Objective To assess the clinical efficacy of sodium hyaluronate （0.3%） eye drops combined with herbal self-heating steam eye mask in the treatment of dry eye disease. Methods A prospective randomized controlled clinical trial was performed on 60 patients diagnosed with dry eye at the ophthalmic clinic of a Grade A, Class Ⅲ hospital in Shanghai from June 2023 to September 2024. Specifically, patients were randomly divided into control group and study group. Patients in the control group were treated with sodium hyaluronate （0.3%） eye drops for six weeks; while in the study group, patients received the eye drops combined with the herbal self-heating steam eye mask mainly containing powders of Flos Buddlejae. Subsequently, comparisons and analysis were performed before and after treatment between the two groups in the clinical symptom questionnaire score traditional Chinese medicine （TCM syndrome score），the Chinese dry eye questionnaire score and determination of tear film fluorscein breakup time （FBUT）, and curative effect. Results The quality control standard of the herbal powder in the self-heating steam eye mask was established through TLC and HPLC, and good heating behavior of the herbal self-heating steam eye mask was ascertained heating temperature （43±5）℃; heating duration （≥20 min）, meeting requirements of the product quality control. After treatment for 6 weeks, FBUT was increased, while TCM syndrome score and the Chinese dry eye questionnaire score were both decreased in the study group （P<0.001）. Besides, compared with the control group, TCM syndrome score and the Chinese dry eye questionnaire score were much lower, while the FBUT were higher in the study group （P<0.001）. Moreover, the overall response rate in the study group （81.7%） was much better than that in the control group （25.9%）. Conclusion The combination of sodium hyaluronate （0.3%） eye drops with herbal self-heating steam eye mask could be applied to the clinical treatment of dry eye disease due to its good clinical effects on relieving dry eye symptoms.

Objective: To systematically evaluate the effect of exercise intervention on lipid metabolism among overweight or obese children and adolescents, providing evidence for improving lipid metabolism. Methods: Literature were retrieved and screened from PubMed, Web of Science, Cochrane Library, EBSCO, Embase, CNKI, Wanfang, and VIP databases regarding the impact of exercise intervention on lipid metabolism among overweight or obese children and adolescents, with a search period from 1,January 2000 to 30,April 2025. Data extraction and quality assessment of included studies were performed, and network Meta analysis was conducted by using RevMan 5.3 and Stata 18.0 software, with standardized mean difference (SMD) and 95% CI as the effect measures. Results: A total of 15 eligible randomized controlled trials were included, with 13 reporting outcomes for total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C), and 14 for triglycerides (TG) and high density lipoprotein cholesterol (HDL-C). Network Meta analysis results showed that compared with the control group, aerobic exercise (AE) ( SMD = -0.51, 95% CI =-0.97 to -0.06) and combined aerobic and resistance exercise (COM) ( SMD =-0.54, 95% CI =-1.03 to -0.05) effectively reduced TC levels; AE ( SMD =-0.98, 95% CI =-1.64 to -0.32) and high intensity interval training (HIIT) ( SMD =-1.58, 95% CI = -2.52 to -0.64) effectively reduced TG levels; AE ( SMD =-0.60, 95% CI =-1.05 to -0.14), COM( SMD =-1.10, 95% CI =-1.72 to -0.48) and HIIT ( SMD =-1.05, 95% CI =-1.68 to -0.43) all effectively reduced LDL-C levels; only HIIT ( SMD = 1.03 , 95% CI =0.05-2.00) significantly increased HDL-C levels(all P <0.05). Conclusions Exercise intervention is beneficial to improve the dyslipidemia among children and adolescents, and the intervention effects of different exercise on different types of dyslipidemia are different.

