Background:Cardiovascular (CV) comorbidities can affect drug tolerability and health outcomes in patients with idiopathic pulmonary fibrosis (IPF). This systematic review and meta-analysis aimed to quantify the magnitudes of association between IPF and both overall and specific categories of CV disease. Methods:The PRISMA guidelines and PICO model were followed. We searched PubMed, Embase, Web of Science, Cochrane Library, and Chinese Biomedical Literature Service System (Sinomed) from inception to April 2025 for studies investigating CV disease in IPF patients. Study quality was assessed using the Newcastle-Ottawa Scale (NOS). Pooled odds ratio (OR) for case-control/cross-sectional datasets and relative risk (RR) for cohort datasets were calculated using Review Manager 5.4. The I 2 test was used to evaluate the heterogeneity and the sources of heterogeneity were explored through sensitivity analyses, meta-regression, and subgroup analyses. The funnel plot and Egger's test were used to evaluate publication bias. Results:A total of 28 studies comprising 29 case-control/cross-sectional datasets and four cohort datasets were included, which indicated a positive association between IPF and CV disease (OR 2.44, 95% CI 1.84-3.24, P < 0.001; RR 1.44, 95% CI 1.07-1.92, P = 0.02). Meta-regression and maximized subgroup analyses confirmed the influence of control characteristics (P < 0.001), data source (P = 0.027), Newcastle-Ottawa Scale (NOS) score (P = 0.022), certainty of CV disease diagnosis (P = 0.027), body mass index (BMI), smoking status, and diabetes prevalence on both heterogeneity and risk estimates in the case-control/cross-sectional datasets. The OR varied across the CV disease category, with 1.14- to 2.51-fold increased risks for ischemic heart disease, thromboembolic disease, pulmonary hypertension, and other forms of heart disease. Conclusion:Idiopathic pulmonary fibrosis is significantly associated with CV disease, emphasizing the urgent need for systematic screening and risk reduction strategies in IPF patients. Systematic review registration:https://www.crd.york.ac.uk/PROSPERO/view/CRD420251013917, identifier CRD420251013917.

BackgroundIdiopathic Pulmonary Fibrosis (IPF), an interstitial lung disease of unknown etiology, remains incurable with current therapies, which fail to halt disease progression or restore lung function. However, Feibi Recipe No. 2 (FBR2), a clinically validated traditional Chinese medicine formula, exhibits potential as an IPF treatment.ObjectiveThis study aimed to investigate the regulatory effect of FBR2 on ferroptosis through the SIRT3/p53 pathway and its therapeutic potential in improving IPF.MethodsPulmonary fibrosis was induced in C57BL/6J mice by intratracheal instillation of Bleomycin (BLM), followed by FBR2 treatment via gavage. Assessments encompassed histopathology, ELISA for cytokine detection, IHC and Western blot for protein expression analysis, and qRT-PCR for gene expression quantification. Transmission electron microscopy (TEM) was used to observe mitochondrial morphology. The roles of Erastin and the SIRT3 inhibitor 3-TYP were also explored to elucidate FBR2’s mechanisms of action.ResultsFBR2 treatment significantly mitigated BLM-induced lung injury in mice, as evidenced by improved body weight and survival rates, and reduced levels of inflammatory cytokines, including IL-6 and TNF-α. FBR2 decreased collagen deposition in lung tissue, as shown by Masson’s staining and IHC detection of Col-I and α-SMA, confirming its anti-fibrotic effects. It also reduced iron and MDA levels in lung tissue, increased GSH-Px activity, improved mitochondrial morphology, and enhanced the expression of GPX4 and SLC7A11, indicating its ferroptosis-inhibitory capacity. Furthermore, FBR2 increased SIRT3 levels and suppressed p53 and its acetylated forms, promoting the translocation of p53 from the nucleus to the cytoplasm where it co-localized with SIRT3. The protective effects of FBR2 were reversed by Erastin, confirming the central role of ferroptosis in pulmonary fibrosis treatment. The use of 3-TYP further confirmed FBR2’s intervention in ferroptosis and cellular senescence through the SIRT3/p53 pathway.ConclusionFBR2 shows therapeutic potential in a BLM-induced pulmonary fibrosis mouse model, with its effects mediated through modulation of the ferroptosis pathway via the SIRT3/p53 mechanism. This study provides novel evidence for the targeted treatment of IPF and offers further insights into its pathogenesis.

