Luteolin attenuates type 2 inflammation in asthmatic mice induced by OVA by regulating IL-33/ST2- GSK3β-M2 macrophage polarization.

Allergic asthma is a prevalent non-infectious inflammatory disease characterized by type 2 inflammation. Although multiple treatment options are available, their efficacy is often limited due to the heterogeneous nature of asthma. Luteolin (LUT), a naturally occurring flavonoid, has demonstrated therapeutic potential in various inflammatory conditions.

Baseline type 2 biomarker levels and clinical remission predictors in children with asthma.

Background: Few studies have investigated the relationship between baseline type 2 biomarker levels and clinical features in pediatric asthma, particularly in different asthma stages, which may inform prognosis and remission.

Objective: To explore the association between baseline Th2 biomarker levels and clinical manifestations in pediatric asthma, identifying predictors of clinical remission.

Methods: The study included 172 children with a mean age of 6.

Astragaloside III inhibits MAPK-mediated M2 tumor-associated macrophages to suppress the progression of lung Cancer cells via Akt/mTOR signaling pathway.

Tumor-associated macrophages (TAMs) play a key role in facilitating a range of cancerous processes by modulating the tumor microenvironment thus being a target for cancer treatment. Astragaloside III (AS-III), a compound derived from Astragalus triterpenoid saponins, has demonstrated immunomodulatory and anticancer properties, but the underlying mechanism remains unclear. Here, we demonstrated that AS-III suppressed metastasis, angiogenesis and induced apoptosis of lung cancer in vitro and in vivo by inhibiting macrophage M2 polarization and inducing M1 phenotype transformation.

Elevated MRPS23 expression facilitates aggressive phenotypes in breast cancer cells.

Mitochondrial ribosomal protein S23 (MRPS23), encoded by a nuclear gene, is a well-known driver of proliferation in cancer. It participates in mitochondrial protein translation, and its expression association has been explored in many types of cancer. However, MRPS23 expression associations are rarely reported in breast cancer (BC).

FXR1 associates with and degrades PDZK1IP1 and ATOH8 mRNAs and promotes esophageal cancer progression.

Background: The growing body of evidence suggests that RNA-binding proteins (RBPs) have an important function in cancer biology. This research characterizes the expression status of fragile X-related protein 1 (FXR1) in esophageal cancer (ESCA) cell lines and understands its mechanistic importance in ESCA tumor biology.

Methods: The role of FXR1, PDZK1IP1, and ATOH8 in the malignant biological behaviors of ESCA cells was investigated using in-vitro and in-vivo experiments.

A clinically applicable model more suitable for predicting malignancy or benignity of pulmonary ground glass nodules in women patients.

Background: In recent years, clinicians often encounter patients with multiple pulmonary nodules in their clinical practices. As most of these ground glass nodules (GGNs) are small in volume and show no spicule sign, it is difficult to use Mayo Clinic Model to make early diagnosis of lung cancer accurately, especially in large numbers of nonsmoking women who have no tumor history. Other clinical models are disadvantaged by a relatively high false-positive or false-negative rate.

Music Therapy and Music Intervention for NSCLC Patients Undergoing PET with Fear of Cancer Recurrence.

Cancer and psychiatric symptoms are associated. Fear of cancer recurrence (FCR) is the most common psychological problem for cancer survivors. Pharmacological interventions can help, but also have major drawbacks.

Psoralen attenuates cigarette smoke extract-induced inflammation by modulating CD8 T lymphocyte recruitment and chemokines via the JAK2/STAT1 signaling pathway.

Chronic obstructive pulmonary disease (COPD) is a respiratory inflammatory disease. Psoralen (PSO) is the main pharmacological component identified from Bu-Shen-Fang-Chuan formula which has been traditionally used in treatment of COPD, yet its efficacy in COPD inflammation were unreported. In this study, we aimed to elucidate the anti-inflammatory potential of PSO in COPD and unravel the underlying mechanisms, focusing on T lymphocyte recruitment and the modulation of chemokines, namely monokine induced by interferon-gamma (CXCL9), interferon inducible protein 10 (CXCL10), and interferon inducible T-Cell alpha chemoattractant (CXCL11).

Icariin attenuates asthmatic airway inflammation via modulating alveolar macrophage activation based on network pharmacology and in vivo experiments.

