Objective: To explore the complications of long-term placement of Montgomery T silicone stent (T-tube) in the treatment of subglottic benign airway stenosis (SBAS) and the timing of successful T-tube removal. Methods: We retrospectively collected the clinical data of 32 patients with SBAS who underwent the treatment of T-tube and analyzed their placement and successful removal of the T-tube. Results: There were 22 males and 10 females, aged from 21 to 79 years (60.9 ± 13.7 years). The T-tubes were successfully placed in all 32 patients, and 6 patients (18.8%) with mild stenosis were placed by the intravenous conscious sedation. The longest follow-up period was 60.4 months, and 17 patients (53.1%) had the T-tubes for more than 12 months; 5 patients (15.6%) were changed to the tracheostomy cannula after unplanned removal of the T-tubes for various reasons; the T-tubes were successfully removed in 9 patients (28.1%), and the duration of T-tubes placement was 5.2-22.7 months (12.1 ± 6.3 months), among them anatomical stenosis in 9 patients (100%). Secretion retention was observed in 32 patients (100%), granulation tissue hyperplasia was observed in 9 patients (28.1%), and the normal ventilation was not affected in most patients by bronchoscopic treatment and follow-up; the T-tubes were removed in 3 patients due to severe complications. There was no significant difference in the incidences of secretion retention and granulation tissue hyperplasia between the time point at 1 week, 1 month, 3 months, and 12 months, p > 0.05. In patients with T-tube more than 12 months, the severity of secretion retention at 1 week, 1 month, 3 months, and 12 months was significantly different, p < 0.05, however, there was no significant difference in the severity of granulation tissue hyperplasia, p > 0.05. Conclusions: T-tube is safe and effective in the treatment of SBAS. The severity of secretion retention increased in patients with long-term placement of the T-tube. For patients with mild stenosis and anatomical stenosis, the T-tube removal can be attempted at about 1 year of follow-up.
目的探讨长期放置蒙哥马利 T 型硅胶支架(T 型管)治疗声门下良性气道狭窄(SBAS)的并发症以及成功拔除 T 型管的时机。方法我们回顾性地收集了 32 例接受 T 型管治疗的 SBAS 患者的临床资料,并分析了他们放置和成功拔除 T 型管的情况。结果:男 22 例,女 10 例:其中男性 22 例,女性 10 例,年龄从 21 岁到 79 岁(60.9±13.7)岁。所有 32 名患者都成功置入了 T 型管,其中 6 名轻度狭窄患者(18.8%)在静脉清醒镇静的情况下置入了 T 型管。最长随访时间为 60.4 个月,17 名患者(53.1%)留置 T 型管超过 12 个月;5 名患者(15.6%)因各种原因意外拔除 T 型管后改用气管造口插管;9 名患者(28.1%)成功拔除 T 型管,留置 T 型管时间为 5.2-22.7 个月(12.1±6.3 个月),其中 9 名患者(100%)为解剖性狭窄。32 例患者(100%)出现分泌物潴留,9 例患者(28.1%)出现肉芽组织增生,通过支气管镜治疗和随访,大多数患者的正常通气未受影响;3 例患者因严重并发症而拔除 T 型管。1周、1个月、3个月和12个月时点的分泌物潴留和肉芽组织增生发生率无明显差异,P>0.05。在插管超过 12 个月的患者中,1 周、1 个月、3 个月和 12 个月时分泌物潴留的严重程度有显著差异(P < 0.05),但肉芽组织增生的严重程度无显著差异(P > 0.05)。结论T管治疗SBAS安全有效。长期放置 T 型管的患者分泌物潴留的严重程度增加。对于轻度狭窄和解剖性狭窄的患者,可在随访 1 年左右时尝试拔除 T 型管。
{"title":"Clinical Analysis of 32 Cases of Subglottic Benign Airway Stenosis Treated With Montgomery T Silicone Stent.","authors":"Zhenyu Yang, Xiaoli Zhou, Wenying Pan, Daxiong Zeng, Junhong Jiang","doi":"10.1155/2024/2145560","DOIUrl":"10.1155/2024/2145560","url":null,"abstract":"<p><p><b>Objective:</b> To explore the complications of long-term placement of Montgomery T silicone stent (T<i>-</i>tube) in the treatment of subglottic benign airway stenosis (SBAS) and the timing of successful T<i>-</i>tube removal. <b>Methods:</b> We retrospectively collected the clinical data of 32 patients with SBAS who underwent the treatment of T<i>-</i>tube and analyzed their placement and successful removal of the T<i>-</i>tube. <b>Results:</b> There were 22 males and 10 females, aged from 21 to 79 years (60.9 ± 13.7 years). The T<i>-</i>tubes were successfully placed in all 32 patients, and 6 patients (18.8%) with mild stenosis were placed by the intravenous conscious sedation. The longest follow-up period was 60.4 months, and 17 patients (53.1%) had the T<i>-</i>tubes for more than 12 months; 5 patients (15.6%) were changed to the tracheostomy cannula after unplanned removal of the T<i>-</i>tubes for various reasons; the T<i>-</i>tubes were successfully removed in 9 patients (28.1%), and the duration of T<i>-</i>tubes placement was 5.2-22.7 months (12.1 ± 6.3 months), among them anatomical stenosis in 9 patients (100%). Secretion retention was observed in 32 patients (100%), granulation tissue hyperplasia was observed in 9 patients (28.1%), and the normal ventilation was not affected in most patients by bronchoscopic treatment and follow-up; the T<i>-</i>tubes were removed in 3 patients due to severe complications. There was no significant difference in the incidences of secretion retention and granulation tissue hyperplasia between the time point at 1 week, 1 month, 3 months, and 12 months, <i>p</i> > 0.05. In patients with T<i>-</i>tube more than 12 months, the severity of secretion retention at 1 week, 1 month, 3 months, and 12 months was significantly different, <i>p</i> < 0.05, however, there was no significant difference in the severity of granulation tissue hyperplasia, <i>p</i> > 0.05. <b>Conclusions:</b> T<i>-</i>tube is safe and effective in the treatment of SBAS. The severity of secretion retention increased in patients with long-term placement of the T<i>-</i>tube. For patients with mild stenosis and anatomical stenosis, the T<i>-</i>tube removal can be attempted at about 1 year of follow-up.</p>","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"2024 ","pages":"2145560"},"PeriodicalIF":2.1,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11498979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495643","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nafeisa Dilixiati,Mengyu Lian,Ziliang Hou,Jie Song,Jingjing Yang,Ruiyan Lin,Jinxiang Wang
