This study aimed to investigate the mechanism of compound Agrimonia pilosula enteritis capsules (CAPEC) on ulcerative colitis (UC) in mice with dampness-heat syndrome. The mice were randomly divided into five groups: the control group, the model group, the positive drug (5-aminosalicylic acid, 5-ASA) group, the low-dose CAPEC (CAPEC-L) group and the high-dose CAPEC (CAPEC-H) group. The mice models were established by using high-fat high-sucrose diet, feeding with distilled spirit and dextran sulfate sodium (DSS). The effects of CAPEC on bile acids (BAs) metabolic profiles in bile and the FXR-SREBP-1 signaling pathway were investigated in the model of UC in mice with dampness-heat syndrome by ELISA, qRT-PCR, UHPLC-QQQ/MS, and histopathological analysis. The results showed that, compared with the model group, the CAPEC-L group and the CAPEC-H group significantly reduced the disease activity index (DAI), and proinflammatory cytokine levels (including IL-6, IL-1β, and TNF-α) in both serum and colon tissues. Additionally, CAPEC markedly ameliorated intestinal inflammation, hepatic lipid accumulation, and pathological alterations in tongue tissue. The CAPEC-H group significantly attenuated the abnormal elevation of BAs profiles in bile, and up-regulated hepatic mRNA levels of Cyp7a1, Cyp7b1, Cyp27a1, Bsep, Fxr, and Shp, while down-regulating Srebp-1 and Cyp8b1 expression. The experimental results suggest that CAPEC alleviates UC with dampness-heat syndrome by ameliorating BAs metabolic disorders, hepatic lipid accumulation, and intestinal inflammation. These findings provide mechanistic insights into CAPEC’s traditional effects of clearing heat and drying dampness, and strengthening the spleen to relieve diarrhea.

Background Silicosis, caused by inhalation of silica (SiO₂) dust, remains the most prevalent occupational pneumoconiosis in China. While galectin-3 (Gal-3) is known to play pro-inflammatory and pro-fibrotic roles in various diseases, its specific mechanism in the pathogenesis of silicosis has not been fully clarified. Objective To investigate the role and underlying mechanisms of Gal-3 in silicosis using clinical samples of silicosis and a silicosis mouse model. Methods Lung nodule biopsy samples were collected from patients with stage III pneumoconiosis. Concurrently a silicosis mouse model was constructed via non-exposed tracheal intubation with instillation of a SiO₂ suspension. The expression levels of Gal-3 mRNA and protein in the lung tissues of the silicosis model mice were then detected using real-time quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC) staining. Single-cell transcriptomic sequencing (scRNA-seq) was performed on both human and murine lung samples to analyze the expression of the Gal-3-encoding gene Lgals3 across different cell types. In vitro, RAW264.7 macrophages were treated with varying concentrations of SiO₂ suspension for 24 h and 48 h; the expression levels of Gal-3 mRNA and protein were measured by RT-qPCR and Western blot. The Gal-3 inhibitor TD139 was used to intervene in the SiO₂-induced in vitro macrophage model, and Western blot was used to detect the intracellular expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and transforming growth factor-β1 (TGF-β1). Finally, mouse embryonic lung fibroblasts NIH/3T3 and Mlg2908 were treated with varying concentrations of recombinant mouse Gal-3 protein (rmGal-3) for 48 h, and Western blot was used to detect the expression of fibrosis markers [(Collagen I, Collagen III, Fibronectin, and α smooth muscle actin (α-SMA)] and proteins associated with the TGF-β1/Smads signaling pathway. Results RT-qPCR and IHC staining showed that both the gene and protein expression levels of Gal-3 were significantly elevated at all consecutive time points in the silicosis mouse model (P < 0.05). scRNA-seq revealed that Lgals3 was aberrantly highly expressed in lung tissues from pneumoconiosis patients and silicosis mouse models, with the highest expression observed in macrophages. After treatment of macrophages with different concentrations of SiO₂ for 24 h and 48 h, the mRNA and protein expression levels of Gal-3 were significantly upregulated compared with the control group (P < 0.05). Following TD139 intervention, the protein expression levels of IL-1β, TNF-α, and TGF-β1 in dust-exposed macrophages were markedly downregulated (P < 0.0001). After 48 h of stimulation with rmGal-3, the protein expression levels of Collagen I, Fibronectin, and α-SMA in mouse embryonic lung fibroblasts (NIH/3T3 and Mlg2908) were significantly increased in all treatment groups compared with the control group (P < 0.01). Moreover, Gal-3 treatment markedly upregulated TGF-β1 protein expression in Mlg2908 cells and enhanced the phosphorylation levels of Smad2 and Smad3 (P < 0.0001). Conclusion Gal-3 is abnormally expressed in silicotic lung tissues, which primarily originates from macrophages, and inhibition of Gal-3 suppresses SiO₂-induced inflammatory and pro-fibrotic responses. In addition, Gal-3 promotes fibroblast differentiation and extracellular matrix production by activating the TGF-β1/Smads signaling pathway.

