Adipose tissue serves as a key endocrine organ for dynamic lipid metabolism in the human body, in which adipocytes store and consume energy, secrete adipokines, and participate in diverse biological processes. Adipose-derived stem cells exhibit a robust capacity for adipogenic differentiation. The hypothalamus, a critical brain region within the central nervous system, regulates systemic lipid metabolism by modulating energy homeostasis, feeding behavior, immune responses, and gut microbiota equilibrium. Lipid droplets function as essential organelles within adipocytes. Collectively, adipose tissue and the hypothalamus maintain systemic lipid metabolic homeostasis. Acupuncture exerts beneficial regulatory effects on lipid metabolism by modulating the central regulatory functions of the hypothalamus, thereby influencing the neuro-endocrine-immune axis. In the process of acupuncture-mediated regulation of lipid metabolism, the autonomic nervous system serves as both an afferent and an efferent pathway, playing a pivotal role in signal transduction. This review synthesizes the current research on how acupuncture transmits stimulation signals to the central nervous system, modulates sympathetic and parasympathetic signaling, and subsequently affects the structure and function of adipose tissue to promote lipid metabolic homeostasis. However, fundamental and clinical investigations into the “neuro-endocrine-adipose tissue” axis underlying acupuncture-mediated lipid metabolism regulation require further elucidation. This article aims to systematically review the interconnected pathways through which acupuncture regulates lipid metabolism via the neuro-endocrine-adipose axis. It provides an in-depth exploration of how acupuncture stimulation, via peripheral and central neural pathways, modulates the hypothalamic–pituitary–target gland axis and the autonomic nervous system, ultimately influencing the function and interaction of white and brown adipose tissues, as well as the process of “white adipose browning.” By integrating recent research advances, this review seeks to clarify the scientific basis of acupuncture in treating lipid metabolism disorders and to propose theoretical frameworks and directions for future mechanistic studies.

BACKGROUND:Sepsis-induced cardiomyopathy (SICM) is a life-threatening complication with limited therapeutic options. Macrophage-driven inflammation and pyroptosis are central to SICM pathogenesis, but the role of myeloid CD38, the primary NAD+ hydrolase, in SIC remains unexplored. METHODS:Myeloid-specific CD38 knockout (CD38ᴹᴷᴼ) mice and CD38ᶠˡ°ˣ controls were subjected to cecal ligation and puncture (CLP) to induce sepsis. Cardiac function, myocardial inflammation, pyroptosis, and oxidative stress were assessed. Bone marrow-derived macrophages (BMDMs) and conditioned medium studies were used to investigate mechanisms and paracrine effects on cardiomyocytes. RESULTS:CD38 was upregulated in cardiac macrophages of septic mice. Myeloid CD38 deletion improved cardiac function, reduced injury markers, and attenuated myocardial inflammation, pyroptosis, and oxidative stress. CD38ᴹᴷᴼ mice exhibited reduced M1 and enhanced M2 macrophage polarization. CD38-deficient BMDMs showed suppressed NF-κB activation, NLRP3 inflammasome assembly, and glycolysis-related gene expression (HIF1α, SLC2A1), with concomitant NAD+ accumulation and SIRT1 upregulation. SIRT1 inhibition reversed these protective effects. Conditioned medium from CD38ᴹᴷᴼ macrophages protected cardiomyocytes from oxidative injury. Proteomic analysis revealed enrichment of mitochondrial proteins in the CD38-deficient macrophage secretome. CONCLUSIONS:Myeloid CD38 deficiency protects against SIC by activating the SIRT1/NF-κB/NLRP3 axis, promoting M2 polarization, suppressing pyroptosis, and remodeling the macrophage secretome. Targeting myeloid CD38 represents a promising therapeutic strategy for SICM.