Background: Icariin (ICA) inhibits inflammatory response in various diseases, but the mechanism underlying ICA treating airway inflammation in asthma needs further understood. We aimed to predict and validate the potential targets of ICA against asthma-associated airway inflammation using network pharmacology and experiments.

Methods: The ovalbumin-induced asthma-associated airway inflammation mice model was established.

Icariside II in NSCLC and COVID-19: Network pharmacology and molecular docking study.

Background: Patients with non-small cell lung cancer (NSCLC) are susceptible to coronavirus disease-2019 (COVID-19), but current treatments are limited. Icariside II (IS), a flavonoid compound derived from the plant epimedin, showed anti-cancer,anti-inflammation and immunoregulation effects. The present study aimed to evaluate the possible effect and underlying mechanisms of IS on NSCLC patients with COVID-19 (NSCLC/COVID-19).

Regulatory roles of N6-methyladenosine (mA) methylation in RNA processing and non-communicable diseases.

Post-transcriptional RNA modification is an emerging epigenetic control mechanism in cells that is important in many different cellular and organismal processes. N6-methyladenosine (mA) is one of the most prevalent, prolific, and ubiquitous internal transcriptional alterations in eukaryotic mRNAs, making it an important topic in the field of Epigenetics. mA methylation acts as a dynamical regulatory process that regulates the activity of genes and participates in multiple physiological processes, by supporting multiple aspects of essential mRNA metabolic processes, including pre-mRNA splicing, nuclear export, translation, miRNA synthesis, and stability.

Icariside II modulates pulmonary fibrosis via PI3K/Akt/β-catenin pathway inhibition of M2 macrophage program.

Background: Idiopathic pulmonary fibrosis (IPF) is a debilitating interstitial lung disorder characterized by its limited therapeutic interventions. Macrophages, particularly the alternatively activated macrophages (M2 subtype), have been acknowledged for their substantial involvement in the development of pulmonary fibrosis. Hence, targeting macrophages emerges as a plausible therapeutic avenue for IPF.

Astragaloside IV targeting autophagy of T cells improves inflammation of asthma.

Astragaloside IV (AST) has been confirmed to have antiasthmatic effects. However, the underline mechanism is unclear. The study aimed to explore the treatment mechanism of AST based on autophagy of memory T cells.

Proteomic analysis reveals the molecular mechanism of Astragaloside in the treatment of non-small cell lung cancer by inducing apoptosis.

Background: Astragaloside III (AS III), a saponin-like metabolite derived from the traditional Chinese medicine Astragali Radix, has been shown to be effective in the treatment of cancer and heart failure, and a variety of digestive disorders. However, its molecular mechanism in the treatment of non-small cell lung cancer (NSCLC) is unknown.

Methods: Human lung cancer A549 cells and NCI-H460 cells and a normal human lung epithelial cell BEAS-2B were treated with different concentrations of AS III.

Modified Bushen Yiqi Formula mitigates pulmonary inflammation and airway remodeling by inhibiting neutrophils chemotaxis and IL17 signaling pathway in rats with COPD.

Ethnopharmacological Relevance: Chronic obstructive pulmonary disease (COPD) is a major global health concern characterized by pulmonary inflammation and airway remodeling. Traditional Chinese medicine, such as Modified Jiawei Bushen Yiqi Formula (MBYF), has been used as a complementary therapy for COPD in China.

Aim Of The Study: To investigate the therapeutic potential of MBYF in a rat model of COPD induced by cigarette smoke (CS) exposure and explore the underlying mechanism.

Identification of immune-related gene signatures for chronic obstructive pulmonary disease with metabolic syndrome: evidence from integrated bulk and single-cell RNA sequencing data.

Chronic obstructive pulmonary disease (COPD) is closely related to innate and adaptive inflammatory immune responses. It is increasingly becoming evident that metabolic syndrome (MetS) affects a significant portion of COPD patients. Through this investigation, we identify shared immune-related candidate biological markers.

Network pharmacology prediction and molecular docking analysis reveal the mechanism of modified Bushen Yiqi formulas on chronic obstructive pulmonary disease.

Background: The present study aimed to explore the mechanism of the modified Bushen Yiqi formula (MBYF) in the treatment of chronic obstructive pulmonary disease (COPD) based on network pharmacology and molecular docking.