ObjectiveIdentification and analysis, animal regression test, and drug susceptibility study were conducted on a pathogenic strain causing diarrhea in cynomolgus monkeys, aiming to provide a practical basis for the clinical treatment of Citrobacter freundii. MethodsFresh fecal samples were collected from nine diarrheal cynomolgus monkeys and streaked on Salmonella-Shigella (SS) medium, LB medium, and Columbia blood agar medium, and incubated at 37 ℃ for 24 h. Subsequently, the isolated strain was identified by colony morphology observation, Gram staining, biochemical tests and 16S rRNA gene sequencing, and PCR was used to detect its major virulence genes. After propagation, the isolate was intragastrically administered to healthy cynomolgus monkeys and C57BL/6 mice for animal regression tests to evaluate its pathogenicity. Finally, the disk-diffusion method was used to detect the antimicrobial susceptibility of the isolate. ResultsA single bacterial strain, designated MF071743, was isolated from 9 fecal samples collected from diarrheal cynomolgus monkeys. The isolate formed pink, smooth, round colonies on SS medium; translucent, smooth, moist, shiny colonies with neat edges on LB medium; and smooth, moist, off-white colonies on Columbia blood agar medium. Gram staining revealed that the isolate was a Gram-negative, spore-free short bacillus. Biochemical tests showed that the isolate was positive for motility test, mannitol test, hydrogen sulfide test, methyl red test, citrate utilization test, gas production from glucose test, raffinose test, sorbitol test, and D-xylose test, but negative for phenylalanine test, gluconate test, indole test, Voges Proskauer (VP) test, urease test, lysine test, ornithine test, and adonitol test. The results of 16S rRNA gene sequencing showed that the gene sequence similarity between strain MF071743 and Citrobacter freundii was 99.0%. PCR results showed that this strain carries genes encoding the urease accessory proteins UreD, UreE, and UreF. Animal intragastric administration assays demonstrated that the strain caused loose stools in cynomolgus monkeys, and all C57BL/6 mice died within 72 h. Drug susceptibility test results indicated that the isolate was sensitive to 16 antibiotics, including ceftriaxone, amikacin, gentamicin, ceftazidime, and levofloxacin, while it exhibited resistance to 5 antibiotics, including ampicillin, cefazolin, vancomycin, erythromycin, and cephalexin. ConclusionA strain of Citrobacter freundii with certain drug resistance was isolated from the feces of diarrheal cynomolgus monkeys. The results of this study provide a reference for the diagnosis and treatment of gastrointestinal diseases in captive laboratory monkeys.

ObjectiveStroke poses a heavy burden due to its high mortality and morbidity rates. Accurate and real-time detection of lesions is pivotal for prompt clinical intervention and favorable prognosis. Electrical impedance tomography (EIT) and microwave tomography (MWT) have emerged as compelling alternatives for stroke screening, owing to their non-ionizing, non-invasive and portable nature. EIT provides information on tissue conductivity, and MWT offers high sensitivity to changes in dielectric properties. However, single-modality imaging is inherently limited, EIT suffers from low sensitivity to deep-seated tissues and severe ill-posedness of inverse problems, whereas MWT is challenged by strong nonlinearity in inverse scattering and susceptibility to modeling errors. Consequently, the clinical utility of standalone EIT or MWT for stroke diagnosis remains constrained by poor spatial resolution and imaging artifacts. To improve the accuracy and robustness of stroke imaging, a dual-modality fusion conditional denoising diffusion probabilistic model (DM-DDPM) was proposed for high-precision dual-modality image reconstruction. MethodsA dual-encoder network with a symmetric architecture and independently trained parameters was constructed to extract heterogeneous features separately from EIT boundary voltage measurements and MWT scattered field signals. Attentional feature fusion (AFF) is employed to integrate complementary information from the two modalities adaptively, generating robust fused priors that suppress redundant noise while preserving key physical characteristics. Subsequently, the fused priors are embedded into a Transformer-based diffusion model via a cross attention mechanism to guide the reverse denoising process. This approach effectively reduces artifacts and enhances the stability of conductivity distribution reconstruction. Time step embedding is introduced to enable the network to perceive the diffusion stage and further improve the accuracy of noise prediction. ResultsSimulated experiments demonstrated that DM-DDPM significantly outperforms single-modality and multi-modality networks under various noise levels. A head model simulation dataset was constructed based on COMSOL Multiphysics, and tests were carried out under 50 dB, 40 dB and 30 dB signal-to-noise ratio levels. At 30 dB, the average relative error (RE) was below 0.20, while the structural similarity index measure (SSIM) and correlation coefficient (CC) remained above 0.90 and 0.89, respectively. Compared with single-modality and multi-modality networks, artifacts were significantly reduced, lesion edges were clearer, and localization was more accurate. The model maintains high reconstruction quality and strong robustness for single, double, and triple lesions simultaneously. Furthermore, physical experiments were conducted using a 16-electrode EIT system and a 16-antenna MWT system with asynchronous data acquisition. These experiments confirmed the feasibility of the method in real-world scenarios and demonstrated that it can robustly reconstruct simulated lesions despite environmental interference and measurement noise, validating its reliability for practical clinical applications. ConclusionThe proposed method effectively combines complementary dual-modality information with a conditional diffusion model. Low accuracy and poor noise resistance in single-modality imaging were effectively addressed, while the noise amplification issue caused by direct multimodal data fusion was avoided. The proposed algorithm exhibits strong anti-noise interference ability and high imaging stability in both simulation and physical experiments. Precise localization of stroke lesions with different quantities was achieved, providing a high-precision, and practical technical support for clinical stroke detection.

Atherosclerosis (AS) remains the core pathological basis underlying the high incidence and high rates of mortality and disability associated with cardiovascular disease (CVD) worldwide. Its essence is not merely lipid deposition, but rather an immune-mediated disease of the vascular wall characterized by an interplay of lipid metabolism disorders and chronic inflammation, with damage to vascular endothelial cells serving as the initiating event. As the disease progresses, it involves complex synergistic interactions among various cellular components, including endothelial cells, macrophages, and inflammatory cells, ultimately leading to plaque formation, instability, and even fatal thrombotic events. In recent years, the central driving role of lipid metabolic reprogramming in the progression of AS has garnered increasing attention from the scientific community. Among the vast array of lipid molecules, long-chain fatty acids (LCFAs) have become a primary focus of research due to their exceptional physiological functions. Traditional views have primarily emphasized the basic physiological functions of LCFAs: serving as highly efficient energy substrates through mitochondrial β-oxidation and acting as key structural components of cellular phospholipid membranes. However, emerging evidence clearly indicates that the functions of LCFAs extend far beyond those of mere metabolic fuel. They also act as potent bioactive signaling molecules, playing an indispensable multidimensional role in the pathogenesis of AS. Equally noteworthy and representing a paradigm shift in cardiovascular research is the emerging theory of the “gut-heart axis”. This theoretical framework views the human gut microbiota—comprising trillions of microorganisms—as a critical and metabolically active “bioreactor”. A wealth of clinical and multi-cohort epidemiological studies have conclusively demonstrated that imbalances in the composition and function of the gut microbiota are highly correlated with the clinical risk and severity of AS. Within this axis, the gut microbiota serves as the primary processing hub for dietary lipids. It actively participates in the digestion and biochemical remodeling of LCFAs, thereby altering their saturation and chemical structure and generating a wide variety of gut microbial metabolites. The effects of these gut-derived lipid metabolites extend far beyond the local intestinal microenvironment. Upon entering the bloodstream, these circulating microbiota metabolites act as endocrine signals. Given the extreme complexity of the underlying mechanisms, a comprehensive elucidation of the synergistic and bidirectional interactions between LCFAs and the gut microbiota in vascular pathology is particularly urgent. Therefore, this article aims to provide a systematic review of the multidimensional regulatory mechanisms of LCFAs and their associated gut microbiota metabolites in the onset, progression, and clinical manifestations of AS. By thoroughly exploring the interaction patterns within the “LCFAs-gut microbiota-AS” triad, this review seeks to fundamentally expand our understanding of the pathogenesis of CVDs. More importantly, translating these mechanistic insights into clinical practice holds tremendous promise. We hope to provide a solid theoretical foundation for the future development of novel AS prevention and treatment strategies based on non-traditional approaches. These include precision nutritional interventions (i.e., dietary lipid intake plans tailored to an individual’s unique microbiome profile) and targeted microbiome modulation therapies (such as next-generation probiotics, prebiotics, or specific metabolite supplements). Targeting the gut as a “reactor” to treat vascular wall lesions represents a promising direction for future cardiovascular medicine.

