王守君.急诊集束化治疗急性心力衰竭患者的疗效[J].内科急危重症杂志,2019,25(5):404-406
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| DOI：10.11768/nkjwzzzz20190515 |
| 中文关键词: 急诊集束化 急性心力衰竭 疗效 气管插管率 心肺功能 |
| 英文关键词:Pirfnidone Lung fibroblasts p38MAPK Collagen TGF-β1 |
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| 中文摘要: |
| 目的：探讨急诊集束化治疗急性心力衰竭患者的影响。方法：选取急性心力衰竭患者100例，实施信封随机化方式分为对照组和观察组，各50例组，对照组采用常规急诊治疗方案，观察组采用急诊集束化干预。结果：观察组患者左心室舒张早期最大血流（E峰）、左心室射血分数(LVEF)、左心室收缩末期内径(LVESD）、左心室舒张末期内径(LVEDD）、动脉血氧分压(PaO2）、收缩压(SBP）、呼吸(RR）、氧饱和度(SaO2)、1秒用力呼气量(FEV1)、最大肺活量(FVC）、FEV1/FVC、气短缓解时间、不良事件发生率、气管插管率、总有效率均优于对照组（均P＜0.05）。结论：急诊集束化治疗用于急性心力衰竭患者效果显著，能降低气管插管率，提高患者疗效，改善患者心肺功能。 |
| 英文摘要: |
| Objective: To investigate the effect of pirfnidone on collagen synthesis induced by TGF-β 1 in lung fibroblasts and its mechanism. Methods: Human embryonic lung fibroblast MRC-5 cells were used as objects of study. TGF-β 1 induced collagen synthesis in lung fibroblasts. The cells were treated with pirfnidone, cell proliferation was measured by MTT, Western blotting was used to detect the expression of Col III and Col I protein, and the level of p38MAPK phosphorylation in cells. The p38MAPK signal inhibitor SB203580 and pirfnidone were used to treat TGF-β1-induced lung fibroblasts. MTT was used to detect cell proliferation, Western blotting was used to detect the expression of Col III and Col I protein, and the level of p38MAPK phosphorylation in cells. Results TGF-β 1 induced increased proliferation of lung fibroblasts after treatment, and the phosphorylation level of Col III, Col I and p38MAPK increased in cells. Pirfidone treatment could reduce the proliferation of lung fibroblasts induced by TGF-β 1, and inhibit the expression of Col III, Col I and p38MAPK phosphorylation proteins in cells. The treatment of SB203580 could cooperate with pirfenidone to reduce the proliferation of lung fibroblasts induced by TGF-β1 and the phosphorylation levels of Col III, Col I and p38 MAPK. Conclusion: Pirfnidone inhibits TGF-β1-induced collagen synthesis in lung fibroblasts by inhibiting the p38MAPK signaling. |
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