This study explored the therapeutic potential of Number 2 Feibi Recipe (FBR2), a traditional Chinese medicine prescription, in the treatment of idiopathic pulmonary fibrosis (IPF). Specifically, it investigated whether FBR2 mediated its effects by modulating miR-199a-5p expression, activating the SIRT1/AMPK/mTOR pathway and then promoting autophagy. Eighty-four mice were divided into seven groups: Control, bleomycin (BLM), FBR2, self-complementary adeno-associated virus expressing miR-199a-5p (scAAV-miR-199a-5p), scAAV-negative control (scAAV-NC), FBR2 + BLM + scAAV-miR-199a-5p, and FBR2 + BLM + scAAV-NC. Fluorescence staining, miR-199a-5p expression levels, histopathological changes, protein expression and autophagy activity were assessed using various techniques, including RT-qPCR, histopathological staining, Western blotting, Elisa and transmission electron microscopy (TEM). FBR2 treatment significantly reduced miR-199a-5p expression elevated by BLM and improved histopathology, reduced levels of α-smooth muscle actin (α-SMA) and collagen-III, and increased E-cadherin expression. FBR2 also enhanced autophagy, as evidenced by elevated LC3-II and Beclin-1 levels and reduced p62 expression. Additionally, it activated the SIRT1/AMPK/mTOR pathway. Finally, network pharmacology identified 227 compounds in FBR2, among which Kaempferol and Quercetin (two major shared constituents) showed strong binding to miR-199a-5p in molecular docking, suggesting their potential as key active components. This study showed FBR2 attenuated BLM-induced pulmonary fibrosis in mice by reducing miR-199a-5p expression and promoting autophagy which may be achieved by modulating the SIRT1/AMPK/mTOR pathway. These findings provide novel insights into the mechanism of FBR2 and its potential as a therapeutic approach for IPF.

Background: Jinwei decoction can enhance the anti-inflammatory effect of glucocorticoid (GC) on chronic obstructive pulmonary disease (COPD) by restoring the activity of human histone deacetylase-2 (HDAC2). However the upstream mechanism of Jinwei decoction on HDAC2 expression is not clear. Objective: To explore the target of Jinwei decoction to enhance the anti-inflammatory effect of GC on COPD through microRNA155-5p (miR-155-5p) by network pharmacology and experimental verification. Methods: The TCMSP database was used to screen active ingredients and target genes of Jinwei decoction, and miRWalk2.0 was used to predict downstream target genes of miR-155-5p. COPD-related genes were identified by searching GeneCards, Grugbank and OMIM databases; Venny 2.1 was used to screen intersection genes; Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of intersection genes were analyzed by R software. Protein-protein interactions (PPIs) were analyzed by Cytoscape 3.7.2 software to identify core genes. Finally, interactions between main compounds and potential targets were verified by molecular docking. A COPD cell model was established by 5% cigarette smoke extract (CSE)- induced bronchial epithelial cell (BEAS-2B), and the results of network pharmacology were verified by in vitro experiments. Results: Two hundred thirty-one active ingredients, 352 Jinwei decoction drug targets, 5949 miR-155-5p target genes, 8286 COPD target genes, and 127 intersection genes were identified. Twelve core proteins of PPI networks may be involved. GO enrichment analysis showed that regulation of membrane potential， response to steroid hormone, and histone modification were involved; KEGG pathway enrichment analysis concentrated in the PI3K-Akt, mitogen-activated protein kinase (MAPK), HIF-1, and other signaling pathways. The molecular docking results showed that quercetin, luteolin and stigmasterol have higher affinity with PTGS2, HIF1A and AKT1. The results of cell experiments revealed that Jinwei decoction not only enhances the anti- inflammatory effect of GC in the COPD cell model but also reverses the high expression of miR-155-5p、PI3k、Akt, and low expression of HDAC2, thereby inhibiting the inflammatory response of COPD. Conclusion: Jinwei decoction can regulate HDAC2 activity and enhance the anti-inflammatory effect of GC on COPD by modulating miR-155-5p. Its mechanism of action may be related to its effect on the PI3K-Akt through miR-155-5p.