Methods: First, the active ingredients and corresponding targets in MBYF were mined through the Traditional Chinese Medicine Systems Pharmacology database. Subsequently, Online Mendelian Inheritance in Man, DrugBank, and GeneCard were used to screen COPD-related targets.

Modified Bushen Yiqi formula enhances antitumor immunity by reducing the chemotactic recruitment of M2-TAMs and PMN-MDSCs in Lewis lung cancer-bearing mice.

Ethnopharmacological Relevance: Modified Bushen Yiqi formula (MBYF) has shown efficacy as an herbal combination therapy with anti-PD-1 for lung cancer patients. However, the underlying mechanisms of its antitumor effects in lung cancer remain unclear.

Aim Of The Study: This study aims to observe the antitumor effect of MBYF and explore its synergistic mechanism in combination with anti-PD-1 based on the tumor immune microenvironment.

Exploring the Mechanisms of Modified Bu-Shen-Yi-Qi Decoction for COPD-Related Osteoporosis Therapy via Transcriptomics and Network Pharmacology Approach.

Purpose: To investigate the effectiveness of modified Bu-Shen-Yi-Qi decoction (MBSYQ) in the treatment of osteoporosis associated with chronic obstructive pulmonary disease (COPD) and its underlying mechanisms of action.

Methods: Disease targets, active ingredients and targets were predicted by TTD, CTD, DisGeNET, HERB (BenCaoZuJian as its Chinese name), and multiple-TCM databases; In addition, the screened targets were performed via the online platforms DAVID 6.8 and Metascape for GO and KEGG pathway enrichment analysis; The relationship between the MBSYQ and core targets were verified by molecular docking technique.

TMT-based quantitative proteomics revealed protective efficacy of Icariside II against airway inflammation and remodeling via inhibiting LAMP2, CTSD and CTSS expression in OVA-induced chronic asthma mice.

Background: Asthma is a chronic inflammatory disorder in airways with typical pathologic features of airflow limitation, airway inflammation and remodeling. Icariside II (IS), derived from herbal medicine Herba Epimedii, exerts an anti-inflammatory property. However, underlying mechanisms with specifically targeted molecular expression by IS in asthma have not been fully understood, and whether IS could inhibit remodeling and EMT still remains unclear.

Icariside Ⅱ attenuates bleomycin-induced pulmonary fibrosis by modulating macrophage polarization.

Ethnopharmacological Relevance: Numerous studies have provided evidence supporting the significant roles of icariin, in the prevention of multiple chronic diseases like diabetes, liver fibrosis, cardiac fibrosis, renal fibrosis, and pulmonary fibrosis. In particular, Icariside II (ISE II), a prominent flavonoid glycoside derived from Epimedium brevicornum Maxim, the principal metabolite of icariin, has demonstrated noteworthy anti-inflammatory and anti-oxidant properties, along with its ability to protect against lung remodeling. However, the research exploring ISE Ⅱ's application in treating pulmonary fibrosis remains limited.

Network pharmacology and experiments in vivo and in vitro reveal that the Jia-Wei-Bu-Shen-Yi-Qi formula (JWBSYQF) and its active ingredient baicalein ameliorate BLM-induced lung fibrosis in mice via PI3K/Akt signaling pathway.

Ethnopharmacological Relevance: Jia-Wei-Bu-Shen-Yi-Qi formula (JWBSYQF), a classical traditional Chinese herbal formula consisting of five herbs, is used clinically in China to treat inflammatory lung diseases, including asthma, chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). Its mechanism for treating asthma and COPD has been reported, however, how it works against IPF remains unclear.

Research Purpose: Our study aims to observe the therapeutic effect of JWBSYQF on pulmonary fibrosis and further identify the potential active ingredients and molecular pathways.

Albumin-based formononetin nanomedicines for lung injury and fibrosis therapy via blocking macrophage pyroptosis.

Pulmonary fibrosis that occurs following lung injury is a progressive and fatal disease since continual damage to lung tissue triggers the dysregulated inflammation response and accompanying abnormal healing process. Pyroptosis of alveolar macrophages has been found to play an essential role in the deterioration of lung injury and fibrosis. However, the lack of inhibitors against this inflammatory cell death in macrophages and the dense stroma pose major barriers to lung injury and fibrosis treatment.