This study aimed to develop nomograms to predict high hospitalization costs and prolonged stays in hospitalized acute exacerbations of chronic obstructive pulmonary disease (AECOPD) patients with community-acquired pneumonia (CAP), also known as pAECOPD. A total of 635 patients with pAECOPD were included in this observational study and divided into training and testing sets. Variables were initially screened using univariate analysis, and then further selected using a backward stepwise regression. Multivariable logistic regression was performed to establish nomograms. The predictive performance of the model was evaluated using the receiver operating characteristic (ROC) curve, area under the curve (AUC), calibration curve, and decision curve analysis (DCA) in both the training and testing sets. Finally, the logistic regression analysis showed that elevated white blood cell count (WBC>10 × 109 cells/l), hypoalbuminemia, pulmonary encephalopathy, respiratory failure, diabetes, and respiratory intensive care unit (RICU) admissions were risk factors for predicting high hospitalization costs in pAECOPD patients. The AUC value was 0.756 (95% CI: 0.699-0.812) in the training set and 0.792 (95% CI: 0.718-0.867) in the testing set. The calibration plot and DCA curve indicated the model had good predictive performance. Furthermore, decreased total protein, pulmonary encephalopathy, reflux esophagitis, and RICU admissions were risk factors for predicting prolonged stays in pAECOPD patients. The AUC value was 0.629 (95% CI: 0.575-0.682) in the training set and 0.620 (95% CI: 0.539-0.701) in the testing set. The calibration plot and DCA curve indicated the model had good predictive performance. We developed and validated two nomograms for predicting high hospitalization costs and prolonged stay, respectively, among hospitalized patients with pAECOPD. This trial is registered with ChiCTR2000039959.
{"title":"Nomograms for Predicting High Hospitalization Costs and Prolonged Stay among Hospitalized Patients with pAECOPD.","authors":"Nafeisa Dilixiati,Mengyu Lian,Ziliang Hou,Jie Song,Jingjing Yang,Ruiyan Lin,Jinxiang Wang","doi":"10.1155/2024/2639080","DOIUrl":"https://doi.org/10.1155/2024/2639080","url":null,"abstract":"This study aimed to develop nomograms to predict high hospitalization costs and prolonged stays in hospitalized acute exacerbations of chronic obstructive pulmonary disease (AECOPD) patients with community-acquired pneumonia (CAP), also known as pAECOPD. A total of 635 patients with pAECOPD were included in this observational study and divided into training and testing sets. Variables were initially screened using univariate analysis, and then further selected using a backward stepwise regression. Multivariable logistic regression was performed to establish nomograms. The predictive performance of the model was evaluated using the receiver operating characteristic (ROC) curve, area under the curve (AUC), calibration curve, and decision curve analysis (DCA) in both the training and testing sets. Finally, the logistic regression analysis showed that elevated white blood cell count (WBC>10 × 109 cells/l), hypoalbuminemia, pulmonary encephalopathy, respiratory failure, diabetes, and respiratory intensive care unit (RICU) admissions were risk factors for predicting high hospitalization costs in pAECOPD patients. The AUC value was 0.756 (95% CI: 0.699-0.812) in the training set and 0.792 (95% CI: 0.718-0.867) in the testing set. The calibration plot and DCA curve indicated the model had good predictive performance. Furthermore, decreased total protein, pulmonary encephalopathy, reflux esophagitis, and RICU admissions were risk factors for predicting prolonged stays in pAECOPD patients. The AUC value was 0.629 (95% CI: 0.575-0.682) in the training set and 0.620 (95% CI: 0.539-0.701) in the testing set. The calibration plot and DCA curve indicated the model had good predictive performance. We developed and validated two nomograms for predicting high hospitalization costs and prolonged stay, respectively, among hospitalized patients with pAECOPD. This trial is registered with ChiCTR2000039959.","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"27 1","pages":"2639080"},"PeriodicalIF":2.2,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142261823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sepsis is a systemic inflammatory reaction syndrome caused by infections. Acute lung injury (ALI) occurs first and most frequently in patients with sepsis. Gentiopicroside (GPS), which originates mostly from Gentiana, is classified as a secoiridoid glycosides. Terpenoid glycosides have various biological effects, including liver protection, blood glucose and cholesterol level management, and anti-inflammatory and antitumor effects. However, presently, the biochemical foundation and mechanism of the anti-inflammatory effects of GPS in sepsis-induced ALI have not been explained. In the present study, we established a rat model of sepsis ALI induced by cecal ligation and puncture. This enables us to observe the effects of GPS therapy, which significantly reduced the inflammatory response (TNF-α, IL-1β, and IL-6), nitrogen stress, oxidative stress, and severity of ALI at both the whole animal and molecular levels. In addition, GPS ameliorates LPS-induced ALI via regulation of inflammatory response and cell proptosis in BEAS-2B. This study provides a theoretical basis for treating sepsis-induced ALI with GPS.
