PubMed:32340415 JSONTXT

{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":139},"obj":"Sentence"},{"id":"T2","span":{"begin":140,"end":150},"obj":"Sentence"},{"id":"T3","span":{"begin":151,"end":309},"obj":"Sentence"},{"id":"T4","span":{"begin":310,"end":549},"obj":"Sentence"},{"id":"T5","span":{"begin":550,"end":685},"obj":"Sentence"},{"id":"T6","span":{"begin":686,"end":1060},"obj":"Sentence"},{"id":"T7","span":{"begin":1061,"end":1133},"obj":"Sentence"},{"id":"T8","span":{"begin":1134,"end":1218},"obj":"Sentence"},{"id":"T9","span":{"begin":1219,"end":1403},"obj":"Sentence"},{"id":"T10","span":{"begin":1404,"end":1458},"obj":"Sentence"},{"id":"T11","span":{"begin":1459,"end":1600},"obj":"Sentence"},{"id":"T12","span":{"begin":1601,"end":1647},"obj":"Sentence"},{"id":"T13","span":{"begin":1648,"end":1857},"obj":"Sentence"},{"id":"T14","span":{"begin":1858,"end":1963},"obj":"Sentence"},{"id":"T15","span":{"begin":1964,"end":2078},"obj":"Sentence"},{"id":"T16","span":{"begin":2079,"end":2617},"obj":"Sentence"},{"id":"T17","span":{"begin":2618,"end":2764},"obj":"Sentence"},{"id":"T18","span":{"begin":2765,"end":2777},"obj":"Sentence"},{"id":"T19","span":{"begin":2778,"end":2825},"obj":"Sentence"},{"id":"T20","span":{"begin":2826,"end":3004},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":139},"obj":"Sentence"},{"id":"T2","span":{"begin":140,"end":150},"obj":"Sentence"},{"id":"T3","span":{"begin":151,"end":309},"obj":"Sentence"},{"id":"T4","span":{"begin":310,"end":549},"obj":"Sentence"},{"id":"T5","span":{"begin":550,"end":685},"obj":"Sentence"},{"id":"T6","span":{"begin":686,"end":1060},"obj":"Sentence"},{"id":"T7","span":{"begin":1061,"end":1133},"obj":"Sentence"},{"id":"T8","span":{"begin":1134,"end":1218},"obj":"Sentence"},{"id":"T9","span":{"begin":1219,"end":1403},"obj":"Sentence"},{"id":"T10","span":{"begin":1404,"end":1458},"obj":"Sentence"},{"id":"T11","span":{"begin":1459,"end":1600},"obj":"Sentence"},{"id":"T12","span":{"begin":1601,"end":1647},"obj":"Sentence"},{"id":"T13","span":{"begin":1648,"end":1857},"obj":"Sentence"},{"id":"T14","span":{"begin":1858,"end":1963},"obj":"Sentence"},{"id":"T15","span":{"begin":1964,"end":2078},"obj":"Sentence"},{"id":"T16","span":{"begin":2079,"end":2617},"obj":"Sentence"},{"id":"T17","span":{"begin":2618,"end":2764},"obj":"Sentence"},{"id":"T18","span":{"begin":2765,"end":2777},"obj":"Sentence"},{"id":"T19","span":{"begin":2778,"end":2825},"obj":"Sentence"},{"id":"T20","span":{"begin":2826,"end":3004},"obj":"Sentence"}],"text":"[Role of 14-3-3σgene in the regulation of endotoxin/lipopolysaccharide-induced inflammatory responses in human pulmonary epithelial cells].\nObjective: To explore the mechanism of 14-3-3σgene in regulating inflammatory response of human pulmonary epithelial cells induced by endotoxin/lipopolysaccharide (LPS). Methods: (1) Cells of human normal pulmonary epithelial cell line BEAS-2B cultured in logarithmic growth period were collected and divided into control group and PCMV6-14-3-3σgroup using the random number table, with 3 wells in each group. Cells in control group were transfected with empty plasmid, and cells in PCMV6-14-3-3σgroup were transfected with PCMV6-14-3-3σplasmid. The protein expression of 14-3-3σin cell was detected by Western blotting at 48 hours after transfection. (2) Cells of human normal pulmonary epithelial cell line BEAS-2B cultured in logarithmic growth period were collected and divided into control group, PCMV6-14-3-3σgroup, PCMV6-14-3-3σ+ LPS group, and LPS group using the random number table, with 3 wells in each group. Cells in control group were transfected with empty plasmid for 42 hours. Cells in PCMV6-14-3-3σgroup were transfected with PCMV6-14-3-3σplasmid for 42 hours. Cells in PCMV6-14-3-3σ+ LPS group were stimulated with 1 μg/mL LPS (the same final mass concentration below) for 6 hours after being transfected with PCMV6-14-3-3σplasmid for 42 hours. Cells in LPS group were stimulated by LPS for 6 hours. The protein expressions of Bax and B-cell lymphoma-2 (Bcl-2) were detected by Western blotting, and the ratio of Bax to Bcl-2 was calculated. Apoptotic rate was detected by flow cytometry. The mRNA expressions of tumor necrosis factor alpha (TNF-α) and interleukin 1beta (IL-1β) in cells were detected by real-time fluorescent quantitative reverse transcription polymerase chain reaction technique. Content of TNF-α and IL-1β in cell culture supernatant was detected by enzyme-linked immunosorbent assay. Data were statistically analyzed with t test, one-way analysis of variance, and least significant difference test. Results: (1) At 48 hours after transfection, the protein expression of 14-3-3σin cells of PCMV6-14-3-3σgroup (1.05±0.03) was significantly higher than that in control group (0.78±0.04, t=5.41, P\u003c0.01). (2) Compared with those in control group, the ratio of Bax to Bcl-2, apoptotic rate, mRNA expressions of TNF-α and IL-1β, and content of TNF-α and IL-1β in cell supernatant in PCMV6-14-3-3σgroup showed no significant difference (P\u003e0.05); the above-mentioned indexes of cells in LPS group were significantly higher or increased (P\u003c0.01). Compared with those in LPS group, the above-mentioned indexes of cells in PCMV6-14-3-3σ+ LPS group were significantly lower or decreased (P\u003c0.01). Conclusions: 14-3-3σis a key factor in regulating apoptosis. It can alleviate the LPS-induced inflammatory responses by regulating the ratio of apoptotic regulators Bax to Bcl-2 and inhibiting apoptosis of human pulmonary epithelial cells."}