ObjectiveTo investigate the effects and underlying mechanisms of Shenqi Wenfei prescription （SQWF） on chronic obstructive pulmonary disease （COPD）. MethodsA rat model of COPD with lung Qi deficiency was established using lipopolysaccharide （LPS） combined with cigarette smoke. Forty-eight SD rats were randomly divided into a blank group， a model group， low-， medium-， and high-dose SQWF groups （2.835， 5.67， 11.34 g·kg^-1）， and a Yupingfeng group （1.35 g·kg^-1）. Drug administration began on day 29 after modeling and continued for 2 weeks. The general condition of the rats was observed， and the lung function in each group was assessed. Hematoxylin-eosin （HE） staining was used to observe pathological changes in lung tissue. The proportion of inflammatory cells in bronchoalveolar lavage fluid （BALF） was measured. Apoptosis in lung tissue was examined by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling （TUNEL） staining. The release level of lactate dehydrogenase （LDH） in BALF was detected by a microplate assay. Reactive oxygen species （ROS） levels in lung tissue were detected using fluorescent probes. The levels of malondialdehyde （MDA）， total superoxide dismutase （SOD）， and reduced glutathione （GSH） in BALF were measured by biochemical methods. Ultrastructural changes in lung cells were observed via transmission electron microscopy. Double immunofluorescence staining was performed to detect the expression of thioredoxin-interacting protein （TXNIP） and nucleotide-binding oligomerization domain-like receptor protein 3 （NLRP3） in lung tissue. Western blot analysis was used to detect the protein expression of TXNIP， NLRP3， apoptosis-associated speck-like protein containing a CARD （ASC）， cysteinyl aspartate-specific protease-1 （Caspase-1）， Caspase-1 p20， gasdermin D （GSDMD）， GSDMD N-terminal active fragment （GSDMD-N）， interleukin-1β （IL-1β）， and IL-18 in lung tissue. Serum IL-1β and IL-18 levels were measured by ELISA. ResultsCompared with the blank group， the model group showed lassitude， fatigue， tachypnea， and audible phlegm sounds， and lung function significantly declined （P0.01）. Pulmonary emphysema and inflammatory cell infiltration were obvious. The level of inflammatory cells in BALF increased significantly （P0.05）. The number of TUNEL-positive cells increased （P0.01）. Levels of LDH， ROS， and MDA in BALF increased significantly （P0.01）， while GSH and SOD activities decreased significantly （P0.01）. Lung tissue cells showed irregular morphology， swollen mitochondria， disrupted cell membranes， and abundant vesicles， i.e.， pyroptotic bodies. Protein levels of TXNIP， NLRP3， ASC， Caspase-1， Caspase-1 p20， GSDMD， GSDMD-N， IL-1β， and IL-18 in lung tissue were significantly elevated （P0.01）， and serum IL-1β and IL-18 levels also increased significantly （P0.01）. Compared with the model group， each medication group showed alleviation of qi deficiency symptoms and improved lung function （P0.01）. Pulmonary emphysema and inflammatory cell infiltration were reduced. Inflammatory cell levels decreased （P0.05）. The number of TUNEL-positive cells decreased significantly （P0.01）. Levels of LDH， ROS， and MDA decreased significantly （P0.05）， while GSH and SOD activities significantly increased （P0.01）. Morphological and structural damage in lung tissue was improved to varying degrees. Protein levels of TXNIP， NLRP3， ASC， Caspase-1， Caspase-1 p20， GSDMD， GSDMD-N， IL-1β， and IL-18 in lung tissue significantly decreased （P0.01）， and serum IL-1β and IL-18 levels also decreased significantly （P0.05）. ConclusionSQWF can improve lung function and alleviate inflammatory responses in COPD rats. Its mechanism may be related to regulating the ROS/TXNIP/NLRP3 pathway and inhibiting pyroptosis.