Background Silicosis, caused by inhalation of silica (SiO₂) dust, remains the most prevalent occupational pneumoconiosis in China. While galectin-3 (Gal-3) is known to play pro-inflammatory and pro-fibrotic roles in various diseases, its specific mechanism in the pathogenesis of silicosis has not been fully clarified. Objective To investigate the role and underlying mechanisms of Gal-3 in silicosis using clinical samples of silicosis and a silicosis mouse model. Methods Lung nodule biopsy samples were collected from patients with stage III pneumoconiosis. Concurrently a silicosis mouse model was constructed via non-exposed tracheal intubation with instillation of a SiO₂ suspension. The expression levels of Gal-3 mRNA and protein in the lung tissues of the silicosis model mice were then detected using real-time quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC) staining. Single-cell transcriptomic sequencing (scRNA-seq) was performed on both human and murine lung samples to analyze the expression of the Gal-3-encoding gene Lgals3 across different cell types. In vitro, RAW264.7 macrophages were treated with varying concentrations of SiO₂ suspension for 24 h and 48 h; the expression levels of Gal-3 mRNA and protein were measured by RT-qPCR and Western blot. The Gal-3 inhibitor TD139 was used to intervene in the SiO₂-induced in vitro macrophage model, and Western blot was used to detect the intracellular expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and transforming growth factor-β1 (TGF-β1). Finally, mouse embryonic lung fibroblasts NIH/3T3 and Mlg2908 were treated with varying concentrations of recombinant mouse Gal-3 protein (rmGal-3) for 48 h, and Western blot was used to detect the expression of fibrosis markers [(Collagen I, Collagen III, Fibronectin, and α smooth muscle actin (α-SMA)] and proteins associated with the TGF-β1/Smads signaling pathway. Results RT-qPCR and IHC staining showed that both the gene and protein expression levels of Gal-3 were significantly elevated at all consecutive time points in the silicosis mouse model (P < 0.05). scRNA-seq revealed that Lgals3 was aberrantly highly expressed in lung tissues from pneumoconiosis patients and silicosis mouse models, with the highest expression observed in macrophages. After treatment of macrophages with different concentrations of SiO₂ for 24 h and 48 h, the mRNA and protein expression levels of Gal-3 were significantly upregulated compared with the control group (P < 0.05). Following TD139 intervention, the protein expression levels of IL-1β, TNF-α, and TGF-β1 in dust-exposed macrophages were markedly downregulated (P < 0.0001). After 48 h of stimulation with rmGal-3, the protein expression levels of Collagen I, Fibronectin, and α-SMA in mouse embryonic lung fibroblasts (NIH/3T3 and Mlg2908) were significantly increased in all treatment groups compared with the control group (P < 0.01). Moreover, Gal-3 treatment markedly upregulated TGF-β1 protein expression in Mlg2908 cells and enhanced the phosphorylation levels of Smad2 and Smad3 (P < 0.0001). Conclusion Gal-3 is abnormally expressed in silicotic lung tissues, which primarily originates from macrophages, and inhibition of Gal-3 suppresses SiO₂-induced inflammatory and pro-fibrotic responses. In addition, Gal-3 promotes fibroblast differentiation and extracellular matrix production by activating the TGF-β1/Smads signaling pathway.