Ethnopharmacological relevanceBacterial pneumonia is a major disease worldwide, and its treatment faces the dual challenges of antimicrobial resistance and antibiotic-related side effects. The herbal formula Guben Qingfei Decoction (GBQF) had shown anti-inflammatory activity in acute lung injury models, but its material basis and mechanism in bacterial pneumonia are still unknow.Aim of the studyThe objective of this study was to investigate the mechanism of action of GBQF in ameliorating bacterial pneumonia and to determine its effective components.Materials and methodsA murine pneumonia model was created by intratracheal instillation of E. coli. The therapeutic effects of GBQF were evaluated by lung histopathology and measurement of inflammatory cytokine levels in BALF. Prototype components in GBQF-containing serum were identified by UHPLC-MS/MS, followed by network pharmacology prediction via KEGG pathway and Gene Ontology enrichment analysis. Integrated serum untargeted metabolomics and lung transcriptomics were performed to systematically reveal the regulatory network. Protein expression changes were verified by immunohistochemistry and Western blot. Inflammatory cytokine secretion and key protein expression were assessed using an in vitro model of mouse macrophages challenged with LPS.ResultsGBQF treatment significantly ameliorated lung histopathological injury, reduced pulmonary bacterial load, and suppressed BALF levels of TNF-α, IL-6, and IL-1β. Nine prototype components were identified in GBQF-containing serum. Integrated serum pharmacochemistry, network pharmacology, transcriptomics and metabolomics indicated that the anti-inflammatory action of GBQF was largely exerted via PPAR signaling pathway and arachidonic acid metabolism. At the protein level, GBQF upregulated the expression of PPARγ, PPARα and RXRα while suppressing COX-2 expression in lung tissue. In vitro, GBQF-containing serum not only inhibited LPS-induced release of IL-6, TNF-α, IL-1β and PGE2 from macrophages, but also recapitulated the same molecular regulation pattern (upregulation of PPARγ, PPARα, RXRα and downregulation of COX-2). Based on molecular docking, three prototype compounds of GBQF (puerarin, pectolinarigenin, and wogonoside) with the highest binding affinity to COX-2 were selected. In LPS-stimulated macrophages, each compound suppressed TNF-α, IL-1β, IL-6, and PGE2 production.ConclusionsThis novel strategy first identified the effective components of GBQF, thereby facilitating elucidation of its therapeutic mechanism against bacterial pneumonia and serving as a reference for discovering active components and quality markers for TCM formula quality control.

Objectives: To investigate the underlying mechanism of Xiaoyou decoction (XYD) in inducing apoptosis and modulating the inflammatory response in human immortalised cervical epithelial H8 cells through the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/Nf-kappaB (NF-kappa B) signalling pathway. Methods: H8 cells in logarithmic growth phase were treated with blank medium, recombinant human interferon alpha-2b (13 000 IU/mL), oxymatrine (4.80 mg/mL), and XYD (2.80 mg/mL) for 48 hours. Subsequently, cell counting kit-8 assay, flow cytometry apoptosis assay, acridine orange hydrochloride and Hoechst double staining, western blot, and Quantitative Real-time-PCR were performed to assess apoptosis, inflammation, and key pathway-related indices in each group. Results: In vitro experiments revealed that all treatments, including XYD and the control groups, exerted some degree of growth inhibition on H8 cells. However, XYD displayed the most significant inhibitory effect. Western blot and Quantitative Real-time-PCR analyses confirmed that XYD promoted apoptosis in H8 cells by suppressing the activation of the PI3K/AKT signalling pathway. Furthermore, it modulated the levels of inflammatory and immune-related factors in H8 cells by inhibiting the activation of the NF-kappa B signalling pathway. Conclusions: This study validates the molecular mechanism of XYD in promoting apoptosis and suppressing the inflammatory response in H8 cells by inhibiting the activation of the PI3K/AKT/NF-kappa B signalling pathway.