ObjectiveTo investigate the effects and underlying mechanisms of Shenqi Wenfei prescription （SQWF） on chronic obstructive pulmonary disease （COPD）. MethodsA rat model of COPD with lung Qi deficiency was established using lipopolysaccharide （LPS） combined with cigarette smoke. Forty-eight SD rats were randomly divided into a blank group， a model group， low-， medium-， and high-dose SQWF groups （2.835， 5.67， 11.34 g·kg^-1）， and a Yupingfeng group （1.35 g·kg^-1）. Drug administration began on day 29 after modeling and continued for 2 weeks. The general condition of the rats was observed， and the lung function in each group was assessed. Hematoxylin-eosin （HE） staining was used to observe pathological changes in lung tissue. The proportion of inflammatory cells in bronchoalveolar lavage fluid （BALF） was measured. Apoptosis in lung tissue was examined by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling （TUNEL） staining. The release level of lactate dehydrogenase （LDH） in BALF was detected by a microplate assay. Reactive oxygen species （ROS） levels in lung tissue were detected using fluorescent probes. The levels of malondialdehyde （MDA）， total superoxide dismutase （SOD）， and reduced glutathione （GSH） in BALF were measured by biochemical methods. Ultrastructural changes in lung cells were observed via transmission electron microscopy. Double immunofluorescence staining was performed to detect the expression of thioredoxin-interacting protein （TXNIP） and nucleotide-binding oligomerization domain-like receptor protein 3 （NLRP3） in lung tissue. Western blot analysis was used to detect the protein expression of TXNIP， NLRP3， apoptosis-associated speck-like protein containing a CARD （ASC）， cysteinyl aspartate-specific protease-1 （Caspase-1）， Caspase-1 p20， gasdermin D （GSDMD）， GSDMD N-terminal active fragment （GSDMD-N）， interleukin-1β （IL-1β）， and IL-18 in lung tissue. Serum IL-1β and IL-18 levels were measured by ELISA. ResultsCompared with the blank group， the model group showed lassitude， fatigue， tachypnea， and audible phlegm sounds， and lung function significantly declined （P0.01）. Pulmonary emphysema and inflammatory cell infiltration were obvious. The level of inflammatory cells in BALF increased significantly （P0.05）. The number of TUNEL-positive cells increased （P0.01）. Levels of LDH， ROS， and MDA in BALF increased significantly （P0.01）， while GSH and SOD activities decreased significantly （P0.01）. Lung tissue cells showed irregular morphology， swollen mitochondria， disrupted cell membranes， and abundant vesicles， i.e.， pyroptotic bodies. Protein levels of TXNIP， NLRP3， ASC， Caspase-1， Caspase-1 p20， GSDMD， GSDMD-N， IL-1β， and IL-18 in lung tissue were significantly elevated （P0.01）， and serum IL-1β and IL-18 levels also increased significantly （P0.01）. Compared with the model group， each medication group showed alleviation of qi deficiency symptoms and improved lung function （P0.01）. Pulmonary emphysema and inflammatory cell infiltration were reduced. Inflammatory cell levels decreased （P0.05）. The number of TUNEL-positive cells decreased significantly （P0.01）. Levels of LDH， ROS， and MDA decreased significantly （P0.05）， while GSH and SOD activities significantly increased （P0.01）. Morphological and structural damage in lung tissue was improved to varying degrees. Protein levels of TXNIP， NLRP3， ASC， Caspase-1， Caspase-1 p20， GSDMD， GSDMD-N， IL-1β， and IL-18 in lung tissue significantly decreased （P0.01）， and serum IL-1β and IL-18 levels also decreased significantly （P0.05）. ConclusionSQWF can improve lung function and alleviate inflammatory responses in COPD rats. Its mechanism may be related to regulating the ROS/TXNIP/NLRP3 pathway and inhibiting pyroptosis.

