Department of Anesthesiology, The Second People's Hospital of Yunnan Province, Kunming, Yunnan, China.
PLoS One. 2024 Jun 14;19(6):e0305409. doi: 10.1371/journal.pone.0305409. eCollection 2024.
Pulmonary fibrosis caused by lung injury is accompanied by varying degrees of inflammation, and diazepam can reduce the levels of inflammatory factors. Therefore, the purpose of this study was to determine whether diazepam can inhibit inflammation and ameliorate pulmonary fibrosis by regulating the let-7a-5p/myeloid differentiation factor 88 (MYD88) axis.
Lipopolysaccharide (LPS) was used to induce cell pyroptosis in an animal model of pulmonary fibrosis. After treatment with diazepam, changes in cell proliferation and apoptosis were observed, and the occurrence of inflammation and pulmonary fibrosis in the mice was detected.
The results showed that LPS can successfully induce cell pyroptosis and inflammatory responses and cause lung fibrosis in mice. Diazepam inhibits the expression of pyroptosis-related factors and inflammatory factors; moreover, it attenuates the occurrence of pulmonary fibrosis in mice. Mechanistically, diazepam can upregulate the expression of let-7a-5p, inhibit the expression of MYD88, and reduce inflammation and inhibit pulmonary fibrosis by regulating the let-7a-5p/MYD88 axis.
Our findings indicated that diazepam can inhibit LPS-induced pyroptosis and inflammatory responses and alleviate pulmonary fibrosis in mice by regulating the let-7a-5p/MYD88 axis.
肺损伤引起的肺纤维化伴有不同程度的炎症，地西泮可以降低炎症因子的水平。因此，本研究旨在确定地西泮是否可以通过调节 let-7a-5p/髓样分化因子 88（MYD88）轴来抑制炎症和改善肺纤维化。
采用脂多糖（LPS）诱导肺纤维化动物模型中的细胞焦亡。用地西泮处理后，观察细胞增殖和凋亡的变化，并检测小鼠的炎症和肺纤维化发生情况。
结果表明，LPS 可成功诱导细胞焦亡和炎症反应，并导致小鼠肺纤维化。地西泮抑制焦亡相关因子和炎症因子的表达；此外，还能减轻小鼠肺纤维化的发生。机制上，地西泮可以上调 let-7a-5p 的表达，抑制 MYD88 的表达，通过调节 let-7a-5p/MYD88 轴来减轻炎症和抑制肺纤维化。
本研究结果表明，地西泮通过调节 let-7a-5p/MYD88 轴，可抑制 LPS 诱导的细胞焦亡和炎症反应，减轻小鼠肺纤维化。
