目的研究支气管哮喘患儿血清中环状RNA(circular RNA,circRNA)同源域相互作用蛋白激酶3(circRNA homeodomain-iteracting protein kinase 3,circHIPK3)表达水平与气道重塑的关系。方法纳入2019年10月—2021年12月我院收治的支气管哮喘患...目的研究支气管哮喘患儿血清中环状RNA(circular RNA,circRNA)同源域相互作用蛋白激酶3(circRNA homeodomain-iteracting protein kinase 3,circHIPK3)表达水平与气道重塑的关系。方法纳入2019年10月—2021年12月我院收治的支气管哮喘患儿90例(支气管哮喘组),按2018版哮喘分级标准,分为间歇状态组54例,轻度组22例,中重度组14例;选择同期本院体检的健康者95例为对照组,实时荧光定量PCR检测血清中circHIPK3表达,检测肺功能指标及气道重塑指标。收集儿童哮喘控制测试(childhood asthma control test,C-ACT)评分。Pearson法分析circHIPK3表达水平与肺功能指标及气道重塑指标的相关性。结果与对照组相比,支气管哮喘组血清circHIPK3表达水平较高,差异有统计学意义(P<0.05);与对照组相比,支气管哮喘组支气管壁占支气管总横截面积的百分比(WA)、支气管管壁厚度与外直径的比值(T/D)较高,第一秒用力呼气容积(forced expiratory volume in one second,FEV1)、FEV1/用力肺活量(forced vital capacity,FVC)、最大呼气中期流量(maximum mid-expiratory flow,MMEF)较低,差异均具有统计学意义(P<0.05)。对照组、间歇状态组、轻度组、中重度组circHIPK3表达、WA、T/D依次升高,FEV1、FEV1/FVC、MMEF、C-ACT评分依次降低,差异均具有统计学意义(P<0.05)。与circHIPK3低表达组相比,circHIPK3高表达组WA、T/D较高,FEV1、FEV1/FVC、MMEF、C-ACT评分较低,差异均具有统计学意义(P<0.05)。Pearson法分析显示,circHIPK3与FEV1、FEV1/FVC、MMEF、C-ACT评分呈负相关(P<0.05),与WA、T/D呈正相关(P<0.05)。结论支气管哮喘患儿血清中circHIPK3表达上调,可能与患儿气道重塑有关。展开更多
Objective: To investigate the effect and potential mechanism of dihydromyricetin(Dmy) on H9C2 cell proliferation, apoptosis, and autophagy. Methods: H9C2 cells were randomly divided into 7 groups, namely control, mode...Objective: To investigate the effect and potential mechanism of dihydromyricetin(Dmy) on H9C2 cell proliferation, apoptosis, and autophagy. Methods: H9C2 cells were randomly divided into 7 groups, namely control, model, EV(empty p CDH-CMV-MCS-EF1-Cop GFP-T2A-Puro vector), IV(circHIPK3 interference), Dmy(50 μmol/L), Dmy+IV, and Dmy+EV groups. Cell proliferation and apoptosis were detected by cell counting kit-8 assay and flow cytometry, respectivley. Western blot was used to evaluate the levels of light chain 3 Ⅱ/Ⅰ(LC3Ⅱ/Ⅰ), phospho-phosphoinositide 3-kinase(p-PI3K), protein kinase B(p-AKT), and phospho-mammalian target of rapamycin(p-mTOR). The level of circHIPK3 was determined using reverse transcriptase polymerase chain reaction. Electron microscopy was used to observe autophagosomes in H9C2 cells. Results: Compared to H9C2 cells, the expression of circHIPK in H9C2 hypoxia model cells increased significantly(P<0.05). Compared to the control group, the cell apoptosis and autophagosomes increased, cell proliferation rate decreased significantly, and the expression of LC3Ⅱ/Ⅰ significantly increased(all P<0.05). Compared to the model group, the rate of apoptosis and autophagosomes in IV, Dmy, and Dmy+IV group decreased, the cell proliferation rate increased, and the expression of LC3Ⅱ/Ⅰ decreased significantly(all P<0.05). Compared to the control group, the expressions of p-PI3K, p-AKT, and p-mTOR in the model group significantly reduced(P<0.05), whereas after treatment with Dmy and sh-circHIPK3, the above situation was reversed(P<0.05). Conclusion: Dmy plays a protective role in H9C2 cells by inhibiting circHIPK expression and cell apoptosis and autophagy, and the mechanism may be related to PI3K/AKT/mTOR pathway.展开更多
