Department of General Medical, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, 030032, China.
Department of Pulmonary and Critical Care Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, No. 99 Longcheng Street, Taiyuan, 030032, China.
Appl Biochem Biotechnol. 2024 Jun;196(6):3374-3386. doi: 10.1007/s12010-023-04671-y. Epub 2023 Sep 1.
To investigate the effects of Baicalin on the apoptosis of human bronchial epithelial cells (16HBE) induced by cigarette smoke extract (CSE) and the release of inflammatory factors, and to clarify its possible mechanism. CSE was used to treat 16HBE cells and construct COPD cell model. The activity of 16HBE cells was detected by CCK-8 and BrdU. Real-time fluorescence quantitative PCR (RT-QPCR) was used to detect the expression level of miR-125a in each group of 16HBE cells. At the same time, the levels of 16HBE inflammatory cytokines IL-1β, IL-8, IL-6, and TNF-α were detected. The apoptosis rate of 16HBE cells in each group was detected by TUNEL. Compared with the control group, the proliferation of 16HBE cells in CSE group was decreased. Baicalin reversed the effect of 2% CSE on the proliferation of 16HBE cells. Baicalin also reversed the effect of 2% CSE on apoptosis and inflammatory factors in 16HBE cells. miR-125a is highly expressed in COPD, and Baicalin can inhibit the expression of miR-125a. Silencing miR-125a reduces apoptosis and inflammatory response of 16HBE cells in COPD. miR-125a reversed the effects of Baicalin on apoptosis and inflammation of 16HBE cells. Baicalin can reduce CSE-induced apoptosis of human bronchial epithelial cells and release of inflammatory factors, and its mechanism may be related to the inhibition of miR-125a.
为了研究黄芩素对香烟烟雾提取物（CSE）诱导的人支气管上皮细胞（16HBE）凋亡和炎症因子释放的影响，并阐明其可能的机制。用 CSE 处理 16HBE 细胞，构建 COPD 细胞模型。通过 CCK-8 和 BrdU 检测 16HBE 细胞的活性。实时荧光定量 PCR（RT-QPCR）检测各组 16HBE 细胞中 miR-125a 的表达水平。同时，检测各组 16HBE 炎症因子 IL-1β、IL-8、IL-6 和 TNF-α的水平。TUNEL 检测各组 16HBE 细胞的凋亡率。与对照组相比，CSE 组 16HBE 细胞的增殖减少。黄芩素逆转了 2% CSE 对 16HBE 细胞增殖的影响。黄芩素还逆转了 2% CSE 对 16HBE 细胞凋亡和炎症因子的影响。miR-125a 在 COPD 中高表达，黄芩素可以抑制 miR-125a 的表达。沉默 miR-125a 可减少 COPD 中 16HBE 细胞的凋亡和炎症反应。miR-125a 逆转了黄芩素对 16HBE 细胞凋亡和炎症的作用。黄芩素可降低 CSE 诱导的人支气管上皮细胞凋亡和炎症因子释放，其机制可能与抑制 miR-125a 有关。