ObjectiveTo investigate the mechanisms by which Liuwei Buqi prescription （LWBQ） regulates alveolar macrophage efferocytosis and improves inflammatory responses in rats with chronic obstructive pulmonary disease （COPD） characterized by lung-kidney Qi deficiency based on the nuclear factor erythroid 2-related factor 2 （Nrf2）/macrophage receptor with collagenous structure （MARCO） pathway. MethodsSuccessfully modeled rats were randomly divided into a model group， low-dose LWBQ group （LWBQ-L， 2.25 g·kg^-1·d^-1）， medium-dose LWBQ group （LWBQ-M， 4.5 g·kg^-1·d^-1）， high-dose LWBQ group （LWBQ-H， 9 g·kg^-1·d^-1）， and aminophylline group （AMIN， 50 mg·kg^-1·d^-1）， with 8 rats in each group. Another 8 healthy rats were included as the blank group. Except for the blank group， rats in the remaining groups were subjected to smoke exposure combined with forced swimming， intratracheal lipopolysaccharide （LPS） instillation， and subcutaneous hydrocortisone injection to establish a COPD model with lung-kidney Qi deficiency. After successful modeling， rats were administered different doses of LWBQ or AMIN by gavage. Body weight， fur condition， and oral secretions were observed. Pulmonary function was measured using an animal lung function analyzer. Enzyme-linked immunosorbent assay （ELISA） was used to detect the expression levels of interferon-γ （IFN-γ）， interleukin-6 （IL-6）， interleukin-1 （IL-1）， and tumor necrosis factor-α （TNF-α） in bronchoalveolar lavage fluid （BALF） and serum （SER）. Hematoxylin-eosin （HE） staining was used to examine pathological changes in lung tissue. Giemsa staining was performed to detect eosinophils， basophils， and neutrophils in BALF. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） was used to detect apoptosis in lung tissue. Western blot and real-time polymerase chain reaction （Real-time PCR） were employed to determine the protein and mRNA expression levels of efferocytosis-related proteins growth arrest-specific gene 6 （GAS6）， milk fat globule-epidermal growth factor 8 （MFG-E8）， and pathway-related proteins Nrf2 and MARCO in lung tissue. ResultsCompared with the blank group， the model group showed reduced food intake， nasal and oral secretions with sputum， and decreased body weight （P<0.01）， decreased peak expiratory flow （PEF） （P<0.01）， increased forced vital capacity （FVC） （P<0.01）， and decreased forced expiratory volume in 0.3 s/forced vital capacity ［FEV0.3/FVC （%）］ （P<0.01）. The expression levels of IFN-γ， IL-6， IL-1， and TNF-α in BALF and SER were increased （P<0.01）. Lung tissue exhibited structural destruction， hyperplasia， inflammatory exudation， increased apoptotic cells， and increased mean optical density （P<0.01）. The protein and mRNA expression levels of GAS6， MFG-E8， and MARCO， as well as Nrf2 mRNA expression， were increased （P<0.01）. Compared with the model group， the LWBQ groups showed increased food intake， reduced nasal and oral secretions with sputum， and increased body weight （P<0.05， P<0.01）. PEF was increased （P<0.01）. FVC was increased in rats treated with low- and medium-dose LWBQ （P<0.01）， and FEV0.3/FVC （%） was increased in rats treated with medium- and high-dose LWBQ （P<0.05， P<0.01）. The expression levels of IFN-γ， IL-6， IL-1， and TNF-α in BALF and SER were decreased （P<0.01）. Lung tissue structure was relatively intact， with improvement in hyperplasia and inflammatory exudation. The number of apoptotic cells in lung tissue was reduced， and mean optical density was decreased （P<0.05， P<0.01）. The protein and mRNA expression levels of efferocytosis-related proteins GAS6 and MFG-E8 and pathway-related proteins Nrf2 and MARCO were increased （P<0.01）. ConclusionLWBQ can alleviate pulmonary and systemic inflammation， improve lung function， and reduce lung tissue damage in rats with COPD characterized by lung-kidney Qi deficiency. The mechanism may be related to enhancement of alveolar macrophage efferocytosis through regulation of the Nrf2/MARCO pathway.