文摘目的研究支气管哮喘患儿血清中环状RNA(circular RNA,circRNA)同源域相互作用蛋白激酶3(circRNA homeodomain-iteracting protein kinase 3,circHIPK3)表达水平与气道重塑的关系。方法纳入2019年10月—2021年12月我院收治的支气管哮喘患儿90例(支气管哮喘组),按2018版哮喘分级标准,分为间歇状态组54例,轻度组22例,中重度组14例;选择同期本院体检的健康者95例为对照组,实时荧光定量PCR检测血清中circHIPK3表达,检测肺功能指标及气道重塑指标。收集儿童哮喘控制测试(childhood asthma control test,C-ACT)评分。Pearson法分析circHIPK3表达水平与肺功能指标及气道重塑指标的相关性。结果与对照组相比,支气管哮喘组血清circHIPK3表达水平较高,差异有统计学意义(P<0.05);与对照组相比,支气管哮喘组支气管壁占支气管总横截面积的百分比(WA)、支气管管壁厚度与外直径的比值(T/D)较高,第一秒用力呼气容积(forced expiratory volume in one second,FEV1)、FEV1/用力肺活量(forced vital capacity,FVC)、最大呼气中期流量(maximum mid-expiratory flow,MMEF)较低,差异均具有统计学意义(P<0.05)。对照组、间歇状态组、轻度组、中重度组circHIPK3表达、WA、T/D依次升高,FEV1、FEV1/FVC、MMEF、C-ACT评分依次降低,差异均具有统计学意义(P<0.05)。与circHIPK3低表达组相比,circHIPK3高表达组WA、T/D较高,FEV1、FEV1/FVC、MMEF、C-ACT评分较低,差异均具有统计学意义(P<0.05)。Pearson法分析显示,circHIPK3与FEV1、FEV1/FVC、MMEF、C-ACT评分呈负相关(P<0.05),与WA、T/D呈正相关(P<0.05)。结论支气管哮喘患儿血清中circHIPK3表达上调,可能与患儿气道重塑有关。
基金Supported by Science Foundation of Education Department of Shaanxi Provincial Government (No.19JK0890)Natural Science Foundation of Xizang (Tibet) Autonomous Region (No.XZ202001ZR0089G)+1 种基金Major Training Project of Xizang Minzu University (Nos.18MDZ03 and 20MDT03)Funded Project of Young Scholar Cultivation Program of Xizang Minzu University (No.21MDX04)。
文摘Objective: To investigate the effect and potential mechanism of dihydromyricetin(Dmy) on H9C2 cell proliferation, apoptosis, and autophagy. Methods: H9C2 cells were randomly divided into 7 groups, namely control, model, EV(empty p CDH-CMV-MCS-EF1-Cop GFP-T2A-Puro vector), IV(circHIPK3 interference), Dmy(50 μmol/L), Dmy+IV, and Dmy+EV groups. Cell proliferation and apoptosis were detected by cell counting kit-8 assay and flow cytometry, respectivley. Western blot was used to evaluate the levels of light chain 3 Ⅱ/Ⅰ(LC3Ⅱ/Ⅰ), phospho-phosphoinositide 3-kinase(p-PI3K), protein kinase B(p-AKT), and phospho-mammalian target of rapamycin(p-mTOR). The level of circHIPK3 was determined using reverse transcriptase polymerase chain reaction. Electron microscopy was used to observe autophagosomes in H9C2 cells. Results: Compared to H9C2 cells, the expression of circHIPK in H9C2 hypoxia model cells increased significantly(P<0.05). Compared to the control group, the cell apoptosis and autophagosomes increased, cell proliferation rate decreased significantly, and the expression of LC3Ⅱ/Ⅰ significantly increased(all P<0.05). Compared to the model group, the rate of apoptosis and autophagosomes in IV, Dmy, and Dmy+IV group decreased, the cell proliferation rate increased, and the expression of LC3Ⅱ/Ⅰ decreased significantly(all P<0.05). Compared to the control group, the expressions of p-PI3K, p-AKT, and p-mTOR in the model group significantly reduced(P<0.05), whereas after treatment with Dmy and sh-circHIPK3, the above situation was reversed(P<0.05). Conclusion: Dmy plays a protective role in H9C2 cells by inhibiting circHIPK expression and cell apoptosis and autophagy, and the mechanism may be related to PI3K/AKT/mTOR pathway.
