A simple hydrothermal process for fabrication of hematite
(α-Fe2O3) nanostructures with narrow size
distribution
was developed by using PVP as surfactant and NaAc as precipitation
agent. The influence of experimental parameters including the concentration
of the precursor, precipitation agent, stabilizing agent, and reaction
time was systematically investigated to study the possible formation
mechanism of α-Fe2O3. Finally, the electrochemical
properties of the obtained hematite particles were studied using cyclic
voltammetry and galvanostatic charge–discharge measurement
by a three-electrode system. The results reveal that their specific
capacitances are related to their sizes. By virtue of large surface
area, the as-prepared hematite nanoparticles can present the highest
capacitance (340.5 F·g–1) and an excellent
long cycle life within the operated voltage window (−0.1 to
0.44 V), demonstrating that the as-prepared hematite nanoparticles
can serve as one of the most excellent electrode materials for supercapacitors.
Background Berberine is a natural isoquinoline alkaloid that has been shown to have antitumor properties in a growing number of studies. However, its role in renal cell carcinoma remains unclear. This study investigates berberine's effect and mechanism in renal cell carcinoma.
Methods The methyl-tetrazolium, colony formation, and lactate dehydrogenase assay were used to detect proliferation and cytotoxicity, respectively. Flow cytometry, caspase-Glo 3/7 assay, and adenosine triphosphate assay were used to detect apoptosis and the adenosine triphosphate levels. Wound healing and transwell assay were used to examine the migration ability of renal cell carcinoma cells. Besides, the level of reactive oxygen species (ROS) was explored using a DCFH-DA-based kit. Additionally, western blot and Immunofluorescence assay was taken to determine the levels of relative proteins.
Results In vitro, our findings indicated that the proliferation and migration of renal cell carcinoma cells treated with berberine in various concentrations were inhibited, while the level of ROS and apoptosis rate were increased. Furthermore, The results of western blot showed that the expression of Bax, Bad, Bak, Cyto c, Clv-Caspase 3, Clv-Caspase 9, E-cadherin, TIMP-1and γH2AX were up-regulated, while Bcl-2, N-cadherin, Vimentin, Snail, Rad51 and PCNA were down-regulated after treating with berberine with various concentration.
Conclusion The result of this study revealed that berberine inhibits renal cell carcinoma progression via regulating ROS generation and inducing DNA break.
Background Berberine is a natural isoquinoline alkaloid that has been shown to have antitumor properties in a growing number of studies. However, its role in renal cell carcinoma remains unclear. This study investigates berberine's effect and mechanism in renal cell carcinoma.Methods The methyl-tetrazolium, colony formation, and lactate dehydrogenase assay were used to detect proliferation and cytotoxicity, respectively. Flow cytometry, caspase-Glo 3/7 assay, and adenosine triphosphate assay were used to detect apoptosis and the adenosine triphosphate levels. Wound healing and transwell assay were used to examine the migration ability of renal cell carcinoma cells. Besides, the level of reactive oxygen species (ROS) was explored using a DCFH-DA-based kit. Additionally, western blot and Immuno uorescence assay was taken to determine the levels of relative proteins.
ResultsIn vitro, our ndings indicated that the proliferation and migration of renal cell carcinoma cells treated with berberine in various concentrations were inhibited, while the level of ROS and apoptosis rate were increased. Furthermore, The results of western blot showed that the expression of Bax, Bad, Bak, Cyto c, Clv-Caspase 3, Clv-Caspase 9, E-cadherin, TIMP-1and γH2AX were up-regulated, while Bcl-2, Ncadherin, Vimentin, Snail, Rad51 and PCNA were down-regulated after treating with berberine with various concentration.
ConclusionThe result of this study revealed that berberine inhibits renal cell carcinoma progression via regulating ROS generation and inducing DNA break.
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