The physicochemical properties of plasma-activated water(PAW)generated under different process conditions were investigated,and their changes under different storage conditions were also studied.The results showed tha...The physicochemical properties of plasma-activated water(PAW)generated under different process conditions were investigated,and their changes under different storage conditions were also studied.The results showed that increasing the processing time and power,and decreasing generated water volume,could cause an increase in the redox potential,conductivity,and temperature of PAW,and a decrease in its pH.A slower dissipation of the reactive oxygen and nitrogen species in PAW was found on storage at 4℃in a sealed conical flask than on storage at room temperature.The inactivation ability of plasma-activated lactic acid(LA)to Listeria monocytogenes(L.monocytogenes)and Pseudomonas aeruginosa(P.aeruginosa)was higher than that of PAW or LA alone under the same experimental conditions.The results of this study may provide theoretical information for the application of PAW as a potential antimicrobial agent in the future.展开更多
Portal hypertension （PHT） gastropathy is a frequent complication of fiver cirrhosis and one of the leading causes of death from cirrhosis. Apoptosis is widely considered to be an active energy-dependent mode of cell...Portal hypertension （PHT） gastropathy is a frequent complication of fiver cirrhosis and one of the leading causes of death from cirrhosis. Apoptosis is widely considered to be an active energy-dependent mode of cell death and a distinct entity from necrotic cell death. It is unclear whether gastric mucosal apoptosis is involved in PHT gastropa- thy. Prostaglandins （PGs） produced through cyclooxygenase （COX） are thought to play a key role in protection of the gastrointestinal mucosa from injury and apoptosis. However, the role of COX in PHT gastropathy is still not clearly understood. The aims of this study were to investigate whether （1） gastric mucosal apoptosis is involved in PHT gas- tropathy and （2） downregulation of COX contributes to this apoptosis. In this study, we show that gastric mucosal apoptosis was remarkably increased while mucosal proliferation was inhibited in PHT rats. Gastric mucosal COX- 1 was significantly suppressed at both the mRNA and protein levels, and PGE2 was reduced in PHT rats. Further, PGE2 treatment suppressed gastric mucosal apoptosis in PHT rats. However, gastric mucosal COX-2 levels did not differ between sham-operated rats and PHT rats. Gastric mucosal levels of tumor necrosis factor-α （TNF-α） and Fas ligand, but not TNF-related apoptosis-inducing ligand, were increased, and activated caspase-8 and caspase-3 levels were upregulated in PHT rats. The release of cytochrome c from the mitochondria to the cytosol was not observed in PHT rats. Our data indicate that downregulation of COX-1 is involved in gastric mucosal apoptosis via death signal- ing-mediated type-I cell death in PHT rats.展开更多
基金National Natural Science Foundation of China(No.32260643)for financial support of this study。
文摘The physicochemical properties of plasma-activated water(PAW)generated under different process conditions were investigated,and their changes under different storage conditions were also studied.The results showed that increasing the processing time and power,and decreasing generated water volume,could cause an increase in the redox potential,conductivity,and temperature of PAW,and a decrease in its pH.A slower dissipation of the reactive oxygen and nitrogen species in PAW was found on storage at 4℃in a sealed conical flask than on storage at room temperature.The inactivation ability of plasma-activated lactic acid(LA)to Listeria monocytogenes(L.monocytogenes)and Pseudomonas aeruginosa(P.aeruginosa)was higher than that of PAW or LA alone under the same experimental conditions.The results of this study may provide theoretical information for the application of PAW as a potential antimicrobial agent in the future.
文摘Portal hypertension （PHT） gastropathy is a frequent complication of fiver cirrhosis and one of the leading causes of death from cirrhosis. Apoptosis is widely considered to be an active energy-dependent mode of cell death and a distinct entity from necrotic cell death. It is unclear whether gastric mucosal apoptosis is involved in PHT gastropa- thy. Prostaglandins （PGs） produced through cyclooxygenase （COX） are thought to play a key role in protection of the gastrointestinal mucosa from injury and apoptosis. However, the role of COX in PHT gastropathy is still not clearly understood. The aims of this study were to investigate whether （1） gastric mucosal apoptosis is involved in PHT gas- tropathy and （2） downregulation of COX contributes to this apoptosis. In this study, we show that gastric mucosal apoptosis was remarkably increased while mucosal proliferation was inhibited in PHT rats. Gastric mucosal COX- 1 was significantly suppressed at both the mRNA and protein levels, and PGE2 was reduced in PHT rats. Further, PGE2 treatment suppressed gastric mucosal apoptosis in PHT rats. However, gastric mucosal COX-2 levels did not differ between sham-operated rats and PHT rats. Gastric mucosal levels of tumor necrosis factor-α （TNF-α） and Fas ligand, but not TNF-related apoptosis-inducing ligand, were increased, and activated caspase-8 and caspase-3 levels were upregulated in PHT rats. The release of cytochrome c from the mitochondria to the cytosol was not observed in PHT rats. Our data indicate that downregulation of COX-1 is involved in gastric mucosal apoptosis via death signal- ing-mediated type-I cell death in PHT rats.