败血症是一种由感染引起的全身炎症反应综合征。急性肺损伤(ALI)在败血症患者中最先发生,也最常见。龙胆草甙(Gentiopicroside,GPS)主要来源于龙胆草,属于仲萜类甙。萜类苷具有多种生物效应,包括保护肝脏、控制血糖和胆固醇水平、抗炎和抗肿瘤作用。然而,目前 GPS 在败血症引起的 ALI 中抗炎作用的生化基础和机制尚未得到解释。在本研究中,我们建立了一个由盲肠结扎和穿刺诱导的大鼠败血症 ALI 模型。GPS能在动物整体和分子水平上显著降低炎症反应(TNF-α、IL-1β和IL-6)、氮应激、氧化应激和ALI的严重程度。此外,GPS 还能通过调节 BEAS-2B 的炎症反应和细胞突眼来改善 LPS 诱导的 ALI。这项研究为利用 GPS 治疗败血症诱发的 ALI 提供了理论依据。
{"title":"Gentiopicroside Ameliorates Sepsis-Induced Acute Lung Injury via Inhibiting Inflammatory Response.","authors":"Mu Hu,Hangxiang Du,Yang Xu,Yan Wang","doi":"10.1155/2024/1068326","DOIUrl":"https://doi.org/10.1155/2024/1068326","url":null,"abstract":"Sepsis is a systemic inflammatory reaction syndrome caused by infections. Acute lung injury (ALI) occurs first and most frequently in patients with sepsis. Gentiopicroside (GPS), which originates mostly from Gentiana, is classified as a secoiridoid glycosides. Terpenoid glycosides have various biological effects, including liver protection, blood glucose and cholesterol level management, and anti-inflammatory and antitumor effects. However, presently, the biochemical foundation and mechanism of the anti-inflammatory effects of GPS in sepsis-induced ALI have not been explained. In the present study, we established a rat model of sepsis ALI induced by cecal ligation and puncture. This enables us to observe the effects of GPS therapy, which significantly reduced the inflammatory response (TNF-α, IL-1β, and IL-6), nitrogen stress, oxidative stress, and severity of ALI at both the whole animal and molecular levels. In addition, GPS ameliorates LPS-induced ALI via regulation of inflammatory response and cell proptosis in BEAS-2B. This study provides a theoretical basis for treating sepsis-induced ALI with GPS.","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"47 1","pages":"1068326"},"PeriodicalIF":2.2,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142261881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-19eCollection Date: 2024-01-01DOI: 10.1155/2024/5812829
Yufeng Li, Qiaoqiao Hu, Wenjie Wang, Changhong Du, Siwen Fan, Linlin Xu, Songmei Li, Bei Chen
Objective: This study aims to evaluate a novel prone position ventilation device designed to enhance patient safety, improve comfort, and reduce adverse events, facilitating prolonged tolerance in critically ill patients.
Methods: A randomized controlled trial was conducted on 60 critically ill patients from January 2020 to June 2023. Of which, one self-discharged during treatment and another was terminated due to decreased oxygenation, leaving an effective sample of 58 patients. Patients were allocated to either a control group receiving traditional prone positioning aids (ordinary sponge pads and pillows) or an intervention group using a newly developed adjustable prone positioning device. A subset of patients in each group also received life support technologies such as extracorporeal membrane oxygenation (ECMO) and continuous renal replacement therapy (CRRT). We assessed prone position ventilation tolerance, oxygen saturation increments postintervention, duration of prone positioning, CRRT filter lifespan, and the incidence of adverse events.
Results: The intervention group exhibited significantly longer average tolerance to prone positioning (16.6 hours vs. 8.3 hours, P < 0.001 with a difference of 8.3 (4.4, 12.2) hours), higher increases in oxygen saturation postventilation (9% vs. 6%, P < 0.001 with a difference of 3.0 (1.5, 4.5)), and reduced time required for medical staff to position patients (11.7 min vs. 21.8 min, P < 0.001 with a difference of -10.1 (-11.9, -8.3)). Adverse events, including catheter displacement or blockage, facial edema, pressure injuries, and vomiting or aspiration, were markedly lower in the intervention group, with statistical significance (P < 0.05). In patients receiving combined life support, the intervention group demonstrated improved catheter blood drainage and extended CRRT filter longevity.
Conclusion: The newly developed adjustable prone ventilation device significantly improves tolerance to prone positioning, enhances oxygenation, and minimizes adverse events in critically ill patients, thereby also facilitating the effective application of life support technologies.