Acute lung injury （ALI） is a critical respiratory emergency caused by various non-cardiogenic factors， including severe pulmonary and extrapulmonary infections， lung contusion， and sepsis. Its pathological features are centered on alveolar-capillary barrier dysfunction， uncontrolled inflammatory responses， and impaired alveolar fluid clearance， manifesting as refractory hypoxemia and respiratory distress， with a poor clinical prognosis. Modern studies have revealed that mitochondrial dysfunction and glucose metabolic reprogramming in macrophages， characterized by hyperactivated glycolysis， drive pro-inflammatory polarization and represent a key mechanism leading to excessive inflammatory responses and disease progression in ALI. Therefore， targeting macrophage glycolysis may be a potential therapeutic strategy for ALI. The Plain Questions： Special Discussion on Channels and Vessels in Huangdi's Internal Classic states that "The spleen disseminates essence upward to the lungs". When the spleen fails in transport and transformation， the distribution of refined nutrients becomes disordered， resulting in the endogenous generation of turbid pathogens that obstruct the pulmonary collaterals， causing failure of lung dispersion and descent and leading to dyspneic reversal. This forms the dynamic pathological pattern of ''deficiency in the root with excess in the manifestation''， thereby proposing the core pathogenesis of ALI as ''spleen deficiency with transport dysfunction and turbid pathogens obstructing the lungs''. This process is intrinsically associated with the inflammatory cascade triggered by disordered macrophage glucose metabolism. Taking the theory of ''spleen failing to disperse essence'' as the entry point， the present study systematically elucidates the progressive pathological mechanism of "energy metabolism disorder-cytokine storm'' in ALI from the perspectives of the ''spleen deficiency-turbid obstruction'' pathogenesis and macrophage glycolysis-pro-inflammatory polarization. In addition， we summarize Chinese medicine compound formulas and monomeric components that ''restore spleen transport and eliminate turbid pathogens''， and explore their potential mechanisms in the treatment of ALI by regulating macrophage metabolic phenotypes to improve the state of ''spleen failing to disperse essence''. This provides a molecular basis for elucidating the ''spleen-lung'' energy metabolism dialogue， deepens understanding of the multi-target regulatory mechanisms of herbal prescriptions， and promotes the deep integration of classical theory with modern medicine.

ObjectiveTo investigate the therapeutic effect of wall-broken ganoderma lucidum spore powder （GLS） on a mouse model of hepatocellular carcinoma and to explore its underlying mechanism. MethodsFifty 2-week-old C57BL/6J mice were divided into a control group， a model group and low， medium and high-dose GLS groups（0.25， 0.5， 1.0 g/kg ）， with 10 mice in each group. A DEN/CCL₄ mouse hepatocellular carcinoma model was established， and GLS was administered by gavage starting from the 8th week， once a day for 14 weeks. At the end of the final administration， the number of liver nodules was observed ， and the serum alpha-fetoprotein （AFP） was detected using enzyme-linked immunosorbent assay. The content of catalase （CAT） in serum and liver tissue was determined by ammonium molybdate method. The content of reduced glutathione （GSH） in serum and liver tissue was measured by microplate assay. The content of glutathione peroxidase （GSH-PX） in serum and liver tissue was detected by colorimetric method. Immunohistochemistry （IHC-P） was employed to detect the protein expression of proliferating cell nuclear antigen （PCNA）. R eal-time fluorescence quantitative polymerase chain reaction was utilized to detect the relative expression of nuclear factor E2-related factor 2 （Nrf2）， Kelch-like epichlorohydrin-associated protein 1 （Keap1）， NAD（P）H quinone oxidoreductase 1 （Nqo1）， heme oxygenase-1 （Ho-1） and glutamate cysteine ligase catalytic subunit （Gclc） mRNA. ResultsCompared with the control group， the content of serum AFP were significantly higher in the model group （P<0.01）， while the contents of CAT， GSH and GSH-PX in liver and serum were significantly lower in the model group （P<0.01）. The relative expression of Keap1 and Nqo1 mRNA was significantly higher （P<0.01）， the relative expression of Nrf2， Ho-1， Gclc mRNA relative expression was significantly lower （P<0.01）， and the positive expression rate of PCNA was significantly higher （P<0.01）. Compared with the model group， the total number of liver nodules and content of serum AFP in the administered group were significantly lower （P<0.01）， and the contents of CAT， GSH， and GSH-PX in the liver and serum of mice significantly increased （P<0.05 or P<0.01）. The expression of Keap1 and Nqo1 mRNA significantly decreased （P<0.05）. The expression of Nrf2， Ho-1 and Gclc mRNA significantly increased （P<0.05）， and positive expression rate of PCNA significantly decreased （P<0.01）. ConclusionGLS has a significant protective effect on DEN/CCL4 -induced mouse hepatocellular carcinoma model， and the mechanism of action is related to the regulation of oxidative stress in mouse liver.

ObjectiveTo investigate the therapeutic effect of paeoniflorin on metabolic dysfunction-associated fatty liver disease （MASLD） combined with insulin resistance （IR）， and to elucidate its regulatory mechanisms on the Toll-like receptor 4 （TLR4）/nuclear transcription factor （NF）-κB-insulin receptor substrate 1 （IRS1） inflammation-insulin signaling axis. MethodsMASLD mouse model was established using a 60% high-fat diet. Mice were randomly assigned to a normal control group， a MASLD model group， and paeoniflorin groups （low dose： 25 mg·kg^-1·d^-1， medium dose： 50 mg·kg^-1·d^-1， high dose： 100 mg·kg^-1·d^-1）， receiving intragastric administration for consecutive 12 weeks. Concurrently， a palmitic acid/oleic acid （PA/OA）-induced lipid deposition model was established in HepG2 cells. Cell counting kit-8 （CCK-8） assay was performed to determine the optimal concentrations of PA/OA and paeoniflorin for intervention. Mice body weight， liver index， and serum levels of alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， triglycerides （TG）， and total cholesterol （TC） were measured. Fasting blood glucose （FBG） and fasting insulin （FINS） levels were measured， and the homeostatic model assessment of insulin resistance （HOMA-IR） was calculated， while an oral glucose tolerance test （OGTT） was performed to evaluate glucose metabolism. Hematoxylin and eosin （HE） staining was used to observe pathological changes and inflammatory cell infiltration in liver tissue， and oil red O staining was used to evaluate lipid droplet deposition in liver tissue and HepG2 cells. Potential targets were screened using network pharmacology and molecular docking. Western blot analysis was performed to detect the expression of HSP90AA1， TLR4， p-NF-κB p65， p-IRS1， and p-Akt proteins in liver tissue and HepG2 cells. ResultsCompared with the normal control group， mice in the MASLD model group exhibited significantly increased body weight， liver index， and serum levels of ALT， AST， TG， and TC， as well as markedly elevated FBG， FINS， and HOMA-IR， and impaired glucose tolerance （P<0.01）. HE staining revealed marked hepatic steatosis and inflammatory cell infiltration， while oil red O staining showed a significant increase in lipid droplet deposition. Compared with the MASLD model group， after intervention with various doses of paeoniflorin， the increase in body weight and liver index was reduced， serum ALT， AST， TG， and TC levels decreased， and FBG， FINS， and HOMA-IR were significantly lowered， with glucose tolerance markedly improved （P<0.05， P<0.01）， showing a certain dose-dependent trend. HE and oil red O staining results showed a marked reduction in hepatic steatosis and lipid deposition. In vitro experiments demonstrated that， compared with the control group， PA/OA treatment significantly induced increased lipid deposition in HepG2 cells. Compared with the model group， paeoniflorin intervention significantly reduced intracellular lipid droplets， and lipid deposition showed a dose-dependent decreasing trend. Mechanism studies indicated that， compared with the normal control group， the MASLD model group exhibited significantly elevated expression of TLR4， HSP90AA1， and p-NF-κB p65， while p-IRS1 （Ser307） expression was elevated and p-Akt （Ser473） expression was reduced （P<0.01）. Compared with the model group， the expression of the aforementioned proteins was significantly reversed in all treatment groups following intervention （P<0.05， P<0.01）. ConclusionPaeoniflorin significantly alleviates lipid deposition and insulin resistance in MASLD mice. Its mechanism of action may involve targeting HSP90AA1， TLR4， and NF-κB1 to regulate the TLR4/NF-κB-IRS1 inflammation-insulin signaling axis. This regulation suppresses inflammatory responses and restores insulin signaling， thereby ameliorating abnormalities in glucose and lipid metabolism.