Ferroptosis is a key driver of the onset and progression of chronic obstructive pulmonary disease （COPD）. By exploring the role of ferroptosis in COPD from the perspective of "qi deficiency with retention and stagnation"， it is considered that mitochondrial dysfunction and imbalanced antioxidant defenses are the microscopic manifestations of "qi deficiency"， whereas iron accumulation and lipid peroxide deposition constitute the pathological basis of "retention and stagnation". In traditional Chinese medicine （TCM）， the treatment principle is tonifying deficiency and benefiting qi， scattering retention and unblocking stagnation. Its mechanism involves improving the antioxidant system and mitochondrial function to enhance cellular resistance to ferroptosis， as well as relieving pulmonary iron overload， excessive lipid peroxidation， and inflammatory factor release to reduce the accumulation of pathological products， thereby exerting therapeutic effects on COPD.

Chronic obstructive pulmonary disease （COPD） is a respiratory disease characterized by airflow limitation， and its high morbidity and disability rates pose a severe challenge to global public health. Traditional Chinese medicine （TCM） has demonstrated definite efficacy and distinctive characteristics in the treatment of COPD. Based on the understanding of ancient and modern physicians regarding the etiology， pathogenesis， and stage-based syndrome differentiation of COPD， this article systematically elaborates on the etiology， pathogenesis， and clinical principles of syndrome differentiation and treatment of COPD. COPD is characterized by deficiency at root and excess in manifestation， with the coexistence of deficiency and excess. Qi deficiency is the fundamental pathogenesis underlying the occurrence and development of COPD and runs throughout the entire disease course. The disease begins with deficiency of lung qi and gradually affects the spleen and kidney， leading to the internal generation of dampness， phlegm， and blood stasis. Phlegm and blood stasis are not only pathological products but also deep-rooted causes of recurrent disease. Together with qi deficiency， they are mutually causal and form a vicious cycle. During the acute exacerbation stage of COPD， phlegm and blood stasis constitute the predominant underlying pathology and are often induced by invasion of pathogenic factors due to deficiency of healthy Qi. In addition， innovative understandings of the etiology and pathogenesis of COPD have emerged from the perspectives of collateral disease， latent pathogens， smoke toxins， and dysfunction of the Shaoyang pivot. During the stable stage， deficiency of Qi in the lung， spleen， and kidney predominates and is often accompanied by phlegm and blood stasis. In the clinical differentiation and treatment of COPD， treatment should be based on different disease stages and syndrome characteristics. During the acute exacerbation stage， eliminating pathogenic factors is the primary principle， with treatment determined according to syndrome differentiation. For wind-cold attacking the lung， the treatment is to ventilate the lung， disperse cold， and relieve cough. For phlegm-dampness accumulating in the lung， the treatment is to dry dampness， resolve phlegm， and direct qi downward. For phlegm-heat obstructing the lung， the treatment is to clear the lung， resolve phlegm， and relieve asthma. For phlegm and blood stasis obstructing the lung， the treatment is to eliminate phlegm， remove blood stasis， and relieve asthma. During the stable stage， reinforcing healthy Qi is the key principle. For lung-spleen qi deficiency， the treatment is to tonify the lung and strengthen the spleen， resolve phlegm， and direct Qi downward to relieve asthma. For deficiency of both lung and kidney， the treatment is to tonify the lung and benefit the kidney， resolve phlegm， promote Qi reception， and relieve asthma. When accompanied by phlegm and blood stasis， the treatment should focus on tonifying deficiency， resolving phlegm， and removing blood stasis. This article aims to systematically summarize the TCM etiology， pathogenesis， syndrome differentiation and treatment principles of COPD， as well as the current shortcomings in related research， in order to provide a reference for the clinical treatment of COPD with TCM， give full play to the advantages of TCM in the prevention and treatment of COPD， and optimize the whole-course management of COPD.