Ethnopharmacological relevance Pulmonary hypertension (PH) is a serious and progressive disease, posing a significant challenge to patient survival and quality of life. However, current treatments have limited effectiveness. Tianlong Kechuanling (TL) is a traditional Chinese medicine (TCM) compound formulation commonly used in clinical practice for the treatment of pulmonary heart disease, but its underlying mechanism is unknown. Aim of the study This study aimed to validate the mitigating effect of TL on PH and to further investigate its mechanism. Materials and methods A rat model of PH was induced by SU5416 combined with hypoxia (SuHx). The effects of TL on PH were evaluated through right ventricular systolic pressure (RVSP), Right ventricular hypertrophy index (RVHI) and histopathological analysis. The serum levels of HIF-1α, VEGFA in rats were detected by ELISA; VEGFR2, Vimentin and CD31 were detected by immunohistochemistry to explore the mechanism of action of TL. Human pulmonary artery endothelial cells (HPAECs) were induced by hypoxia, and the effects of TL were confirmed by RT-PCR and Western Blotting. Liquid chromatography-mass spectrometry (LC-MS) analysis was used to identify the chemical composition of TL. Results TL ameliorated PH through modulation of the HIF-1α/VEGFA pathway and endothelial-to-mesenchymal transition (End-MT). The study also identified the key chemical components responsible for these effects. Conclusions The study demonstrates that TL can improve PH by inhibiting End-MT, supporting the further development of TL as an effective therapeutic option for PH.

ETHNOPHARMACOLOGICAL RELEVANCE:Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal disease. Baihe Gujin decoction (BHGJ), a traditional Chinese medicine consisting of ten medicine food homology herbs, has shown therapeutic effects in various lung diseases; however, its efficacy in ameliorating IPF and the underlying mechanisms remain unclear. AIM OF THE STUDY:This study aimed to evaluate the effects of BHGJ on IPF and investigate its potential mechanisms. MATERIALS AND METHODS:We established a bleomycin (BLM)-induced IPF model and performed proteomic analysis. The therapeutic effects of BHGJ on IPF were assessed by measuring lung index, hydroxyproline (HYP) content, lung function parameters, and histopathological changes. Mechanistic insights were further explored using Western blot and RT-qPCR analyses. RESULTS:Our results demonstrated that BHGJ significantly alleviated BLM-induced IPF, improved lung function, reduced histopathological damage, and decreased collagen deposition. BHGF reduced apoptosis and inhibited EMT in TGF-β-induced A549 cells. Proteomic analysis revealed that its effects were associated with the modulation of the proline metabolism pathway. CONCLUSIONS:BHGJ effectively attenuated IPF progression via regulating proline metabolism, providing a potential therapeutic strategy for pulmonary fibrosis.

ETHNOPHARMACOLOGICAL RELEVANCE:Klebsiella pneumoniae (Kp) is a significant pathogen responsible for various clinical bacterial infections, including pneumonia, sepsis, and even death. However, effective treatment options remain limited due to the rising prevalence of antimicrobial resistance. Traditional Chinese medicine (TCM) has shown potential in the treatment of bacterial pneumonia. Qingfei Litan decoction (QFLT) has been reported to alleviate symptoms in patients with bacterial pneumonia, though its precise mechanisms in regulating pulmonary inflammation remain unclear. AIM OF THE STUDY:This study aimed to investigate the therapeutic potential of QFLT in Kp-induced pneumonia and to elucidate its underlying molecular mechanisms. MATERIAL AND METHODS:In vivo, a murine pneumonia model was established through intratracheal instillation of Kp, and QFLT was administered by oral gavage. miR-146a-5p expression was downregulated by tail vein injection of an antagomir. The therapeutic effects of QFLT on pulmonary pathology, inflammatory factors, and miR-146a-5p expression were evaluated using qRT-PCR, flow cytometry, and other methods. Bioinformatics tools were employed to predict miR-146a-5p targets and associated inflammatory pathways. In vitro, an alveolar macrophage inflammation model was established by stimulating MH-S cells with heat-inactivated Klebsiella pneumoniae (iKp), followed by QFLT treatment. Inhibition of miR-146a-5p was achieved through transfection with specific inhibitors. The effects of QFLT on inflammatory responses, miR-146a-5p expression, and TLR4/MyD88/NF-κB signaling were assessed using qRT-PCR, Western blotting (WB) and other methods. RESULTS:Kp infection significantly exacerbated pulmonary inflammation and downregulated miR-146a-5p expression in both lung tissues and MH-S cells. QFLT treatment alleviated inflammatory responses and upregulated miR-146a-5p expression. Bioinformatics analysis demonstrated that miR-146a-5p targeted TRAF6, a key mediator of the TLR4/MyD88/NF-κB pathway. Western blot analysis further confirmed that QFLT reduced Kp-induced upregulation of the TLR4/MyD88/NF-κB pathway in MH-S cells. Moreover, inhibition of miR-146a-5p exacerbated inflammatory responses in both lung tissues and MH-S cells, whereas QFLT treatment effectively attenuated these inflammatory effects. Furthermore, miR-146a-5p suppression resulted in elevated expression of proteins in the TLR4/MyD88/NF-κB signaling pathway in MH-S cells, while QFLT administration significantly reduced the expression levels of these signaling components. CONCLUSIONS:These findings demonstrated that QFLT ameliorated Kp-induced pneumonia by modulating the TLR4/MyD88/NF-κB axis via miR-146a-5p.