This study aimed to construct an evidence map and conduct a comprehensive analysis of clinical research literature on the treatment of pulmonary fibrosis with proprietary Chinese medicines published over the past three decades,so as to systematically evaluate the effectiveness and limitations of existing evidence and provide a scientific basis for subsequent clinical practice,research directions,and policy-making.A systematic search was conducted across 7 databases in both Chinese and English from the inception of the databases to June 1,2024.The clinical research characteristics and methodological quality of the included literature were assessed.A total of 123 pieces of literature were ultimately included,comprising 108 interventional studies,3 observational studies,10 secondary study,and 2 expert consensuses.These studies involved 33 kinds of proprietary Chinese medicines,with Danhong Injection being the most widely used.Most studies had a duration of 1-3 months and a sample size ranging from 50 to 100 cases,and they were often used in combination with steroids or conventional western medicine.There was a common phenomenon of off-label use of proprietary Chinese medicines.The main outcome indicators included pulmonary function,blood gas analysis,and total effective rate,with issues such as insufficient safety reporting,lack of distinctive traditional Chinese medicine(TCM)features,absence of long-term outcome indicators,and strong subjective evaluation.In terms of methodological quality assessment,randomized controlled trial(RCT)had biases in randomization and outcome indicator measurement and a risk of selective reporting.Meta-analysis lacked reporting on protocol registration,literature exclusion lists,and disclosure of conflicts of interest.Expert consensuses lacked standards in terms of rigor,scientific basis,and applicability.The quality of clinical research evidence on the treatment of pulmonary fibrosis with proprietary Chinese medicines urgently needs improvement.It is recommended that future research should pay more attention to the scientific and rigorous design to enhance the standardization and reproducibility of the research.At the same time,it should integrate TCM theories to establish an outcome indicator evaluation system suitable for the treatment of pulmonary fibrosis with proprietary Chinese medicines,so as to fully explore the potential of proprietary Chinese medicines in treating pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a disease of unknown etiology characterized by a constant incidence rate. Unfortunately, effective pharmacological treatments for this condition are lacking and the identification of novel therapeutic approaches and underlying pathological mechanisms are required. This study investigated the potential of quercetin in alleviating pulmonary fibrosis by promoting autophagy and activation of the SIRT1/AMPK pathway. Mouse models of IPF were divided into four treatment groups: control, bleomycin (BLM), quercetin (Q), and quercetin + EX-527 (Q + E) treatment. Pulmonary fibrosis was induced in the mouse models through intratracheal instillation of BLM. Various indexes were identified through histological staining, Western blotting analysis, enzyme-linked immunosorbent assay, immunohistochemistry, and transmission electron microscopy. Quercetin treatment ameliorated the pathology of BLM-induced pulmonary fibrosis of mice by reducing α-smooth muscle actin (α-SMA), collagen I (Col I), and collagen III (Col III) levels, and also improved the level of E-cadherin in lung tissue. Furthermore, Quercetin significantly enhanced LC3II/LC3I levels, decreased P62 expression, and increased the number of autophagosomes in lung tissue. These effects were accompanied by the activation of the SIRT1/AMPK pathway. Treatment with EX-527, an inhibitor for SIRT1, reversed all effects induced by quercetin. This study showed that quercetin could alleviate pulmonary fibrosis and improve epithelial-mesenchymal transition by acting on the SIRT1/AMPK signaling pathway, which may be achieved by regulating the level of autophagy.

Background: Some patients with chronic obstructive pulmonary disease (COPD) benefit from glucocorticoid (GC) treatment, but its mechanism is unclear.Objective: With the help of the Gene Expression Omnibus (GEO) database, the key genes and miRNA-mRNA related to the treatment of COPD by GCs were discussed, and the potential mechanism was explained.Methods: The miRNA microarray dataset (GSE76774) and mRNA microarray dataset (GSE36221) were downloaded, and differential expression analysis were performed.Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the differentially expressed genes (DEGs).The protein interaction network of the DEGs in the regulatory network was constructed with the STRING database, and the key genes were screened through Cytoscape.Potential downstream target genes regulated by differentially expressed miRNAs (DEMs) were predicted by the miRWalk3.0database, and miRNA-mRNA regulatory networks were constructed.Finally, some research results were validated.Results: ① Four DEMs and 83 DEGs were screened; ② GO and KEGG enrichment analysis mainly focused on the PI3K/Akt signalling pathway, ECM receptor interaction, etc.; ③ CD2, SLAMF7, etc. may be the key targets of GC in the treatment of COPD; ④ 18 intersection genes were predicted by the mirwalk 3.0 database, and 9 pairs of miRNA-mRNA regulatory networks were identified; ⑤ The expression of miR-320d-2 and TFCP2L1 were upregulated by dexamethasone in the COPD cell model, while the expression of miR-181a-2-3p and SLAMF7 were downregulated. Conclusion:In COPD, GC may mediate the expression of the PI3K/Akt signalling pathway through miR-181a-2-3p, miR-320d-2, miR-650, and miR-155-5p, targeting its downstream signal factors.The research results provide new ideas for RNA therapy strategies of COPD, and also lay a foundation for further research.