Chronic obstructive pulmonary disease （COPD） is a respiratory disease characterized by airflow limitation， and its high morbidity and disability rates pose a severe challenge to global public health. Traditional Chinese medicine （TCM） has demonstrated definite efficacy and distinctive characteristics in the treatment of COPD. Based on the understanding of ancient and modern physicians regarding the etiology， pathogenesis， and stage-based syndrome differentiation of COPD， this article systematically elaborates on the etiology， pathogenesis， and clinical principles of syndrome differentiation and treatment of COPD. COPD is characterized by deficiency at root and excess in manifestation， with the coexistence of deficiency and excess. Qi deficiency is the fundamental pathogenesis underlying the occurrence and development of COPD and runs throughout the entire disease course. The disease begins with deficiency of lung qi and gradually affects the spleen and kidney， leading to the internal generation of dampness， phlegm， and blood stasis. Phlegm and blood stasis are not only pathological products but also deep-rooted causes of recurrent disease. Together with qi deficiency， they are mutually causal and form a vicious cycle. During the acute exacerbation stage of COPD， phlegm and blood stasis constitute the predominant underlying pathology and are often induced by invasion of pathogenic factors due to deficiency of healthy Qi. In addition， innovative understandings of the etiology and pathogenesis of COPD have emerged from the perspectives of collateral disease， latent pathogens， smoke toxins， and dysfunction of the Shaoyang pivot. During the stable stage， deficiency of Qi in the lung， spleen， and kidney predominates and is often accompanied by phlegm and blood stasis. In the clinical differentiation and treatment of COPD， treatment should be based on different disease stages and syndrome characteristics. During the acute exacerbation stage， eliminating pathogenic factors is the primary principle， with treatment determined according to syndrome differentiation. For wind-cold attacking the lung， the treatment is to ventilate the lung， disperse cold， and relieve cough. For phlegm-dampness accumulating in the lung， the treatment is to dry dampness， resolve phlegm， and direct qi downward. For phlegm-heat obstructing the lung， the treatment is to clear the lung， resolve phlegm， and relieve asthma. For phlegm and blood stasis obstructing the lung， the treatment is to eliminate phlegm， remove blood stasis， and relieve asthma. During the stable stage， reinforcing healthy Qi is the key principle. For lung-spleen qi deficiency， the treatment is to tonify the lung and strengthen the spleen， resolve phlegm， and direct Qi downward to relieve asthma. For deficiency of both lung and kidney， the treatment is to tonify the lung and benefit the kidney， resolve phlegm， promote Qi reception， and relieve asthma. When accompanied by phlegm and blood stasis， the treatment should focus on tonifying deficiency， resolving phlegm， and removing blood stasis. This article aims to systematically summarize the TCM etiology， pathogenesis， syndrome differentiation and treatment principles of COPD， as well as the current shortcomings in related research， in order to provide a reference for the clinical treatment of COPD with TCM， give full play to the advantages of TCM in the prevention and treatment of COPD， and optimize the whole-course management of COPD.

This article summarizes Professor HAN Mingxiang's clinical experience in treating lung cancer based on the theory of "deficiency-phlegm-stasis-toxin". It is believed that depletion of healthy qi， together with binding of phlegm and stasis forming into toxin is the core pathogenesis of lung cancer occurrence and development. In clinical practice， the core treatment principle should be reinforcing healthy qi， resolving phlegm， removing stasis， and relieving toxins. The treatment should be given based on syndrome differentiation. For the syndrome of lung-spleen qi deficiency， the self-formulated Jianpi Huatan Zhike Decoction （健脾化痰止咳汤） can be applied to fortify the spleen and replenish qi， thereby reinforcing healthy qi. For the syndrome of deficiency of both qi and yin， the self-formulated Shenmai Yuzhu Decoction （参麦玉竹汤） is used to nourish yin and moisten the lungs， thereby clearing the source. For the syndrome of phlegm-dampness accumulating in the lungs， the self-formulated Sizi Wenfei Decoction （四子温肺汤） is applied to warm the lungs and resolve phlegm， thereby diffusing the lung qi. For the syndrome of qi stagnation and blood stasis， the self-formulated Yiqi Zhuyu Decoction （益气逐瘀汤） is used to activate blood and resolve stasis， thereby unblocking the collaterals. For the syndrome of binding of phlegm and stasis， the self-formulated Jiejie Decoction （结节方） is utilized to resolve phlegm and remove stasis， thereby dissipating nodules. For the syndrome of lung deficiency with toxin accumulation， the self-formulated Qiyu Sanlong Decoction （芪玉三龙汤） is applied to reinforce healthy qi and remove toxins， thereby combating cancer. Medications are flexibly prescribed based on syndrome differentiation， with an emphasis on reinforcing healthy qi and eliminating pathogenic factors， and maintaining the balance of zang-fu （脏腑） organ functions as well as qi， blood， yin and yang.