ObjectiveTo investigate the therapeutic effect of paeoniflorin on metabolic dysfunction-associated fatty liver disease （MASLD） combined with insulin resistance （IR）， and to elucidate its regulatory mechanisms on the Toll-like receptor 4 （TLR4）/nuclear transcription factor （NF）-κB-insulin receptor substrate 1 （IRS1） inflammation-insulin signaling axis. MethodsMASLD mouse model was established using a 60% high-fat diet. Mice were randomly assigned to a normal control group， a MASLD model group， and paeoniflorin groups （low dose： 25 mg·kg^-1·d^-1， medium dose： 50 mg·kg^-1·d^-1， high dose： 100 mg·kg^-1·d^-1）， receiving intragastric administration for consecutive 12 weeks. Concurrently， a palmitic acid/oleic acid （PA/OA）-induced lipid deposition model was established in HepG2 cells. Cell counting kit-8 （CCK-8） assay was performed to determine the optimal concentrations of PA/OA and paeoniflorin for intervention. Mice body weight， liver index， and serum levels of alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， triglycerides （TG）， and total cholesterol （TC） were measured. Fasting blood glucose （FBG） and fasting insulin （FINS） levels were measured， and the homeostatic model assessment of insulin resistance （HOMA-IR） was calculated， while an oral glucose tolerance test （OGTT） was performed to evaluate glucose metabolism. Hematoxylin and eosin （HE） staining was used to observe pathological changes and inflammatory cell infiltration in liver tissue， and oil red O staining was used to evaluate lipid droplet deposition in liver tissue and HepG2 cells. Potential targets were screened using network pharmacology and molecular docking. Western blot analysis was performed to detect the expression of HSP90AA1， TLR4， p-NF-κB p65， p-IRS1， and p-Akt proteins in liver tissue and HepG2 cells. ResultsCompared with the normal control group， mice in the MASLD model group exhibited significantly increased body weight， liver index， and serum levels of ALT， AST， TG， and TC， as well as markedly elevated FBG， FINS， and HOMA-IR， and impaired glucose tolerance （P<0.01）. HE staining revealed marked hepatic steatosis and inflammatory cell infiltration， while oil red O staining showed a significant increase in lipid droplet deposition. Compared with the MASLD model group， after intervention with various doses of paeoniflorin， the increase in body weight and liver index was reduced， serum ALT， AST， TG， and TC levels decreased， and FBG， FINS， and HOMA-IR were significantly lowered， with glucose tolerance markedly improved （P<0.05， P<0.01）， showing a certain dose-dependent trend. HE and oil red O staining results showed a marked reduction in hepatic steatosis and lipid deposition. In vitro experiments demonstrated that， compared with the control group， PA/OA treatment significantly induced increased lipid deposition in HepG2 cells. Compared with the model group， paeoniflorin intervention significantly reduced intracellular lipid droplets， and lipid deposition showed a dose-dependent decreasing trend. Mechanism studies indicated that， compared with the normal control group， the MASLD model group exhibited significantly elevated expression of TLR4， HSP90AA1， and p-NF-κB p65， while p-IRS1 （Ser307） expression was elevated and p-Akt （Ser473） expression was reduced （P<0.01）. Compared with the model group， the expression of the aforementioned proteins was significantly reversed in all treatment groups following intervention （P<0.05， P<0.01）. ConclusionPaeoniflorin significantly alleviates lipid deposition and insulin resistance in MASLD mice. Its mechanism of action may involve targeting HSP90AA1， TLR4， and NF-κB1 to regulate the TLR4/NF-κB-IRS1 inflammation-insulin signaling axis. This regulation suppresses inflammatory responses and restores insulin signaling， thereby ameliorating abnormalities in glucose and lipid metabolism.