ETHNOPHARMACOLOGICAL RELEVANCE:COPD-PH is a common and severe complication of COPD, posing significant challenges to patient survival and quality of life due to its poor prognosis. However, current treatment options remain clinically unsatisfactory. Tianlong kechuanling (TL), a traditional Chinese medicine compound hospital preparation, has been clinically employed for treating cor pulmonale, although its underlying mechanisms remain elusive. PURPOSE:This study aimed to investigate the therapeutic effects of TL on COPD-PH and elucidate its molecular mechanisms. MATERIALS AND METHODS:A murine COPD-PH model was established through cigarette smoke exposure, intratracheal lipopolysaccharide instillation, and chronic hypoxia. The therapeutic effects of TL were evaluated by measuring pulmonary function parameters, lung index, right ventricular systolic pressure (RVSP), right ventricular hypertrophy index (RVHI), total cell count in bronchoalveolar lavage fluid (BALF), levels of TNF-α, IL-1β, IL-6, and IL-18, along with histopathological analyses. Immunohistochemistry was performed to examine DNMT3A, GSDMD, Caspase1and NLRP3 expression for mechanistic studies. A pyroptosis model was established using TNF-α-stimulated human pulmonary arterial endothelial cells (HPAECs), with Scanning electron microscopy, qPCR, immunofluorescence, and Western blot analyses conducted to assess TL's effects. To further elucidate the therapeutic mechanism of TL, pharmacological inhibition of DNMT3A was systematically employed. RESULTS:TL administration significantly improved pulmonary function, reduced RVSP and RVHI in COPD-PH mice, attenuated pulmonary inflammation, reduced DNMT3A expression and ameliorated pyroptosis. In HPAECs, TL suppressed the expression of mitigated cellular pyroptosis, revealing a regulatory correlation between DNMT3A and GSDMD. CONCLUSION:TL attenuated COPD-PH progression via inhibiting endothelial pyroptosis by targeting the DNMT3A-GSDMD signaling pathway, offering potential therapeutic avenues for COPD-PH management.