ObjectiveTo investigate the improvement effect of Qibai Pingfei capsules on pulmonary vascular remodeling in rats at different stages of chronic obstructive pulmonary disease （COPD） and to analyze its possible mechanism of action. MethodsMale Sprague-Dawley （SD） rats were randomly divided into a normal group， an early COPD model group， an advanced COPD model group， an early-intervention high-dose group， a late-intervention high-dose group， an early-intervention low-dose group， a late-intervention low-dose group， an early-intervention pyrrolidine dithiocarbamate （PDTC） group， and a late-intervention PDTC group， with 15 rats in each group. A rat model of early COPD was constructed by using cigarette smoke combined with airway infusion using lipopolysaccharide（LPS）， and a rat model of advanced COPD was constructed by using airway infusion with LPS， cigarette smoke， and hypoxia. All groups except the normal group were given LPS airway drops on days 1 and 14 of the experiment， smoked for 1 h per day， and administered the drug once a day for 40 weeks from day 15 onward. In the high- and low-dose groups， rats were given 1 g·kg^-1 and 250 mg·kg^-1 Qibai Pingfei capsules， respectively by gavage， and in PDTC groups， rats were given 100 mg·kg^-1 of PDTC by intraperitoneal injection. The advanced COPD model group underwent 6 h of hypoxia per day in weeks 5-6. Lung function and mean pulmonary artery pressure were tested in rats. Morphologic changes in lung tissues were detected by hematoxylin-eosin（HE）staining. Collagen deposition in lung tissues was examined by Masson staining， and the levels of inflammatory factors including interleukin-1β（IL-1β）， interleukin-6（IL-6）， and tumor necrosis factor-α（TNF-α）in lung tissues were detected by enzyme-linked immunosorbent assay （ELISA）. The number of inflammatory cells in the alveolar lavage fluid of rats in each group was detected by Giemsa staining， and the protein expression of Toll-like receptor 4（TLR4）， myeloid differentiation factor 88（MyD88）， nuclear factor-κB（NF-κB）， TNF-α， vascular endothelial-cadherin（VE-cadherin）， α-smooth muscle actin（α-SMA）， and platelet endothelial cell adhesion molecule-1（CD31） was detected by Western blot in the lung tissues of rats. ResultsCompared with the normal group， the model group showed significantly decreased forced expiratory volume in 0.3 s （FEV_0.3）， forced vital capacity （FVC）， and FEV_0.3/FVC ratio related to lung function （P<0.05）， thickening of pulmonary vasculature， increased collagen deposition in the lungs， and enhanced mean pulmonary arterial pressure and expression levels of IL-6， IL-1β， and TNF-α （P<0.05）. Additionally， the model group also exhibited increased numbers of macrophages， lymphocytes， and neutrophils （P<0.05）， significantly higher protein expression of TLR4， MyD88， NF-κB， TNF-α， and α-SMA （P<0.05）， and significantly lower protein expression of VE-cadherin and CD31 （P<0.05）. Lung function was significantly improved in the Qibai Pingfei capsules groups compared with the model group （P<0.05）， with mean pulmonary arterial pressure reduced and pulmonary vascular thickening and collagen deposition in the lungs ameliorated. The Qibai Pingfei capsules groups also showed reduced expression levels of IL-6， IL-1β， and TNF-α （P<0.05） and decreased numbers of macrophages， lymphocytes， and neutrophils （P<0.05）， as well as reduced protein expression of TLR4， MyD88， NF-κB， TNF-α， and α-SMA （P<0.05） and elevated protein expression of VE-cadherin and CD31 （P<0.05） in rat lung tissues. ConclusionQibai Pingfei capsules inhibits inflammatory response and endothelial-to-mesenchymal transition probably by regulating the TLR4/NF-κB signaling pathway， thus improving pulmonary vascular remodeling in COPD model rats and showing therapeutic effects in the early stage of COPD.