Multiple randomized controlled studies have shown that pirfenidone and nintedanib are effective and safe for treating idiopathic pulmonary fibrosis. This study aimed to evaluate their efficacy, safety, and tolerability in a real-world setting. We searched PubMed, Embase, Cochrane Library, and ClinicalTrials.gov databases for real-world studies published up to March 3, 2023, on pirfenidone and nintedanib for idiopathic pulmonary fibrosis. A total of 74 studies with 23,119 participants were included. After 12 months of treatment, the change from baseline in percent predicted FVC (

Ethnopharmacological relevance: Fu Fang Gang Liu (FFGL) is an effective formula for treating wart proliferation caused by human papillomavirus (HPV) infection and has the potential to treat HPV-related cancers. However, scientific evidence of its anti-tumor activity against cervical cancer, the most common cancer caused by HPV, is lacking.Aim of the study: To clarify the anti-tumor effect of an FFGL aqueous extract on human cervical cancer and its possible mechanism of cell cycle arrest in HeLa cells.Materials and methods: The anti-proliferative effect of FFGL on cervical cancer cells was assessed using the cell counting kit-8 assay. The proportion of apoptotic cells, cell cycle distribution, and cell division rate were determined using flow cytometry. Quantitative proteomics was used to identify differentially expressed proteins after FFGL treatment, and bioinformatics analysis was used to identify key nodal proteins affected by FFGL. Immunofluorescence and western blot analyses were used to explore changes in the expression of related proteins in the cell cycle and DNA damage pathways to elucidate the potential mechanism of action of FFGL against HeLa cell proliferation. Results: FFGL inhibited cervical cancer cell proliferation and caused cell cycle arrest. According to quantitative proteomics, CyclinB1 may play an important role in the anti-proliferative effect of FFGL on HeLa cells. Additional experiments showed that FFGL aqueous extract caused ATM-mediated DNA damage, further phosphorylated CHK2, led to the inactivation of Cdc25C, inhibited the activity of the CDK1/CyclinB1 complex, and resulted in cell cycle arrest. Conclusions: FFGL can inhibit cervical cancer cell proliferation. Furthermore, it can increase CDK1 phosphorylation, block the cell cycle by causing DNA damage, and inhibit HeLa cell proliferation.

病证结合诊疗模式逐渐成为中医诊疗的特色,可提高治疗效果.在生理功能方面,线粒体功能与中医气的推动、气化、防御、温煦作用颇为类似;在病理机制方面,心气虚、脾气虚、肺气虚及其他脏腑气虚均表现出不同程度或不同类型的线粒体功能障碍;在治疗方面,从气虚论治可促进心力衰竭、功能性消化不良、运动性疲劳等不同系统疾病过程中受损线粒体功能的恢复.由此认为,中医气虚与线粒体功能障碍关系密切.为进一步探寻气虚证的生物学基础,本文梳理总结对气虚证患者或动物模型体液或组织的代谢组学及蛋白质组学分析以及补气药的生物信息学分析的相关文献,归纳出气虚证的生物学基础可能是线粒体相关物质和/或能量代谢产物/蛋白及其相关调控通路失调,具体表现在线粒体膜蛋白酶系、线粒体呼吸链复合物及三羧酸循环中间产物的表达异常.从线粒体功能障碍角度探讨中医气虚的生物学基础,将中医辨证与现代医学辨病有机结合,量化中医证型,可以为中医证候的科学化、标准化、规范化提供有力依据.

基于朱震亨"六郁"理论,提出肺结节的形成与气郁、血郁、痰郁、火郁、湿郁、食郁六郁密切相关.认为六郁皆可导致肺结节,其中以气郁为主导,气郁久则化为火郁,导致脾失运化可成痰郁、湿郁、食郁,气不行血则成血郁,六郁相因为病且病机之间相互关联,共同促进肺结节的发生发展.治疗以畅通气机为主,以治疗六郁的经典名方越鞠丸为基本方,并根据六郁偏颇在越鞠丸基础上灵活配伍疏肝理气、清热散结、化痰散结、健脾化湿、消食化积、活血化瘀之品.