ETHNOPHARMACOLOGICAL RELEVANCE:Pulmonary fibrosis is an irreversible lung disease with a high mortality rate. Zhebeimu (ZBM, Fritillaria thunbergii Miq.) is a Chinese medicine commonly used for the treatment of pulmonary fibrosis in China. AIM OF THE STUDY:In this study, the protective effect and mechanism of ZBM extract in the treatment of pulmonary fibrosis were investigated in vivo and in vitro. MATERIALS AND METHODS:The protective effect of ZBM extract was assessed using an in vivo model of bleomycin (BLM) tracheal drip and transforming growth factor-β(TGF-β1)-induced fibroblasts to simulate pulmonary fibrosis, and lung function, lung histopathological status and hydroxyproline were tested. Relevant pathways were detected using protein blotting, immunofluorescence and immunohistochemistry. RESULTS:ZBM extract effectively improved lung function, inflammatory changes and fibrotic deposition in the lungs, and reduced the expression of fibroblast markers in mice. In addition, ZBM extract significantly inhibited TGF-β1-induced hyperphosphorylation of FOXO3, and simultaneously improved the low expression level of FOXO3 prototype protein and significantly reduced the phosphorylation level of PI3K-p85 and AKT1, suggesting that ZBM extract improves lung fibrosis by inhibiting the over-activation of PI3K/AKT/FOXO signalling pathway. CONCLUSION:The PI3K/AKT/FOXO signalling pathway is critical for ZBM extract to improve pulmonary fibrosis.

Myocardial ischemia-reperfusion injury (MIRI) is a complex pathological process that results from the restoration of blood flow to ischemic myocardium, leading to a series of detrimental effects including oxidative stress and inflammation. Stachyose, a naturally occurring oligosaccharide found in traditional Chinese medicinal herbs, has been suggested to possess therapeutic properties against various pathological conditions. However, its impact on MIRI and the underlying mechanisms have not been fully elucidated. In this study, we aimed to investigate the therapeutic effects of stachyose on MIRI and to uncover the molecular mechanisms involved. Using both in vivo and in vitro models of MIRI, we evaluated the effects of stachyose on cardiac function and cell death pathways. Our results indicate that stachyose significantly improves cardiac function and reduces infarct size in MIRI mice. Mechanistically, stachyose modulates the ferroptotic pathway in cardiomyocytes by upregulating the expression of glutathione peroxidase 4 (GPX4) and reducing lipid peroxides and iron levels. Additionally, stachyose inhibits the pyroptotic pathway in macrophages by downregulating the expression of NLRP3, gasdermin D (GSMD-N), and cleaved-caspase-1, leading to decreased levels of proinflammatory cytokines interleukin (IL)-1 beta beta and IL-18. This study demonstrates that stachyose exerts a protective effect against MIRI by targeting both ferroptosis and pyroptosis pathways, suggesting its potential as a novel therapeutic agent for the treatment of MIRI. Further research is warranted to explore the detailed mechanisms and therapeutic potential of stachyose in clinical settings.

The study aimed to unravel the molecular basis of cervical precancerous lesions leveraging bioinformatic tools to pinpoint crucial genes and signaling cascades. A multi-faceted approach was undertaken, commencing with GEO database mining for differential gene expression between CSILs and healthy cervical tissues. STRING 11.0 facilitated protein-protein interaction (PPI) analysis, generating a network visualized in Cytoscape 3.7.2. Gene Ontology (GO) and KEGG pathway enrichment via DAVID illuminated biological functions and pathways associated with identified differentially expressed genes (DEGs). GSEA further refined key genes and enriched modules. Concurrently, qRT-PCR validation on cervical biopsy samples from eligible patients corroborated bioinformatic findings. The analysis pinpointed 371 common DEGs across datasets, leading to the discovery of 102 biological processes, 33 cellular components, 15 molecular functions, 29 significant pathways, and 3 pivotal genes. Clinical assessment linked lesion severity to age, vaginal microbiota characteristics, and ALK gene/PI3K/AKT/NF-κB pathway activity. qRT-PCR verified heightened ALK and PI3K/AKT/NF-κB signaling in high-grade lesions, underscoring their roles in CSIL pathogenesis. The importance of this research lies in its potential to inform the development of targeted therapies and personalized treatment strategies for cervical precancerous lesions. By identifying the molecular drivers of the disease, researchers can design interventions that precisely target these pathways, improving patient outcomes and reducing the burden of cervical cancer.

