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阿托伐他汀鈣對香煙暴露大鼠肺血管炎癥模型組蛋白脫乙酰酶2的影響

目的 探討阿托伐他汀鈣對香煙暴露大鼠肺血管炎癥的作用及對肺組織、血清中組蛋白脫乙酰酶2（HADC2）的影響。方法 將18只雌性SD大鼠隨機分為空白組（A組）、肺血管模型組（B組）、阿托伐他汀鈣干預組（C組），每組6只，使用煙熏加氣道滴入脂多糖經典造模方法對B組和C組大鼠進行香煙暴露肺血管炎癥模型制作，C組于第2天開始，每天熏煙前1 h用阿托伐他汀片灌胃治療，劑量5 mg/（kg·d），A、B組同期予以等量生理鹽水進行灌胃，35 d后處死大鼠。使用蘇木精–伊紅染色對大鼠各組病理組織進行染色，并對血管的炎癥進行評分。酶聯免疫吸附試驗檢測血清中HDAC2水平，蛋白印跡法檢查肺組織中HDAC2蛋白水平，實時熒光定量聚合酶鏈反應檢測肺組織HDAC2 mRNA水平。結果 與A組比較，B、C組的肺血管炎癥明顯，但C組輕于B組。A組炎癥評分為（0.5±0.5）分，略低于C組［（1.7±0.7）分］，顯著低于B組［（2.7±1.0）分］，C組炎癥評分顯著低于B組。A組大鼠血清中HADC2水平為（12.76±0.63）ng/mL，略高于C組［（11.59±0.60）ng/mL］，但C、A組明顯高于B組［（2.27±0.42）ng/mL］，三組之間的差異有統計學意義（P<0.05）。B組大鼠肺組織中HDAC2蛋白表達明顯減少，而通過阿托伐他汀鈣干預后，C組的HDAC2表達（0.30±0.02）相較于B組（0.09±0.01）明顯增加，略低于A組（0.35±0.04）；A組（1.23±0.06）、C組（0.82±0.03）的HDAC2 mRNA水平明顯高于B組（0.27±0.02），三組之間的差異有統計學意義（P<0.05）。結論 阿托伐他汀鈣可減輕香煙暴露大鼠肺血管炎癥的程度，其機制可能與增加HDAC2的表達有關。

骨橋蛋白與肺部疾病關系的研究進展

The effect of azithromycin on pulmonary vascular remodeling in chronic obstructive pulmonary disease rats

ObjectiveTo investigate the effect of azithromycin on chronic obstructive pulmonary disease (COPD) vascular remodeling and its possible mechanism.MethodsEighteen male SD rats were randomly divided into normal control group (group A), model group (group B) and azithromycin intervention group (group C). In group B and group C, the COPD model was established by passive smoking and intratracheal injection of lipopolysaccharide. On the fifteenth day, group C was intragastricly administrated with azithromycin (50 mg/kg) one hour prior to smoking, while group A and group B were given equal amount of normal saline. All the rats were killed 6 weeks later. Hematoxylin-eosin staining was used to observe lung tissue pathological changes and victoria blue + Van Gieson staining was used to observe the pulmonary artery morphology changes. The serum osteopontin (OPN) was determined with ELISA. The protein expression of OPN was measured with immunohistochemistry and OPN mRNA was detected by RT-PCR.ResultsCompared with group A, the degree of pulmonary vascular inflammation and pulmonary vascular remodeling in groups B and C was more serious, but these changes in group C were lighter than those in group B. The serum OPN content, lung tissue OPN protein and OPN mRNA expression in groups B and C were higher than those in group A, while these parameters in group C were lower than those in group B. The content of serum OPN, the expression of OPN protein and OPN mRNA in lung tissue were positively correlated with the degree of pulmonary vascular inflammation and vascular remodeling.ConclusionAzithromycin can alleviate the pulmonary vascular inflammation and pulmonary vascular remodeling in COPD rats, and its mechanism may be related to inhibiting the expression of OPN.

Nomogram modeling of short-term mortality risk in patients with COPD and heart failure comorbidity

Objective The purpose of the current research was to analyze the relevant risk factors for short-term death in patients with chronic obstructive pulmonary disease (COPD) and heart failure (HF), and to build a predictive nomogram. Methods We conducted a retrospective analysis of clinical data from 1 323 COPD and HF comorbidity patients who were admitted to the Affiliated Hospital of Southwest Medical University from January 2018 to January 2022. Samples were divided into survival and death groups based on whether they died during the follow-up. General data and tested index of both groups were analyzed, and the discrepant index was analyzed by single factor and multiple factor Logistic regression analysis. R software was applied to create the nomogram by visualizing the results of the regression analysis. The accuracy of the results was verified by C index, calibration curve, and ROC curve. Results The results from the multiple factor Logistic regression analysis indicated that age (OR=1.085, 95%CI 1.048 to 1.125), duration of smoking (OR=1.247, 95%CI 1.114 to 1.400), duration of COPD (OR=1.078, 95%CI 1.042 to 1.116), comorbidity with respiratory failure (OR=5.564, 95%CI 3.372 to 9.329), level of NT-proBNP (OR=1.000, 95%CI 1.000 to 1.000), level of PCT (OR=1.153, 95%CI 1.083 to 1.237), and level of D-dimer (OR=1.205, 95%CI 1.099 to 1.336) were risk factors for short-term death of COPD and HF comorbidity patients. The level of ALB (OR=0.892, 95%CI 0.843 to 0.942) was a protective factor that was used to build the predictive nomogram with the C index of 0.874, the square under the working characteristics curve of the samples of 0.874, the specify of 82.5%, and the sensitivity of 75.0%. The calibration curve indicated good predictive ability of the model. Conclusion The nomogram diagram built by the current research indicated good predictability of short-term death in COPD and HF comorbidity patients.