BACKGROUND:5-Methylcytosine (m5C) is an mRNA modifier that is associated with the occurrence and development of viral infection, pulmonary fibrosis, lung cancer, and other diseases. However, the role of m5C regulators in chronic obstructive pulmonary disease (COPD) remains unknown. METHODS:In this study, by analysing the GSE42057 dataset, the differential expression of m5c regulators in the COPD group and control group was obtained, and a correlation analysis was conducted. The random forest model and support vector machine model were used to predict the occurrence of COPD. A nomogram model was also constructed to predict the prevalence of COPD. The COPD patients were divided into subtypes by consistent cluster analysis based on m5c methylation regulators. Immune cell infiltration was performed on the m5c methylation subtypes. Differentially expressed genes (DEGs) between m5c methylation subtypes were screened, and the DEGs were analysed by Gene Ontology (GO) Kyoto Encyclopedia of Genes and Genomes (KEGG). Finally, we verified the expression of several m5C regulators and related pathways using a COPD cell model. RESULTS:Seven m5c methylation regulators were differentially expressed. The random forest model based on the above genes was the most accurate for predicting the occurrence of COPD. A nomogram model based on the above genes could also accurately predict the prevalence of COPD, and the implementation of these models could benefit COPD patients. The consistent cluster analysis divided the COPD patients into two subtypes (Cluster A and Cluster B). The main component analysis algorithm determined the m5c methylation subtypes and found that patients in Cluster A had a higher m5c score than those in Cluster B. GO analysis of the DEGs between the m5c methylation COPD patient subtypes revealed that DEGS were mainly enriched in leukocyte-mediated immunity and regulation of T-cell activation. KEGG analysis revealed that DEGS were mainly enriched in Th1 and Th2 cell differentiation, neutrophil extracellular trap formation, and the NF-κB signalling pathway. Immunocyte correlation analysis revealed that Cluster B was associated with neutrophil- and macrophage-mediated immunity, while Cluster A was associated with CD4 + T-cell- and CD8 + T-cell-mediated immunity. Cell experiments have also verified some of the above research results. CONCLUSION:The diagnosis and subtype classification of COPD patients based on m5c regulators may provide a new strategy for the diagnosis and treatment of COPD.

BACKGROUND:Rationale: No other treatment besides lung transplant is effective for idiopathic pulmonary fibrosis (IPF). Patients with IPF have poor prognosis, which may eventually lead to death. Patient concerns: Two female patients were diagnosed with IPF. In our recent follow-up, both these patients maintained a good quality of life.CASE SUMMARY:Diagnosis: Both patients had dry cough and progressive dyspnea. Interventions: The first patient was treated with prednisone, and the second patient was treated with prednisone and tripterygium glycosides. However, the symptoms did not improve and fibrosis was not controlled. Thus, the Feibi recipe was used. Outcomes: No deterioration was observed after the treatment, and the dry cough and its effect were ameliorated. Furthermore, they are still alive and the quality of their lives has improved.CONCLUSION:These two cases suggest that the Feibi recipe and other traditional Chinese medicine therapies could be beneficial for IPF treatment.

目的 利用数据挖掘方法探究周平安教授治疗肺纤维化的组方用药规律和经验方.方法 筛选整理周平安教授治疗肺纤维化医案,分别利用Clementine 12.0 和SPSS 21.0 软件对高频药物进行性味归经分析、关联规则及聚类分析.结果 (1)药物及性味归经分析总结出清热药、补虚药、止咳化痰平喘药位居前三,性温平、味甘苦辛、入肺经药物使用频次较高;(2)关联规则提取出常用药对及药物组合为生黄芪、金银花、穿山龙、石韦、当归中两药或多种药的组合;(3)聚类分析得出四个常用药物组合,其中之一便是周教授经验方"肺痹汤"的基本药物组成.结论 周平安教授临床治疗肺纤维化用药平和,所用核心药物组合恰为经验方肺痹汤的组成,与前期理论相吻合.

