ObjectiveThis study aimed to investigate whether Bushen Tongluo prescription inhibits macrophage polarization by regulating the Wnt3a/β-catenin signaling pathway， thereby reducing epithelial-mesenchymal transition and excessive extracellular matrix deposition， in order to elucidate the anti-pulmonary fibrosis mechanisms of Bushen Tongluo prescription and provide a new theoretical basis for the clinical treatment of pulmonary fibrosis. MethodsFifty male Sprague-Dawley （SD） rats were randomly divided into a blank group， model group， pirfenidone group， and high- and low-dose Bushen Tongluo prescription groups. Except for the blank group， the pulmonary fibrosis model was established by intratracheal instillation of bleomycin. Intervention was initiated on day 28 after modeling. The high- and low-dose Bushen Tongluo prescription groups were administered Bushen Tongluo prescription at doses of 30.88， 15.44 g·kg^-1， respectively， by intragastric gavage. The pirfenidone group was administered pirfenidone capsules at 110 mg·kg^-1 by intragastric gavage. The blank and model groups were given an equal volume of normal saline by gavage， once daily for 90 days. After treatment， the level of transforming growth factor-β₁ （TGF-β₁） in bronchoalveolar lavage fluid （BALF） was detected by enzyme-linked immunosorbent assay （ELISA）. Morphological changes in lung tissue and the collagen volume fraction were compared. The protein distribution and expression of E-cadherin， cytokeratin 19， α-smooth muscle actin （α-SMA）， vimentin， collagen type Ⅰ （Col Ⅰ）， and collagen type Ⅲ （Col Ⅲ） in lung tissue were detected by immunohistochemistry. The protein distribution and expression of CD68， arginase-1 （Arg-1）， inducible nitric oxide synthase （iNOS）， Wnt3a， and β-catenin in lung tissue were detected by immunofluorescence. The protein expression of Wnt3a and β-catenin in lung tissue was detected by Western blot， and the mRNA expression of Wnt3a and β-catenin was detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared with the blank group， a large number of inflammatory cells infiltrated the airway walls， alveolar spaces， and interstitial tissue in the model group， with obvious fibrous tissue hyperplasia. The level of TGF-β₁ in BALF was significantly increased. The protein expression of E-cadherin and cytokeratin 19 in lung tissue was decreased， whereas the protein expression of α-SMA， Vimentin， Wnt3a， β-catenin， Col Ⅰ， and Col Ⅲ was increased. The fluorescence-positive area ratios of CD68， Arg-1， iNOS， Wnt3a， and β-catenin in lung tissue were increased. The protein and mRNA expression levels of Wnt3a and β-catenin in lung tissue were significantly increased （P<0.01）. Compared with the model group， all treatment groups showed varying degrees of improvement in inflammatory cell infiltration and fibrous tissue hyperplasia in the airway walls， alveolar spaces， and interstitial tissue， decreased TGF-β₁ levels in BALF， increased protein expression of E-cadherin and cytokeratin 19 in lung tissue， decreased protein expression of α-SMA， Vimentin， Col Ⅰ， and Col Ⅲ， decreased fluorescence-positive area ratios of CD68， Arg-1， iNOS， Wnt3a， and β-catenin in lung tissue， and decreased protein and mRNA expression levels of Wnt3a and β-catenin in lung tissue （P<0.05， P<0.01）. ConclusionBushen Tongluo prescription can improve bleomycin-induced pulmonary fibrosis in rats by inhibiting epithelial-mesenchymal transition and reducing excessive extracellular matrix deposition. The mechanism may be related to inhibition of the Wnt3a/β-catenin signaling pathway and the macrophage polarization mediated by this pathway.

