Objective: To investigate the effects of emulsified isoflurane on hypoxic pulmonary artery endothelial cells (HPAECs) injury and orphan nuclear receptor subfamily 4A1 (NR4A1) expression. Methods: HPAECs were divided i...Objective: To investigate the effects of emulsified isoflurane on hypoxic pulmonary artery endothelial cells (HPAECs) injury and orphan nuclear receptor subfamily 4A1 (NR4A1) expression. Methods: HPAECs were divided into normal control group, model group and test group. Normal control group was cultured under normoxia. Cells in model group and test group were treated in a hypoxic chamber with oxygen concentration of about 3% (95% N2+ 5% CO2) for 2 h. The final concentration of 1 mmol·L-1 emulsified isoflurane was added to the test group, and 30% Intralipid? was added to the normal control group and the model group. MTT method was used to detect cell proliferation, Hoechst 33258 nuclear staining was used to detect cell apoptosis, Griess method was used to detect the production of NO in cell supernatant, and real-time fluorescence quantitative PCR (q-RT-PCR) was used to detect the expression of NR4A1 in cells. Results: After 12 h of intervention, the cell viability of normal control group, model group and test group were (98.45±2.41)%, (15.46±2.69)%, (79.52±4.16)%, the apoptosis rate were (2.51±0.36)%, (50.12±3.36)%, (22.15±3.42)%respectively, the concentration of NO in the culture supernatant were (59.52±4.1) μmol·L^-1, (25.16±4.85) μmol·L^-1, (43.58±6.19) μmol·L^-1, and the relative expression of NR4A1 were 1.00±0.09, 5.89±0.41, 2.39±0.24, respectively. The difference was statistically significant (P<0.05). Conclusion: Emulsified isoflurane can promote the proliferation, inhibit apoptosis and increase NO production of hypoxic HPAECs. NR4A1 may be involved in the endogenous protective mechanism of endothelial cell injury after hypoxia.展开更多
基金supported by the Seed Fund Program of Shanghai University of Medicine&Health Sciences(Grant No.HMSF-16-22-026).
文摘Objective: To investigate the effects of emulsified isoflurane on hypoxic pulmonary artery endothelial cells (HPAECs) injury and orphan nuclear receptor subfamily 4A1 (NR4A1) expression. Methods: HPAECs were divided into normal control group, model group and test group. Normal control group was cultured under normoxia. Cells in model group and test group were treated in a hypoxic chamber with oxygen concentration of about 3% (95% N2+ 5% CO2) for 2 h. The final concentration of 1 mmol·L-1 emulsified isoflurane was added to the test group, and 30% Intralipid? was added to the normal control group and the model group. MTT method was used to detect cell proliferation, Hoechst 33258 nuclear staining was used to detect cell apoptosis, Griess method was used to detect the production of NO in cell supernatant, and real-time fluorescence quantitative PCR (q-RT-PCR) was used to detect the expression of NR4A1 in cells. Results: After 12 h of intervention, the cell viability of normal control group, model group and test group were (98.45±2.41)%, (15.46±2.69)%, (79.52±4.16)%, the apoptosis rate were (2.51±0.36)%, (50.12±3.36)%, (22.15±3.42)%respectively, the concentration of NO in the culture supernatant were (59.52±4.1) μmol·L^-1, (25.16±4.85) μmol·L^-1, (43.58±6.19) μmol·L^-1, and the relative expression of NR4A1 were 1.00±0.09, 5.89±0.41, 2.39±0.24, respectively. The difference was statistically significant (P<0.05). Conclusion: Emulsified isoflurane can promote the proliferation, inhibit apoptosis and increase NO production of hypoxic HPAECs. NR4A1 may be involved in the endogenous protective mechanism of endothelial cell injury after hypoxia.