Number 2 Feibi Recipe (N2FBR) is a traditional Chinese medicine formula for treating idiopathic pulmonary fibrosis. N2FBR inhibits H2O2-mediated oxidative stress damage in alveolar epithelial cells by increasing autophagy, as we previously demonstrated. However, it is unknown if similar mechanisms occur in vivo. We established a pulmonary fibrosis model by instilling bleomycin (BLM) from the airway to examine the effects of N2FBR on pulmonary fibrosis and investigate its probable mechanism in this work. We discovered that N2FBR treatment effectively alleviated interstitial fibrosis as well as collagen deposition, primarily in upregulating SOD, GSH-Px, T-AOC and downregulating MDA content. N2FBR also increased the expression of LC3B, Beclin-1, LAMP1, TFEB and downregulated the expression of p62, legumain. N2FBR treatment boosted the production of autophagosomes, according to the results of the TEM observation. Furthermore, we explored that N2FBR exerted its anti-oxidative stress and pro-autophagy effects via GSK-3β/mTOR signalling pathway. Therefore, these results provide further evidence for the protective effect of N2FBR in pulmonary fibrosis. Our findings could have ramifications for the development of antifibrosis therapies.

Background Stress urinary incontinence (SUI) in women is a female urogenital disease in which urine leaks out involuntarily due to increased abdominal pressure during coughing or sneezing or physical activity. As one of complementary and alternative medicine, moxibustion therapy has been widely used in the clinical treatment of female SUI, but its efficacy and safety have not been systematically evaluated. Therefore, this study aimed to systematically evaluate the efficacy and safety of moxibustion in the treatment of female SUI. Methods The following electronic databases were searched from database establishment to December 2021: PubMed, Web of Science, Cochrane Library, Embase, China National Knowledge Infrastructure (CNKI), VIP Database, Wanfang Database, and China Biology Medicine Disc (CBM). All randomized controlled trials (RCTs) with moxibustion as an intervention for the treatment of female SUI were included in this study. The primary outcome of included studies was the change from baseline in urine leakage measured by the 1-hour pad test. Secondary outcomes included clinical efficacy, the International Consultation on Incontinence Questionnaire Short-Form (ICIQ-SF) score, mean 24-hour frequency of incontinence episodes, and adverse events. The meta-analysis was performed by STATA software (version 15.0) in this study. Results A total of 13 RCTs were included in this meta-analysis, involving 822 female SUI patients, of which 413 in the experimental group received moxibustion, and 409 in the control group received other conservative treatments (pelvic floor muscle training or acupuncture or Chinese medicine). The results of the meta-analysis showed that compared with receiving pelvic floor muscle training (PFMT) or acupuncture or Chinese medicine treatment, moxibustion intervention for female SUI reduced urine leakage in the one-hour pad test [SMD=-0.86, 95%CI (-1.03,-0.58)], significantly improved clinical efficacy [OR = 3.42, 95%CI (2.32,5.04)], decreased the ICIQ-SF score [SMD=-0.80, 95%CI (-1.03,-0.57)], and reduced average 24-hour incontinence episode frequency [SMD=-0.78, 95%CI (-1.05,-0.54)]. At the same time, no adverse events occurred during the moxibustion intervention. Conclusions Based on this meta-analysis, moxibustion, as one of the complementary and alternative medicine therapies, can be effective and safe in the treatment of female SUI. Moxibustion intervention can reduce urine leakage in the one-hour pad test, improve clinical efficacy, reduce the ICIQ-SF score, and reduce the average 24-hour frequency of urinary incontinence episodes. However, due to the low quality of evidence in this study, higher-quality RCTs are needed for further demonstration. Registration of systematic review: This systematic review and meta-analysis has been registered in the INPLASY International Registry of Prospective Systematic Reviews under the registration number INPLASY2021120052.