Pulmonary sarcoidosis is an immune system disease with an unclear etiology. Guided by the yang-reinforcing method， it is believed that the fundamental pathogenesis of pulmonary sarcoidosis lies in the disharmony between water and fire and the reckless movement of the ministerial fire. The failure of the spleen and stomach to maintain warmth， leading to the production of phlegm and blood stasis， is an important pathogenesis. The invasion of external pathogenic toxins， deeply penetrating into the interior， is considered a triggering factor for the disease. The treatment focuses on supplementing the yang， consolidating the kidney， drawing fire back to its source， warming the yang， benefiting the kidney， and nourishing the spleen to generate metal. It also emphasizes unblocking the yang， transforming turbidity， and eliminating phlegm and blood stasis.

Chronic cough is one of the common complications after pulmonary nodule surgery. Its etiology and pathogenesis are complex， and syndrome differentiation and treatment in traditional Chinese medicine （TCM） require comprehensive consideration of the distinct characteristics across the preoperative， intraoperative， and postoperative phases. Prior to surgery， there may be healthy qi depletion with lingering pathogens in the lungs； during surgery， metal instruments may injure the body， leading to qi and blood damage； after surgery， the depletion of healthy qi worsens， with dual deficiency of lung and spleen qi and yin as the root condition， often complicated by pathogens such as wind， phlegm， stagnation， and stasis. Treatment should follow the principle of comprehensively considering all three phases with a focus on the postoperative phase. Replenishing deficiency is the primary， particularly by tonifying qi and nourishing yin， as well as supplementing the lung and fortifying the spleen. For different accompanying syndromes， therapeutic methods such as dispelling wind， resolving phlegm， relieving stagnation， and unblocking stasis should be applied accordingly， while aggressive purgative herbs should be used with caution to avoid depletion of qi and blood injury.

Refractory chronic cough belongs to the category of "refractory cough" in traditional Chinese medicine， and it is believed that the root cause of intractable chronic cough is wind lodging in the spleen collaterals， with poor spleen yang and deficient kidney essence as the pathologic basis of the disease， which is present throughout the disease. The method advocated is to search the spleen collaterals and eliminate latent wind， warm the spleen yang and smooth the middle jiao， cultivate the kidney essence and consolidate the root， prescribed with modified Fuzi Lizhong Decoction （附子理中汤） plus Erxian Decoction （二仙汤） as the basis. The Fuzi Lizhong Decoction can warm yang and fortify the middle， and smooth the middle jiao， and the Erxian Decoction can cultivate the kidney essence and consolidate the innate. The two prescriptions could combine with Suye （Perilla frutescens）， Jingjie （Dysphania ambrosioides）， Fangfeng （Carum carvi） and other medicinals of cleaning characteristic， or combine with Gouteng （Uncaria rhynchophylla）， Chuanshanlong （Dioscorea nipponica）， Dilong （Kummerowia striata） and other medicinals of worm or cane category， to find the wind and expel pathogen， smooth spleen collaterals.

This article is based on ZHANG Jingyue's theory of yin-yang holism to explore the etiology， pathogenesis， and treatment of acute exacerbation of rheumatoid arthritis-associated interstitial lung disease （RA-ILD）. It is believed that the foundation of acute exacerbation of RA-ILD lies in real yin insufficiency and yin fail to control yang； external pathogen attacking is a common cause of acute exacerbation of RA-ILD. For treatment， it is important to first suppress ministerial fire by prescribing modified Yinhuo Decoction （引火汤）； if ministerial fire submerged， focus should be on nourishing both yin and yang； if real yin deficiency is the main issue， modified Zuogui Pill （左归丸） should be used； if real yang deficiency is prominent as well， modified Yougui Pill （右归丸） can be chosen. When yin and yang balanced， the disease could be solved.