Xinglou Chengqi decoction (XLCQD) is a Chinese formula that offers benefits in ischemic stroke. However, the underlying mechanism of the effects of XLCQD-mediated anti-ischemic stroke effects remains obscure. This study investigates the ferroptosis mechanism of XLCQD against cerebral ischemia/reperfusion (I/R) injury using rat models of middle cerebral artery occlusion/reperfusion (MCAO/R). Ferroptosis differs from traditional cell death pathways and is linked to oxidative stress-induced lipid peroxidation and glutathione (GSH) depletion, which is essential to the development of ischemic stroke. In this study, it is shown that XLCQD improves brain infarction, neurological dysfunction, and histopathological changes caused by MCAO/R exposure, and improving I/R-induced oxidative damage through inhibition of ferroptosis via (Solute Carrier Family 7 Member 11) SLC7A11/ (glutathione peroxidase 4) GPX4 pathway. Interestingly, it is found that XLCQD-mediated protection in I/R is reversed by the silence of SLC7A11. XLCQD intervention significantly promotes GSH content and suppresses Reactive Oxygen Species(ROS), iron accumulation, as well as Malondialdehyde (MDA) generation, are markedly abrogated when SLC7A11 is knockdown by SLC7A11-shRNA transfection, indicating that SLC7A11 is the main target of XLCQD to further trigger intracellular events. In conclusion, XLCQD attenuates in vivo cerebral I/R injury by reducing ferroptosis via the SLC7A11/GPX4 pathway.

Ethnopharmacological relevance Acute lung injury (ALI) is a life-threatening and widespread disease, with exceptionally high morbidity and mortality rates. Unfortunately, effective drugs for ALI treatment are currently lacking. Guben Qingfei decoction (GBQF) is a Chinese herbal compound known for its efficacy in treating viral pneumonia, yet the precise underlying mechanisms remain unknown. Aim of the study: This study aimed to validate the mitigating effect of GBQF on ALI and to further investigate its mechanism. Materials and methods An ALI mice model was established by infusing LPS into the endotracheal tube. The effects of GBQF on ALI were investigated by measuring lung W/D; MPO; BALF total protein concentration; total number of cells; TNF-alpha, IL-1 beta, and IL-6 levels; pathological changes in lung tissue, and oxidation products. Immunohistochemistry and Western Blotting were performed to verify the underlying mechanisms. MH-S and BEAS-2B cells were induced by LPS, and the effects of GBQF were confirmed by RT-PCR and immunofluorescence. Results GBQF significantly reduced LPS-induced ALI in mice, improved lung inflammation, reduced the production of oxidative products, increased the activity of antioxidant enzymes, and reduced the degree of lung tissue damage. GBQF prevents MH-S cells from releasing inflammatory factors and reduces oxidative damage to BEAS-2B cells. In vivo studies have delved deeper into the mechanism of action of GBQF, revealing its correlation with the TLR4/NF-kappa B and Keap1/Nrf2 pathways. Conclusions Our study demonstrates that GBQF is an effective treatment for ALI, providing a new perspective on medication development for ALI treatment.

ETHNOPHARMACOLOGICAL RELEVANCE:Acute lung injury (ALI) is a life-threatening and widespread disease, with exceptionally high morbidity and mortality rates. Unfortunately, effective drugs for ALI treatment are currently lacking. Guben Qingfei decoction (GBQF) is a Chinese herbal compound known for its efficacy in treating viral pneumonia, yet the precise underlying mechanisms remain unknown. AIM OF THE STUDY:This study aimed to validate the mitigating effect of GBQF on ALI and to further investigate its mechanism. MATERIALS AND METHODS:An ALI mice model was established by infusing LPS into the endotracheal tube. The effects of GBQF on ALI were investigated by measuring lung W/D; MPO; BALF total protein concentration; total number of cells; TNF-α, IL-1β, and IL-6 levels; pathological changes in lung tissue, and oxidation products. Immunohistochemistry and Western Blotting were performed to verify the underlying mechanisms. MH-S and BEAS-2B cells were induced by LPS, and the effects of GBQF were confirmed by RT-PCR and immunofluorescence. RESULTS:GBQF significantly reduced LPS-induced ALI in mice, improved lung inflammation, reduced the production of oxidative products, increased the activity of antioxidant enzymes, and reduced the degree of lung tissue damage. GBQF prevents MH-S cells from releasing inflammatory factors and reduces oxidative damage to BEAS-2B cells. In vivo studies have delved deeper into the mechanism of action of GBQF, revealing its correlation with the TLR4/NF-κB and Keap1/Nrf2 pathways. CONCLUSIONS:Our study demonstrates that GBQF is an effective treatment for ALI, providing a new perspective on medication development for ALI treatment.