Background At present, the treatment of silicosis is still limited, and no method is available to cure the disease. miRNAs are involved in the process of fibrosis at the transcriptional level by directly degrading target gene mRNA or inhibiting its translation. However, how miR-130a-3p regulates silicosis fibrosis has not been fully elucidated yet. Objective To investigate whether miR-130a-3p promotes epithelial-mesenchymal transition (EMT) by inhibiting peroxisome proliferators-activated receptors gamma (PPAR-γ), thereby pro-moting the process of silicotic fibrosis. To identify effective new targets for the treatment of silicotic fibrosis. Methods (1) Animal experiments: C57BL/6J mice were intratracheally injected with a one-time dose of 10 mg silica suspension (dissolved in 100 μL saline) as positive lung exposure. A silicosis model group was established 28 d after the exposure. A control group was injected with the same amount of normal saline into the trachea. Hematoxylin-eosin staining and Sirius red staining were used to observe the pathological changes and collagen deposition in lung tissues respectively. Realtime fluorescence-based quantitative polymerase chain reaction (RT-qPCR) was used to assay the expression of miR-130a-3p and PPAR-γ mRNA in lung tissues. Western blotting was used to detect the protein expression of PPAR-γ, transforming growth factor (TGF)-β1, E-cadherin, α-smooth muscle actin (α-SMA), and Collagen Ⅰ in lung tissues. (2) Cells experiments: Mouse lung epithelial cells (MLE-12) were induced with 5 µg·L⁻¹ TGF-β1 for different time (0, 12, 24, 48 h). RT-qPCR was used to detect the expression of miR-130a-3p and PPAR-γ mRNA in cells. The binding relationship between miR-130a-3p and PPAR-γ mRNA was verified by dual luciferase reporter gene assay. MLE-12 cells were stimulated by 5 µg·L⁻¹ TGF-β1 after transfection of miR-130a-3p inhibitor, and Western blotting was used to measure the protein expression of PPAR-γ, E-cadherin, and α-SMA in the TGF-β1-induced cells. Results In the silicosis model group, the alveolar septum was widened and the pulmonary nodules were formed. The Sirius red staining collagen deposition in pulmonary nodules indicated that a silicosis fibrosis model was successfully established. The expressions of TGF-β1, α-SMA, and Collagen Ⅰ proteins were increased, and the expressions of E-cadherin and PPAR-γ proteins were decreased in lung tissues of the silicosis group, compared with the control group (P<0.05 or P<0.01). The expression of miR-130a-3p was increased and the expression of PPAR-γ mRNA was decreased in lung tissues of the silicosis model (P<0.01). The expression of miR-130a-3p was significantly increased, while the expression of PPAR-γ mRNA was decreased in the TGF-β1 induced MLE-12 cells (P<0.05 or P<0.01). The dual luciferase reporter assay showed a direct relationship between miR-130a-3p and PPAR-γ mRNA in MLE-12 cells. The transfection of miR-130a-3p inhibitor in the TGF-β1 induced MLE-12 cells inhibited the decrease of PPAR-γ and E-cadherin proteins, and the increase of α-SMA protein in the MLE-12 cells induced by TGF-β1 (P<0.05 or P<0.01). Conclusion miR-130a-3p promotes the development of silicosis fibrosis by targeting PPAR-γ to increase pulmonary EMT.