{"title":"Development of Prone Position Ventilation Device and Study on the Application Effect of Combined Life Support Technology in Critically Ill Patients.","authors":"Yufeng Li, Qiaoqiao Hu, Wenjie Wang, Changhong Du, Siwen Fan, Linlin Xu, Songmei Li, Bei Chen","doi":"10.1155/2024/5812829","DOIUrl":"10.1155/2024/5812829","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to evaluate a novel prone position ventilation device designed to enhance patient safety, improve comfort, and reduce adverse events, facilitating prolonged tolerance in critically ill patients.</p><p><strong>Methods: </strong>A randomized controlled trial was conducted on 60 critically ill patients from January 2020 to June 2023. Of which, one self-discharged during treatment and another was terminated due to decreased oxygenation, leaving an effective sample of 58 patients. Patients were allocated to either a control group receiving traditional prone positioning aids (ordinary sponge pads and pillows) or an intervention group using a newly developed adjustable prone positioning device. A subset of patients in each group also received life support technologies such as extracorporeal membrane oxygenation (ECMO) and continuous renal replacement therapy (CRRT). We assessed prone position ventilation tolerance, oxygen saturation increments postintervention, duration of prone positioning, CRRT filter lifespan, and the incidence of adverse events.</p><p><strong>Results: </strong>The intervention group exhibited significantly longer average tolerance to prone positioning (16.6 hours vs. 8.3 hours, <i>P</i> < 0.001 with a difference of 8.3 (4.4, 12.2) hours), higher increases in oxygen saturation postventilation (9% vs. 6%, <i>P</i> < 0.001 with a difference of 3.0 (1.5, 4.5)), and reduced time required for medical staff to position patients (11.7 min vs. 21.8 min, <i>P</i> < 0.001 with a difference of -10.1 (-11.9, -8.3)). Adverse events, including catheter displacement or blockage, facial edema, pressure injuries, and vomiting or aspiration, were markedly lower in the intervention group, with statistical significance (<i>P</i> < 0.05). In patients receiving combined life support, the intervention group demonstrated improved catheter blood drainage and extended CRRT filter longevity.</p><p><strong>Conclusion: </strong>The newly developed adjustable prone ventilation device significantly improves tolerance to prone positioning, enhances oxygenation, and minimizes adverse events in critically ill patients, thereby also facilitating the effective application of life support technologies.</p>","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"2024 ","pages":"5812829"},"PeriodicalIF":2.1,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11347033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-06eCollection Date: 2024-01-01DOI: 10.1155/2024/9284430
Tingting Lv, Ziliang Hou, Kaiyuan Yang, Jinxiang Wang
Introduction: The impaired proliferative capacity of alveolar epithelial cells after injury is an important factor causing epithelial repair dysfunction, leading to the occurrence of idiopathic pulmonary fibrosis (IPF). Alveolar type 2 (AT2) cells as the stem cells of alveolar epithelium participate in the repair process after alveolar injury. Lipocalin-2 (LCN2) participates in multiple processes regulating the pathological process of alveolar epithelial cells, but the mechanisms involved are still unclear.
Method: We used a BLM-treated mouse model to characterize the expression of LCN2 in lung fibrosis regions and analyzed the location of LCN2 in alveolar epithelial cells. Moreover, human pulmonary alveolar epithelial cells (HPAEpiCs) were transfected with the LCN2 overexpression plasmid vector in vitro. Recombinant human interleukin-17 (IL-17) protein (rhIL-17) at different concentrations was administered to intervene in HPAEpiCs, observing cell viability and analyzing the concentration-dependent effect of IL-17.
Results: LCN2 was increased in the alveolar epithelium post-BLM injury, and highly expressed LCN2 was mainly concentrated on AT2 cells in BLM-injured lungs. Meanwhile, LCN2-overexpressing HPAEpiCs showed impaired cell viability and cell growth. HPAEpiC intervention with rhIL-17 mildly rescued the impaired cell proliferation induced by LCN2 overexpression, and the effect of IL-17 intervention was partially concentration-dependent.
Conclusions: The results revealed the reversed effect of IL-17 on the impaired proliferative capacity of the alveolar epithelium induced by LCN2 overexpression. The target alveolar epithelial cells regulated by this process were AT2 cells, providing new clues for alveolar epithelium repair after injury and the treatment of lung injury diseases.
{"title":"IL-17 Mildly Rescued the Impaired Proliferation of Alveolar Epithelial Cells Induced by LCN2 Overexpression.","authors":"Tingting Lv, Ziliang Hou, Kaiyuan Yang, Jinxiang Wang","doi":"10.1155/2024/9284430","DOIUrl":"10.1155/2024/9284430","url":null,"abstract":"<p><strong>Introduction: </strong>The impaired proliferative capacity of alveolar epithelial cells after injury is an important factor causing epithelial repair dysfunction, leading to the occurrence of idiopathic pulmonary fibrosis (IPF). Alveolar type 2 (AT2) cells as the stem cells of alveolar epithelium participate in the repair process after alveolar injury. Lipocalin-2 (LCN2) participates in multiple processes regulating the pathological process of alveolar epithelial cells, but the mechanisms involved are still unclear.</p><p><strong>Method: </strong>We used a BLM-treated mouse model to characterize the expression of LCN2 in lung fibrosis regions and analyzed the location of LCN2 in alveolar epithelial cells. Moreover, human pulmonary alveolar epithelial cells (HPAEpiCs) were transfected with the LCN2 overexpression plasmid vector in vitro. Recombinant human interleukin-17 (IL-17) protein (rhIL-17) at different concentrations was administered to intervene in HPAEpiCs, observing cell viability and analyzing the concentration-dependent effect of IL-17.</p><p><strong>Results: </strong>LCN2 was increased in the alveolar epithelium post-BLM injury, and highly expressed LCN2 was mainly concentrated on AT2 cells in BLM-injured lungs. Meanwhile, LCN2-overexpressing HPAEpiCs showed impaired cell viability and cell growth. HPAEpiC intervention with rhIL-17 mildly rescued the impaired cell proliferation induced by LCN2 overexpression, and the effect of IL-17 intervention was partially concentration-dependent.</p><p><strong>Conclusions: </strong>The results revealed the reversed effect of IL-17 on the impaired proliferative capacity of the alveolar epithelium induced by LCN2 overexpression. The target alveolar epithelial cells regulated by this process were AT2 cells, providing new clues for alveolar epithelium repair after injury and the treatment of lung injury diseases.</p>","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"2024 ","pages":"9284430"},"PeriodicalIF":2.1,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11321888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141975086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pulmonary hypertension (PH) is a progressive and complex pulmonary vascular disease with poor prognosis. The aim of this study was to provide a new understanding of the lung pathology of disease and a noninvasive method in monitoring the establishment of animal models for basic and clinical studies of PH, indeed to explore clinical application value of lung ultrasound for patients with PH. Totally 32 male SD rats were randomly divided into control group, MCT (monocrotaline) group, PDTC (pyrrolidine dithiocarbamate) group, and NS (normal saline) group. Rats in the MCT group, PDTC group, and NS group received single intraperitoneal injection of MCT, while the control group received the same dose of NS. Then, PDTC group and NS group received PDTC and NS daily for treatment at the end of the model. Each group received lung ultrasound examination and measurement of pulmonary arterial pressure (PAP). Then, the rats were sacrificed to take the lung specimens to being observed. The ultrasound and pathological results were analyzed with a semiquantitative score. With the pulmonary artery pressure increases, the MCT group had a higher pulmonary ultrasound score and pathological score compared with the control group (p < 0.05). After PDTC treatment, the pulmonary ultrasound score and the pathological score decline (p < 0.05). We investigated both lung ultrasound scores, and the pathological scores were positively correlated with mean pulmonary artery pressure (mPAP) (both r > 0.8, p < 0.0001). Moreover, lung ultrasound scores were positively correlated with pathological scores (r > 0.8, p < 0.0001). We elucidated lung ultrasound evaluation providing more evidence for the management of PH in the rat model. Moreover, lung ultrasound provided a noninvasive method in monitoring the establishment of animal models for basic and clinical studies of PH.