This paper discussed the treatment of chronic cough of phlegm-dampness type based on the theory of “removing the earth stagnation”. It is believed that stagnation of qi in the middle energizer caused malfunction of water metabolism in the human body， which is the key pathogenetic mechanism leading to phlegm-dampness cough. Pathogenesis like cold and dampness attacking the spleen， dampness-heat obstruction， weakness of the middle energizer， failure to ascend clear yang， and internal blazing of yin fire may lead to “earth stagnation”， which triggered phlegm-dampness cough. The treatment advocated “removing the stagnation” to improve qi transformation in the middle energizer， eliminate stagnation， and use different treatment methods such as warming the middle， circulating qi， transforming phlegm and dampness based on different disease cause and mechanism to calm cough. As for prescriptions， Jiangling Banxia Decoction （姜苓半夏汤） could be used for cold-dampness syndrome， Banxia Xiexin Decoction （半夏泻心汤） plus Xiangsu Powder （香苏散） used for damp-heat syndrome， and Buzhong Yiqi Decoction （补中益气汤）， Tiaozhong Yiqi Decoction （调中益气汤）， Shengyang Yiwei Decoction （升阳益胃汤） and Bupiwei Xieyinhuo Shengyang Decoction （补脾胃泻阴火升阳汤） could be selected for spleen-stomach weakness syndrome according to different characteristics and pathogenesis.

It is believed that the fundamental pathogenesis of the connective tissue diseases-associated interstitial lung disease （CTD-ILD） is kidney essence deficiency， with lung collateral obstruction throughout the disease， and environmental toxin pathogen is the important causative factors for the development of CTD-ILD. This article proposed to restore origin and alleviate bi （痹） for CTD-ILD， for which restoring origin means tonifying the lungs， spleen and kidneys to bank up the roots and consolidate the original qi， with modified Erxian Decoction （二仙汤） plus Liu Junzi Decoction （六君子汤）； alleviating bi means expelling wind and dredging collaterals， and eliminating the mass to restore the smoothness of the lung collaterals， with paired medicines of Chuanshanlong （Dioscorea nipponica）-Dilong （Kalanchoe pinnata）， Vinegar-processed Sanleng （Sparganium stoloniferum）-Vinegar-processed Ezhu （Curcuma zedoaria）， and stem-type medicines， and emphasized on removing the environmental toxin pathogens to facilitate the recovery of healthy qi.

Bronchiectasis is a refractory chronic airway disease characterized by chronic cough and phlegm production. Airway mucus hypersecretion is one of the important causative factors for acute exacerbation of bronchiectasis. Thus， reducing airway mucus secretion during the stable phase of bronchiectasis is the key to the treatment. Phlegm-dispelling therapy is commonly used in modern medicine， which， however， fails to radically reduce mucus secretion. At the moment， it is difficult and urgent to find an intervention that can improve the quality of life of patients and reduce the recurrence of disease during the stable phase of bronchiectasis. Chinese medicine shows remarkable efficacy in reducing airway mucus secretion. Nonetheless， there is a lack of research on the airway mucus hypersecretion of bronchiectasis， and no registered research outcome is available. Traditional Chinese medicine boasts a lot of experience in the treatment of phlegm. It combines clearing and tonifying methods and identifies Yin and Yang and internal organs， thus being advantageous in the treatment of airway mucus hypersecretion of bronchiectasis. Therefore， it is an important topic to improve the effectiveness of Chinese medicine on airway mucus hypersecretion of bronchiectasis by focusing on the "generation"， "transformation" and "excretion" of phlegm.

Objective To investigate the regulatory effect of calcitonin gene-related peptide (CGRP) on the mRNA and protein expression of neuronal nitric oxide synthase (NOS), as well as the release of nitric oxide (NO) in cultured human keratinocyte line HaCaT. Methods NO level in the supernatant of cell culture medium was detected with an enzymatic NO detecting kit, the mRNA expression of neuronal NOS was studied with reverse transcription polymerase chain reaction(RT-PCR), and the protein expression of neuronal NOS was studied with immunochemical technique(SP). Results Compared with that in normal culture condition, the mRNA and protein expression of neuronal NOS and the release of NO was significantly upregulated by CGRP in HaCaT cells. Whereas, the expression of neuronal NOS and the release of NO in HaCaT cells induced by CGRP was inhibited by CGRP-8-37, an inhibitor of CGRP receptor. Conclusion The expression of neuronal NOS in keratinocytes and the release of NO from keratinocytes could be upregulated by CGRP.