Objective:To initially explore traditional Chinese medicine patterns in a bleomycin-induced pulmonary fibrosis mouse model.Methods:Thirty-six C57 BL/6 mice were divided by the random number table method（with 12 rats per group） into three groups:a blank group,a model group,and a number 2 Feibi recipe（FBR-2） group.The pulmonary fibrosis mouse model was established by intratracheal instillation of bleomycin.The FBR-2 group was treated with FBR-2 for 4 weeks.Symptoms in the mice such as mental behavior,food/water intake,body weight,body temperature,respiratory rate,and tongue image were observed.The samples were collected on the 14 th day and 28 th day after modeling,and lung tissues were visually assessed and microscopically evaluated by staining with hematoxylin-eosin and Masson.The expression levels of hydroxyproline,interleukin（IL）-33,IL-37,tissue plasminogen activator,and plasminogen activator inhibitor-1 were determined by enzyme-linked immunosorbent assay.Results:Mice in the model group were poor in spirit,less active,slow in response,showed reduced food/water intake,body temperature,and body weight,increased respiratory rate,and their tongue color had changed from light red to dark red.However,treatment with FBR-2 significantly improved these symptoms.Extensive inflammatory cell infiltration and collagen fiber deposition were observed in the lung tissues of the model group.Compared with the blank group,the levels of hydroxyproline,IL-33,and plasminogen activator inhibitor-1 in the model group significantly increased（all P ＜.05）,whereas that of tissue plasminogen activator significantly decreased on the 14 th day and 28 th day（P=.036 and P=.005,respectively）.Moreover,FBR-2 improved lung inflammation and fibrinolysis imbalance and reduced collagen fiber deposition.Conclusion:To some extent,our bleomycin-induced pulmonary fibrosis mouse model exhibited traditional Chinese medicine patterns of qi deficiency,blood stasis,and heat retention.

更年期综合征是妇女在绝经前后因卵巢功能衰退而引起的一系列躯体、精神心理等方面的症状.周平安教授因其突出的情志失调见症及发病特有的年龄特点,主张以"更年期脏躁"为名认识该病.本病以肾精亏虚、阴阳失衡、五脏不安为发病病机,阴阳不平,气血不和,病及周身,致使该病症状复杂多变.周平安教授治疗本病注重调整阴阳,以平为期,寓调平之法于补益之中,选方二仙汤合四物汤为主方,共致平和,安脏除躁,在临床上取得很好的疗效.

作为《金匮要略》五种水气病之一,黄汗病症状表现复杂多样,病机虚实兼见,并涉及多个脏腑.种种原因,导致其理论内涵尚未得到充分的阐发.系统性红斑狼疮是现代医学累及多系统的难治性疾病.其临床表现,发展转归与黄汗病具有极高的契合度,将系统性红斑狼疮归入黄汗病范畴具有合理性.素有肝肾亏虚、阳明热盛,又因调摄不慎,外感寒湿之邪,是系统性红斑狼疮的关键病机.基于《伤寒杂病论》黄汗病以及其余相关理论,针对系统性红斑狼疮肾脏、皮肤黏膜、骨骼肌肉、消化、呼吸、心脏、神经等系统受累所表现出的各种临床表现,以补益肝肾、清解阳明、散寒除湿为原则,分别提出了相应的经方治疗,为系统性红斑狼疮的现代中医诊治提供了思路.

Background Chinese herbs for supplementing qi and activating blood circulation (CH) combined with N-acetylcysteine (NAC) is widely used for idiopathic pulmonary fibrosis (IPF) in China, but there is a lack of literature to evaluate its efficacy and clinical value. Purpose This study compared CH + NAC with other treatments by network meta-analysis to clarify its clinical value. Methods Cochrane Library, PubMed, Embase, Web of Science, China National Knowledge Infrastructure, WanFang Data, VIP Database, and China Biology Medicine were searched. Outcomes included lung function (DLCO (%), VC (%), FVC (%), FVC (L)), 6-min walking distance (6MWD), score of St George’s respiratory questionnaire (SGRQ), blood gas analysis (PaO2, PaCO2). The data were analyzed by Review Manager 5.4, Stata 12.0 and ADDIS 1.16.5. Results 23 studies including 1390 patients (702 in intervention group and 688 in control group) were collected to compare 8 outcome indicators among different treatments involving CH, CH+NAC, CH+PFD, NAC, PFD and PFD+NAC on IPF. Network meta-analysis showed that CH was better than NAC in terms of DLCO (%) (MD = 5.14, 95%CI: 1.01 to 8.68) and 6MWD (MD = 49.17, 95%CI: 25.97 to 71.36) as well as PFD + NAC was better than NAC in terms of FVC (L) (MD = -0.56, 95%CI: -0.83 to -0.31). In rankings results, CH + NAC is the best in terms of FVC (%), SGRQ, PaO2 and PaCO2; CH is the best in terms of DLCO (%), VC (%) and 6MWD; CH + PFD is the best in terms of FVC (L). Conclusion CH related treatments may have advantages in the treatment of IPF and CH + NAC may have clinical application value. However, limited by the quality and quantity of researches included, more rational and scientific randomized controlled trials containing large sample sizes need to be conducted to further verify our conclusions.