{"title":"The Correlation between Lung Ultrasound and Pathology in Rat Model of Monocrotaline-Induced Pulmonary Hypertension.","authors":"Yan-Fen Zhong, Bin-Bin Liang, Xiao-Feng Zhang, Ji-Wu","doi":"10.1155/2024/6619471","DOIUrl":"10.1155/2024/6619471","url":null,"abstract":"<p><p>Pulmonary hypertension (PH) is a progressive and complex pulmonary vascular disease with poor prognosis. The aim of this study was to provide a new understanding of the lung pathology of disease and a noninvasive method in monitoring the establishment of animal models for basic and clinical studies of PH, indeed to explore clinical application value of lung ultrasound for patients with PH. Totally 32 male SD rats were randomly divided into control group, MCT (monocrotaline) group, PDTC (pyrrolidine dithiocarbamate) group, and NS (normal saline) group. Rats in the MCT group, PDTC group, and NS group received single intraperitoneal injection of MCT, while the control group received the same dose of NS. Then, PDTC group and NS group received PDTC and NS daily for treatment at the end of the model. Each group received lung ultrasound examination and measurement of pulmonary arterial pressure (PAP). Then, the rats were sacrificed to take the lung specimens to being observed. The ultrasound and pathological results were analyzed with a semiquantitative score. With the pulmonary artery pressure increases, the MCT group had a higher pulmonary ultrasound score and pathological score compared with the control group (<i>p</i> < 0.05). After PDTC treatment, the pulmonary ultrasound score and the pathological score decline (<i>p</i> < 0.05). We investigated both lung ultrasound scores, and the pathological scores were positively correlated with mean pulmonary artery pressure (mPAP) (both <i>r</i> > 0.8, <i>p</i> < 0.0001). Moreover, lung ultrasound scores were positively correlated with pathological scores (<i>r</i> > 0.8, <i>p</i> < 0.0001). We elucidated lung ultrasound evaluation providing more evidence for the management of PH in the rat model. Moreover, lung ultrasound provided a noninvasive method in monitoring the establishment of animal models for basic and clinical studies of PH.</p>","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"2024 ","pages":"6619471"},"PeriodicalIF":2.1,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11288697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141854931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-03eCollection Date: 2024-01-01DOI: 10.1155/2024/7013576
Laura Tregidgo, Prasheena Naran, Eshrina Gosal, Rebecca F D'Cruz
Hypercapnic respiratory failure arises due to an imbalance in the load-capacity-drive relationship of the respiratory muscle pump, typically arising in patients with chronic obstructive pulmonary disease, obesity-related respiratory failure, and neuromuscular disease. Patients at risk of developing chronic respiratory failure and those with established disease should be referred to a specialist ventilation unit for evaluation and consideration of home noninvasive ventilation (NIV) initiation. Clinical trials demonstrate that, following careful patient selection, home NIV can improve a range of clinical, patient-reported, and physiological outcomes. This narrative review provides an overview of the pathophysiology of chronic respiratory failure, evidence-based applications of home NIV, and monitoring of patients established on home ventilation and describes technological advances in ventilation devices, interfaces, and monitoring to enhance comfort, promote long-term adherence, and optimise gas exchange.
{"title":"Update in Noninvasive Home Mechanical Ventilation: A Narrative Review of Indications, Outcomes, and Monitoring.","authors":"Laura Tregidgo, Prasheena Naran, Eshrina Gosal, Rebecca F D'Cruz","doi":"10.1155/2024/7013576","DOIUrl":"10.1155/2024/7013576","url":null,"abstract":"<p><p>Hypercapnic respiratory failure arises due to an imbalance in the load-capacity-drive relationship of the respiratory muscle pump, typically arising in patients with chronic obstructive pulmonary disease, obesity-related respiratory failure, and neuromuscular disease. Patients at risk of developing chronic respiratory failure and those with established disease should be referred to a specialist ventilation unit for evaluation and consideration of home noninvasive ventilation (NIV) initiation. Clinical trials demonstrate that, following careful patient selection, home NIV can improve a range of clinical, patient-reported, and physiological outcomes. This narrative review provides an overview of the pathophysiology of chronic respiratory failure, evidence-based applications of home NIV, and monitoring of patients established on home ventilation and describes technological advances in ventilation devices, interfaces, and monitoring to enhance comfort, promote long-term adherence, and optimise gas exchange.</p>","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"2024 ","pages":"7013576"},"PeriodicalIF":2.1,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11236466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141579023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-07-02eCollection Date: 2024-01-01DOI: 10.1155/2024/5647813
Jingjing Chen, Wenxiao Qiao, Xiaoming Xue, Dian Li, Ye Zhang, Di Xie, Jinyun Wang, Yaoqin Sun, Shuo Yang, Zhuomin Yang
Background: Chronic obstructive pulmonary disease (COPD) is a common respiratory disease. Currently, no specific treatment strategy has been established; therefore, finding new treatment methods is essential. Clinically, Shenqi Huatan Decoction (SQHT) is a traditional Chinese medicinal formula for COPD treatment; however, its mechanism of action in treatment needs to be clarified.