Ethnopharmacological relevance: Pulmonary fibrosis (PF), a lethal lung disease, can lead to structural destruction of the alveoli until death. Sparganii Rhizoma (SR), primarily distributed in East Asia, has been used clinically for hundreds of years against organ fibrosis and inflammation. Aim of the study: We intended to verify the effect of SR alleviate PF and further explore mechanisms. Methods: Murine model of PF was established by endotracheal infusion of bleomycin. We detected the anti-PF effect of SR through lung coefficient, hydroxyproline content, lung function and pathological staining. Then, we used Western Blot and RT-PCR to verify the mechanism. In vitro experiments, MRC-5 and BEAS-2B were induced to phenotypic transformation by TGF-01 and then RT-PCR, WB and IF were conducted to verify the effect of SR. Results: SR significantly reduced BLM-induced PF in mice, improved lung function, slowed the degree of lung tissue lesions, and reduced collagen deposition. SR alleviated PF by inhibiting fibroblasts differentiation and epithelial-mesenchymal transition. In vivo studies explored the mechanism and found that it was related to TGF01/Smad2/3 pathway. Conclusions: Our research proved SR could effectively treat PF, providing a fresh idea and approach for the treatment of PF with traditional Chinese medicine.

This study aimed to investigate the biological effects and underlying mechanisms of the total ginsenosides from Panax ginseng stems and leaves on lipopolysaccharide(LPS)-induced acute lung injury(ALI) in mice. Sixty male C57BL/6J mice were randomly divided into a control group, a model group, the total ginsenosides from P. ginseng stems and leaves normal administration group(61.65 mg·kg~(-1)), and low-, medium-, and high-dose total ginsenosides from P. ginseng stems and leaves groups(15.412 5, 30.825, and 61.65 mg·kg~(-1)). Mice were administered for seven continuous days before modeling. Twenty-four hours after modeling, mice were sacrificed to obtain lung tissues and calculate lung wet/dry ratio. The number of inflammatory cells in bronchoalveolar lavage fluid(BALF) was detected. The levels of interleukin-1β(IL-1β), interleukin-6(IL-6), and tumor necrosis factor-α(TNF-α) in BALF were detected. The mRNA expression levels of IL-1β, IL-6, and TNF-α, and the levels of myeloperoxidase(MPO), glutathione peroxidase(GSH-Px), superoxide dismutase(SOD), and malondialdehyde(MDA) in lung tissues were determined. Hematoxylin-eosin(HE) staining was used to observe the pathological changes in lung tissues. The gut microbiota was detected by 16S rRNA sequencing, and gas chromatography-mass spectrometry(GC-MS) was applied to detect the content of short-chain fatty acids(SCFAs) in se-rum. The results showed that the total ginsenosides from P. ginseng stems and leaves could reduce lung index, lung wet/dry ratio, and lung damage in LPS-induced ALI mice, decrease the number of inflammatory cells and levels of inflammatory factors in BALF, inhibit the mRNA expression levels of inflammatory factors and levels of MPO and MDA in lung tissues, and potentiate the activity of GSH-Px and SOD in lung tissues. Furthermore, they could also reverse the gut microbiota disorder, restore the diversity of gut microbiota, increase the relative abundance of Lachnospiraceae and Muribaculaceae, decrease the relative abundance of Prevotellaceae, and enhance the content of SCFAs(acetic acid, propionic acid, and butyric acid) in serum. This study suggested that the total ginsenosides from P. ginseng stems and leaves could improve lung edema, inflammatory response, and oxidative stress in ALI mice by regulating gut microbiota and SCFAs metabolism.

