result in apoptosis or necrosis, suggesting that the increases in both mitochondrial membrane potential and reactive oxygen species levels preceded cell death. The data suggest that amyloid-β peptide （25-35） cytotoxicity is associated with adenosine triphosphate-sensitive potassium channels and nitric oxide. Regulation of adenosine triphosphate-sensitive potassium channels suppresses PC12 cell cytotoxicity induced by amyloid-β peptide （25-35）.
基金supported by the Natural Science Foundation of Hubei Province,No.2010CDB09001
文摘Iron overload can lead to cytotoxicity, and it is a risk factor for diabetic peripheral neuropathy. However, the underlying mechanism remains unclear. We conjectured that iron overload-induced neurotoxicity might be associated with oxidative stress and the NF-E2-related factor 2 （Nrf2）/ARE signaling pathway. As an in vitro cellular model of diabetic peripheral neuropathy, PC12 cells ex- posed to high glucose concentration were used in this study. PC12 cells were cultured with ferric ammonium citrate at different concentrations to create iron overload. PC12 cells cultured in ferric ammonium citrate under high glucose concentration had significantly low cell viability, a high rate of apoptosis, and elevated reactive oxygen species and malondialdehyde levels. These changes were dependent on ferric ammonium citrate concentration. Nrf2 mRNA and protein expression in the ferric ammonium citrate groups were inhibited markedly in a dose-dependent manner. All changes could be inhibited by addition of deferoxamine. These results indicate that iron overload aggravates oxidative stress injury in neural cells under high glucose concentration and that the Nrf2/ARE sigfnaling pathway might play an important role in this process.