Methods: The COPD rat model was replicated by cigarette smoking and tracheal injection using the LPS method. The control group and the SQHT groups were treated with dexamethasone and SQHT by gavage, respectively. After treatment, superoxide dismutase (SOD) serum levels, total antioxidant capacity (TAOC), lipid peroxidation, and malondialdehyde (MDA) were detected by enzyme-linked immunosorbent assay (ELISA). Activated protein kinase alpha (AMPK-α), forkhead transcription factor O3a (FOXO3a), manganese SOD (MnSOD), and peroxisome proliferator-activated receptor gamma (PPARγ) were detected using reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) and Western blot. Microribonucleic acid and protein expression levels were measured, and pathological changes in lung tissue were observed using hematoxylin and eosin staining.
Results: The pathological findings suggested that SQHT substantially affects COPD treatment by enhancing alveolar fusion and reducing emphysema. ELISA results showed that SQHT could lower the blood levels of MDA and lipid peroxide and raise SOD and TAOC levels, suggesting that it could lessen oxidative stress. In the lung tissue of rats with COPD, large doses of SQHT intervention dramatically increased AMPK protein expression, AMPK-α, FOXO3a, MnSOD, and PPARγ, indicating that SQHT may reduce oxidative stress by activating the PPARγ-mediated AMPK/FOXO3a signaling pathway. Similar results were obtained using RT-qPCR.
Conclusion: SQHT is effective for COPD treatment. The mechanism of action may be related to the activation of the PPARγ-mediated AMPK/FOXO3a signaling pathway to improve oxidative stress in lung tissue.
{"title":"Amelioration of Oxidative Stress in Rats with Chronic Obstructive Pulmonary Disease through Shenqi Huatan Decoction Activation of Peroxisome Proliferator-Activated Receptor Gamma-Mediated Activated Protein Kinase/Forkhead Transcription Factor O3a Signaling Pathway.","authors":"Jingjing Chen, Wenxiao Qiao, Xiaoming Xue, Dian Li, Ye Zhang, Di Xie, Jinyun Wang, Yaoqin Sun, Shuo Yang, Zhuomin Yang","doi":"10.1155/2024/5647813","DOIUrl":"10.1155/2024/5647813","url":null,"abstract":"<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is a common respiratory disease. Currently, no specific treatment strategy has been established; therefore, finding new treatment methods is essential. Clinically, Shenqi Huatan Decoction (SQHT) is a traditional Chinese medicinal formula for COPD treatment; however, its mechanism of action in treatment needs to be clarified.</p><p><strong>Methods: </strong>The COPD rat model was replicated by cigarette smoking and tracheal injection using the LPS method. The control group and the SQHT groups were treated with dexamethasone and SQHT by gavage, respectively. After treatment, superoxide dismutase (SOD) serum levels, total antioxidant capacity (TAOC), lipid peroxidation, and malondialdehyde (MDA) were detected by enzyme-linked immunosorbent assay (ELISA). Activated protein kinase alpha (AMPK-<i>α</i>), forkhead transcription factor O3a (FOXO3a), manganese SOD (MnSOD), and peroxisome proliferator-activated receptor gamma (PPAR<i>γ</i>) were detected using reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) and Western blot. Microribonucleic acid and protein expression levels were measured, and pathological changes in lung tissue were observed using hematoxylin and eosin staining.</p><p><strong>Results: </strong>The pathological findings suggested that SQHT substantially affects COPD treatment by enhancing alveolar fusion and reducing emphysema. ELISA results showed that SQHT could lower the blood levels of MDA and lipid peroxide and raise SOD and TAOC levels, suggesting that it could lessen oxidative stress. In the lung tissue of rats with COPD, large doses of SQHT intervention dramatically increased AMPK protein expression, AMPK-<i>α</i>, FOXO3a, MnSOD, and PPAR<i>γ</i>, indicating that SQHT may reduce oxidative stress by activating the PPAR<i>γ</i>-mediated AMPK/FOXO3a signaling pathway. Similar results were obtained using RT-qPCR.</p><p><strong>Conclusion: </strong>SQHT is effective for COPD treatment. The mechanism of action may be related to the activation of the PPAR<i>γ</i>-mediated AMPK/FOXO3a signaling pathway to improve oxidative stress in lung tissue.</p>","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"2024 ","pages":"5647813"},"PeriodicalIF":2.1,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11233184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141562642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-06-28eCollection Date: 2024-01-01DOI: 10.1155/2024/2803044
Erkan Topkan, Ahmet Kucuk, Duriye Ozturk, Emine Elif Ozkan, Ali Ayberk Besen, Berrin Pehlivan, Ugur Selek
Objectives: We explored the prognostic utility of the unique combination of C-reactive-protein-to-albumin ratio (CAR) and significant weight loss (WL > 5%) over the preceding 6 months, namely, the CARWL score, in stage IIIC non-small-cell lung cancer (NSCLC) patients who underwent concurrent chemoradiotherapy (CCRT).
Methods: For each patient, the CAR was calculated using C-reactive protein and albumin measurements obtained on the first day of CCRT: CAR = C-reactive protein ÷ albumin. The availability of an ideal CAR cutoff that may categorize patients into two distinct progression-free (PFS) and overall survival (OS) outcomes was explored by employing receiver operating characteristic (ROC) curve analysis. Patients were additionally divided into two groups based on their status of significant WL according to the well-recognized Delphi criteria. Then, the CARWL score was created by combining all feasible combinations of the CAR and significant WL groupings. The potential links between pretreatment CARWL groups and the post-CCRT OS and PFS outcomes were determined as the primary and secondary endpoints.