Asthma is a chronic respiratory disease. Bergamot essential oil (BEO) is extracted from the bergamot peel, which is widely used as a medicinal and food plant in China. Modern pharmacological studies have confirmed that BEO has anti-inflammatory properties, suggesting potential in treating asthma. First, the main active ingredients of BEO were detected and analyzed by gas chromatography-mass spectrometry (GC-MS). Network pharmacology methods were used to explore the possible core targets and main pathways of BEO in asthma treatment. Then ovalbumin (OVA)-induced in vivo and lipopolysaccharide (LPS)-induced in vitro models were established to investigate the antiasthmatic effects of BEO. BEO showed a good antiasthmatic effect by improving lung inflammation and inhibiting collagen deposition. Then, enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qPCR) were used to explore the possible mechanism of BEO in asthma treatment. Furthermore, experimental verification showed that BEO could suppress the release of inflammatory factors in vitro and inhibit the activation of MAPK and JAK-STAT signaling pathways. This study demonstrated the anti-inflammatory effects of BEO against asthma. Moreover, it supplies a theoretical basis for the clinical application of BEO.

Allergic asthma is a prevalent form of asthma that is characterized primarily by airway inflammation. Jiegeng decoction (JGT) is a traditional Chinese herbal formula known for its anti-inflammatory properties and has been used to treat respiratory diseases for centuries. This study aimed to investigate the biological effects and mechanisms of action of JGT in improving allergic asthma. An experimental allergic asthma mouse model was established using ovalbumin. The results showed that JGT significantly improved inflammation cell infiltration in the lung tissue of allergic asthmatic mice and the inflammatory environment of Th2 cells in the bronchoalveolar lavage fluid while also reducing serum IgE levels. Subsequently, 38 components of JGT were identified through liquid chromatography-mass spectrometry. Network pharmacology revealed that regulating inflammation and immune responses is the primary biological process by which JGT improves allergic asthma, with Th2 cell differentiation and the JAK-STAT signaling pathway being the key mechanisms of action. Finally, qPCR, flow cytometry, and Western blotting were used to validate that JGT inhibited Th2 cell differentiation by blocking the JAK1-STAT6 signaling pathway in CD4+ T cells, ultimately improving allergic asthma. This study provides a novel perspective on the therapeutic potential of JGT in the treatment of allergic asthma.

Alcoholic liver disease (ALD) is a liver injury caused by chronic or binge alcohol consumption. Jiubanban (JBB) is a 10-edible-herb- formula. The current study investigated the protective effects and mechanisms of JBB against chronic alcoholic liver injury. The results showed that JBB significantly alleviated chronic alcoholic liver injury caused by chronic-binge alcohol consumption. JBB accelerated ethanol metabolism and had a protective effect on both acute and chronic alcoholic liver injury. By modulating the NFκB, KEAP1, and HIF1 pathways, JBB was shown to reduce the production of cytokines (IL-6 and TNFα), enhanced the activity of anti-oxidative enzymes (SOD and GSH-px), reduced associated products (ROS and MDA), reversing inflammation, oxidative stress, and apoptosis. The study findings suggest that this functional herbal food combination may be a risk-free therapeutic strategy for treating ALD.

急性肺损伤(ALI)/急性呼吸窘迫综合征(ARDS)是继发于肺内或全身的炎症反应过程,它由肺泡损伤导致并形成炎症性非心源性的肺水肿.模式识别受体(PRRs)参与先天免疫系统的激活,PRRs可以启动炎症信号级联反应,并释放促炎细胞因子.本综述对PRRs所包括的跨膜受体TLRs、胞质受体RLRs和NLRs以及下游炎症通路NF-κB、IRF、MAPK、NETs、RAGE和Nrf2信号通路及自噬进行总结,以阐述模式识别受体PRRs在ALI/ARDS发病机制中的作用.