This study systematically elucidates the contemporary understanding of the theory of"the lung and large intestine being interior-exteriorly related"within both traditional Chinese and Western medical theoretical frameworks,while providing an in-depth summary of national medical master Han Mingxiang's clinical experience in diagnosing and treating phlegm-heat obstructing lung syndrome in acute exacerbation chronic obstructive pulmonary disease(AECOPD).Theoretically,this doctrine originates from the Huangdi Neijing and has been developed into a comprehensive system by subsequent medical practitioners.Modern medical research from embryological,microbiological,and other perspectives has confirmed the close physiological and pathological relationship between the lung and intestine,particularly evidenced by the proposed"gut-lung axis"theory.Based on over 6 decades of clinical practice,professor Han identified the core pathogenesis of AECOPD as involving"phlegm,blood stasis,toxins,and deficiency,"with phlegm-heat obstructing lung syndrome being the most prevalent manifestation.The pathological characteristics include impaired lung qi descent,internal accumulation of phlegm-heat,and intestinal obstruction.The therapeutic approach emphasizes"clearing heat and resolving phlegm,relieving cough and asthma"as the primary treatment principle,focusing on"clearing lung heat,eliminating phlegm pathogens,and descending rebellious qi",while adhering to the concept of"simultaneous treatment of lung and intestine."In terms of herbal prescription,professor Han skillfully employs modified Xuanbai Chengqi decoction,which integrates lung-ventilating,phlegm-resolving,and purgative effects.Importantly,he emphasizes the precise timing and dosage of purgative herbs,particularly for patients with deficiency patterns,advocating discontinuation or dose reduction once intestinal patency is achieved to avoid overtreatment.For remission phase management,professor Han advocates the"reinforcing earth to generate metal"approach using modified Bufei decoction combined with Yigong powder,which strengthens spleen qi to nourish lung function.This therapeutic strategy embodies the fundamental treatment principle of"treating the acute manifestations first,then addressing the root cause."This research not only deepens the understanding of classical Chinese medical theories but also provides more scientifically grounded intervention strategies for the clinical prevention and treatment of lung distension.The findings offer valuable insights into integrative approaches for AECOPD management,combining traditional wisdom with contemporary medical understanding.

This paper summarized the experience of Chinese medical master Han Mingxiang in treating pathogenic-damp caused diseases by the method of dispelling dampness.Han Mingxiang believes that refractory diseases are usually caused by pathogenic cold and dampness,and complicated diseases are usually caused by phlegm and stagnation.Predominant dampness causes the inactivation of yang,and warming therapy is not the only one choice for activating yang.In clinical practice,he emphasizes the principles for dispelling dampness mainly by simultaneous treatment of phlegm and qi,lifting lucid yang and lowering turbid yin,nourishing spleen and resolving dampness,expelling and resolving pathogens by elevation and dispersion,relieving exterior and activating yang,which is summed up as"warming,resolving,dispersing and activating,regulating qimovement".For the treatment of the diseases caused by pathogenic-damp,the warm-natured medicines are usually used frequently,and the warm-natured medicines are not limited to the pungent-warm medicine.For dispelling dampness,the method of relieving exterior and promoting qi movement,percolating and draining dampness with aromatics,and relieving fluid retention with pungent-sweet medicine can be chosen flexibly based on syndrome differentiation,thus to reach the goal of activating yang and resolving stagnation and to obtain satisfactory efficacy.