Results: This retrospective cohort study comprised a total of 651 stage IIIC NSCLC patients. ROC curve analysis indicated that rounded 3.0 was the ideal CAR cutoff (area under the curve (AUC): 70.1%; sensitivity: 67.8%; specificity: 65.9%), which categorized the patients into CAR < 3.0 (N = 324) and CAR ≥ 3.0 (N = 327) groups. There were 308 (47.3%) and 343 (52.7%) patients without and with significant WL, respectively. The created CARWL groups were CARWL-0: CAR < 3.0 and WL ≤ 5.0%; CARWL-1: CAR < 3.0 and WL > 5.0%, or CAR ≥ 3.0 and WL ≤ 5.0%; and CARWL-2: CAR > 3.0 and WL > 5.0%. The Kaplan-Meier curves showed that the PFS (14.2 vs. 11.4 vs. 7.5 months; P < 0.001) and OS (37.3 vs. 23.6 vs. 12.8 months; P < 0.001) durations were gradually and significantly lowered from the CARWL-0 to CARWL-2 groups. The CARWL score's significant impacts on PFS and OS outcomes were found to be independent of the other variables in the multivariate analysis (P < 0.001, for each).
Conclusions: Our findings indicate that the novel CARWL score, which accounts for pretreatment CAR and significant WL during the preceding 6 months, can reliably stratify newly diagnosed stage IIIC NSCLC patients into three groups with significantly different PFS and OS after definitive CCRT.
研究目的我们探讨了在接受同期化疗(CCRT)的IIIC期非小细胞肺癌(NSCLC)患者中,C反应蛋白与白蛋白比值(CAR)和前6个月体重显著下降(WL > 5%)的独特组合,即CARWL评分的预后效用:方法:每位患者的 CAR 分值均根据 CCRT 第一天获得的 C 反应蛋白和白蛋白测量值计算得出:CAR = C 反应蛋白 ÷ 白蛋白。通过接收器操作特征曲线(ROC)分析,探讨了是否有一个理想的CAR分界线,可将患者分为两种不同的无进展(PFS)和总生存(OS)结果。此外,根据公认的德尔菲(Delphi)标准,根据患者的显著 WL 状态将其分为两组。然后,结合 CAR 和显著 WL 分组的所有可行组合,得出 CARWL 评分。将治疗前CARWL分组与CCRT后OS和PFS结果之间的潜在联系作为主要和次要终点:这项回顾性队列研究共纳入了 651 例 IIIC 期 NSCLC 患者。ROC曲线分析表明,圆形 3.0 是理想的 CAR 临界值(曲线下面积 (AUC):70.1%;灵敏度:67.0%):70.1%;灵敏度:67.8%;特异性:65.9%),将患者分为 CAR N = 324 组和 CAR ≥ 3.0 组(N = 327)。无明显 WL 和有明显 WL 的患者分别为 308 人(47.3%)和 343 人(52.7%)。创建的 CARWL 组为 CARWL-0:CAR 5.0%,或 CAR ≥ 3.0 且 WL ≤ 5.0%;CARWL-2:CAR > 3.0 且 WL > 5.0%。Kaplan-Meier曲线显示,从CARWL-0组到CARWL-2组,PFS(14.2个月 vs. 11.4个月 vs. 7.5个月;P < 0.001)和OS(37.3个月 vs. 23.6个月 vs. 12.8个月;P < 0.001)持续时间逐渐显著缩短。在多变量分析中发现,CARWL评分对PFS和OS结果的显著影响与其他变量无关(P<0.001):我们的研究结果表明,新的CARWL评分考虑了治疗前的CAR和前6个月的显著WL,可以可靠地将新诊断的IIIC期NSCLC患者分为三组,三组患者在接受明确的CCRT治疗后的PFS和OS显著不同。
{"title":"Prognostic Value of Novel CARWL Score in Stage IIIC Non-Small-Cell Lung Cancer Patients Undergoing Concurrent Chemoradiotherapy.","authors":"Erkan Topkan, Ahmet Kucuk, Duriye Ozturk, Emine Elif Ozkan, Ali Ayberk Besen, Berrin Pehlivan, Ugur Selek","doi":"10.1155/2024/2803044","DOIUrl":"10.1155/2024/2803044","url":null,"abstract":"<p><strong>Objectives: </strong>We explored the prognostic utility of the unique combination of C-reactive-protein-to-albumin ratio (CAR) and significant weight loss (WL > 5%) over the preceding 6 months, namely, the CARWL score, in stage IIIC non-small-cell lung cancer (NSCLC) patients who underwent concurrent chemoradiotherapy (CCRT).</p><p><strong>Methods: </strong>For each patient, the CAR was calculated using C-reactive protein and albumin measurements obtained on the first day of CCRT: CAR = C-reactive protein ÷ albumin. The availability of an ideal CAR cutoff that may categorize patients into two distinct progression-free (PFS) and overall survival (OS) outcomes was explored by employing receiver operating characteristic (ROC) curve analysis. Patients were additionally divided into two groups based on their status of significant WL according to the well-recognized Delphi criteria. Then, the CARWL score was created by combining all feasible combinations of the CAR and significant WL groupings. The potential links between pretreatment CARWL groups and the post-CCRT OS and PFS outcomes were determined as the primary and secondary endpoints.</p><p><strong>Results: </strong>This retrospective cohort study comprised a total of 651 stage IIIC NSCLC patients. ROC curve analysis indicated that rounded 3.0 was the ideal CAR cutoff (area under the curve (AUC): 70.1%; sensitivity: 67.8%; specificity: 65.9%), which categorized the patients into CAR < 3.0 (<i>N</i> = 324) and CAR ≥ 3.0 (<i>N</i> = 327) groups. There were 308 (47.3%) and 343 (52.7%) patients without and with significant WL, respectively. The created CARWL groups were CARWL-0: CAR < 3.0 and WL ≤ 5.0%; CARWL-1: CAR < 3.0 and WL > 5.0%, or CAR ≥ 3.0 and WL ≤ 5.0%; and CARWL-2: CAR > 3.0 and WL > 5.0%. The Kaplan-Meier curves showed that the PFS (14.2 vs. 11.4 vs. 7.5 months; <i>P</i> < 0.001) and OS (37.3 vs. 23.6 vs. 12.8 months; <i>P</i> < 0.001) durations were gradually and significantly lowered from the CARWL-0 to CARWL-2 groups. The CARWL score's significant impacts on PFS and OS outcomes were found to be independent of the other variables in the multivariate analysis (<i>P</i> < 0.001, for each).</p><p><strong>Conclusions: </strong>Our findings indicate that the novel CARWL score, which accounts for pretreatment CAR and significant WL during the preceding 6 months, can reliably stratify newly diagnosed stage IIIC NSCLC patients into three groups with significantly different PFS and OS after definitive CCRT.</p>","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"2024 ","pages":"2803044"},"PeriodicalIF":2.1,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11226337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141554210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Context. Ferroptosis is known to influence the pathogenesis of pulmonary fibrosis. Astragalus and Panax notoginseng are used to treat pulmonary fibrosis; however, the therapeutic mechanisms require further elucidation. Objective. To investigate the mechanism through which Astragalus and Panax notoginseng decoction (APD) facilitates the treatment of ferroptosis-mediated pulmonary fibrosis. Materials and Methods. First, the electromedical measurement systems were used to measure respiratory function in mice; the lungs were then collected for histological staining. Potential pharmacologic targets were predicted via network pharmacology. Finally, tests including immunohistochemistry, reverse transcription-quantitative polymerase chain reaction, and western blotting were used to evaluate the relative expression levels of collagen, transforming growth factor β, α-smooth muscle actin, hydroxyproline, and ferroptosis-related genes (GPX4, SLC7A11, ACSL4, and PTGS2) and candidates involved in the mediation of pathways associated with ferroptosis (Hif-1α and EGFR). Results. APD prevented the occurrence of restrictive ventilation dysfunction induced by ferroptosis. Extracellular matrix and collagen fiber deposition were significantly reduced when the APD group compared with the model group; furthermore, ferroptosis was attenuated, expression of PTGS2 and ACSL4 increased, and expression of GPX4 and SLC7A11 decreased. In the APD group, the candidates related to the mediation of ferroptosis (Hif-1α and EGFR) decreased compared with the model group. Discussion and Conclusions. APD may ameliorate restrictive ventilatory dysfunction through the inhibition of ferroptosis. This was achieved through the attenuation of collagen deposition and inflammatory recruitment in pulmonary fibrosis. The underlying mechanisms might involve Hif-1α and EGFR.
{"title":"Ferroptosis Mediates Pulmonary Fibrosis: Implications for the Effect of Astragalus and Panax notoginseng Decoction","authors":"Jing Wen, Cui Wang, Li-yun Song, Yin-ying Wang, Peng-tao Liang, Wen-lin Pang, Wen Yin, Qiang Zhang, Wei-tian Zhao, Xue-ping Sun, Jin-yuan Yan, Zhong-shan Yang","doi":"10.1155/2024/5554886","DOIUrl":"https://doi.org/10.1155/2024/5554886","url":null,"abstract":"<i>Context</i>. Ferroptosis is known to influence the pathogenesis of pulmonary fibrosis. <i>Astragalus</i> and <i>Panax notoginseng</i> are used to treat pulmonary fibrosis; however, the therapeutic mechanisms require further elucidation. <i>Objective</i>. To investigate the mechanism through which <i>Astragalus</i> and <i>Panax notoginseng</i> decoction (APD) facilitates the treatment of ferroptosis-mediated pulmonary fibrosis. <i>Materials and Methods</i>. First, the electromedical measurement systems were used to measure respiratory function in mice; the lungs were then collected for histological staining. Potential pharmacologic targets were predicted via network pharmacology. Finally, tests including immunohistochemistry, reverse transcription-quantitative polymerase chain reaction, and western blotting were used to evaluate the relative expression levels of collagen, transforming growth factor <i>β</i>, <i>α</i>-smooth muscle actin, hydroxyproline, and ferroptosis-related genes (GPX4, SLC7A11, ACSL4, and PTGS2) and candidates involved in the mediation of pathways associated with ferroptosis (Hif-1<i>α</i> and EGFR). <i>Results</i>. APD prevented the occurrence of restrictive ventilation dysfunction induced by ferroptosis. Extracellular matrix and collagen fiber deposition were significantly reduced when the APD group compared with the model group; furthermore, ferroptosis was attenuated, expression of PTGS2 and ACSL4 increased, and expression of GPX4 and SLC7A11 decreased. In the APD group, the candidates related to the mediation of ferroptosis (Hif-1<i>α</i> and EGFR) decreased compared with the model group. <i>Discussion and Conclusions</i>. APD may ameliorate restrictive ventilatory dysfunction through the inhibition of ferroptosis. This was achieved through the attenuation of collagen deposition and inflammatory recruitment in pulmonary fibrosis. The underlying mechanisms might involve Hif-1<i>α</i> and EGFR.","PeriodicalId":9416,"journal":{"name":"Canadian respiratory journal","volume":"4281 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2024-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140325059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}