ObjectiveTo investigate the effect of protein arginine methyltransferase 5 （PRMT5） on the angiogenesis of colorectal cancer （CRC） through the Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathway. MethodsThe expression and prognostic value of PRMT5 in CRC tissues were analyzed based on the cancer genome atlas （TCGA） and gene expression omnibus （GEO） databases. A total of 105 pairs of cancer tissues and matched adjacent non-tumor tissues were collected from CRC patients， and PRMT5 expression was detected by immunohistochemistry （IHC）； Western blot was used to detect the PRMT5 protein level in normal colonic epithelial cells （FHC） and CRC cell lines （including RKO， SW480）. SW48 and LoVo cells were divided into negative control （NC） group and PRMT5 knockdown interference group. After the stable knockdown cell models were successfully constructed， the effects of conditioned medium on the proliferation， cell cycle， migration and tube formation abilities of human umbilical vein endothelial cells （HUVECs） were detected； the correlation between PRMT5 and vascular endothelial growth factor A （VEGFA） was analyzed by real-time quantitative polymerase chain reaction （RT-qPCR） and enzyme-linked immunosorbent assay （ELISA）. Gene set enrichment analysis （GSEA） and cytoplasm-nucleus separation assay were performed to verify the regulatory pathway. ResultsPRMT5 was highly expressed in CRC tissues and cell lines， which was significantly correlated with poor prognosis and pathological characteristics of patients （all P<0.05）； PRMT5 knockdown could significantly inhibit the angiogenesis-related abilities of HUVECs （all P<0.05） and down-regulate the expression of VEGFA （all P<0.01）. GSEA results indicated that PRMT5 expression was significantly associated with the activation of JAK2/STAT3 signaling pathway （all P<0.001）. PRMT5 knockdown could inhibit the activation of JAK2/STAT3， the nuclear translocation of STAT3 and the protein level of phosphorylated STAT3 （p-STAT3） in the nucleus， thus inhibiting the expression of VEGFA. ConclusionPRMT5 is highly expressed in CRC tissues and indicates poor prognosis of patients. It promotes the nuclear translocation and transcriptional activity of STAT3 by activating the JAK2/STAT3 pathway and drives the expression of VEGFA to promote tumor angiogenesis.

Objective This study reports on the obligatory parasitism of water mites Arrenurus sp. on Anopheles messeae at the Manzhouli Port, Inner Mongolia, China. Methods Duing July 2024, a survey on the mosquito diversity was conducted at the Manzhouli Port. Captured mosquitoes and their ectoparasites were identified to species level. Results A total of 1840 adult mosquitoes were collected, representing species from three genera: Culex(Cx. modestus, Cx. pipiens pallens), Aedes(Ae. dorsalis, Ae. flavidorsalis, Ae. flavescens), and Anopheles (An. messeae). Among all the mosqutioes specimens,3 out of 150 captured An. messeae were found to carry ectoparasitic mites, with number of 2,4,27 mites separately. Morphological and molecular identification reached the same result as water mites(Hydrachnidiae, Hydracrina). COI gene sequence showed 94% similarity with the closest species Arrenurus truncatellus. Conlusions Literature review suggests water mites are host-specific parasitism of mosquito species and herein with the first record of Arrenurus sp. parasiting on An. Messeae in the most high-latitude region globally.

The recombinant human thyroid-stimulating hormone (rhTSH) can be used for differentiated thyroid cancer (DTC) preparation before ¹³¹I therapy, and follow-up. Since its approval by the American Food and Drug Administration (FDA) in 1998, rhTSH has been clinically used in European countries, the United States, and other countries for nearly 30 years. In April 2024, China’s first independently developed rhTSH agent was approved. Based on clinical experience and evidence from domestic and international studies, an expert consensus on the application of rhTSH has been developed following thorough consultations among experts. The consensus offers evidence-based recommendations to guide the appropriate use of rhTSH in clinical practice.

Isoliquiritigenin (ISL) is a chalcone compound isolated from licorice, known for its anti-diabetic, anti-cancer, and antioxidant properties. Our previous study has demonstrated that ISL effectively lowers blood glucose levels in type 2 diabetes mellitus (T2DM) mice and improves disturbances in glucolipid and energy metabolism induced by T2DM. This study aims to further investigate the effects of ISL on alleviating abnormal endoplasmic reticulum stress (ERS) caused by T2DM and to elucidate its molecular mechanisms. In vivo experiments were conducted using 8-week-old SPF male C57BL/6J mice. The T2DM animal model was established by high-fat and high-sugar diet combined with intraperitoneal injections of streptozotocin (STZ), in compliance with the ethical guidelines set by the Animal Welfare Committee of Beijing University of Chinese Medicine (approval number: BUCM-2022021503-1134). In vitro experiments employed human liver cancer HepG2 cells, which were induced with tunicamycin (TM) to establish the ERS cell model. Transcriptomic sequencing was used to analyze changes in gene expression in the liver samples of T2DM mice following ISL treatment. Real-time quantitative polymerase chain reaction (RT-qPCR) was employed to assess the regulatory effects of ISL on key ERS genes. Enzyme-linked immunosorbent assay (ELISA), Western blot (WB), and immunofluorescence techniques were used to evaluate ISL's effects on ERS-related proteins. Results indicate that ISL significantly downregulates the expression of ERS-related genes, reduces the level of glucose-regulated protein 78 (GRP78), and inhibits the phosphorylation of protein kinase RNA-like endoplasmic reticulum kinase (PERK), thereby alleviating abnormal ERS induced by T2DM. Additionally, ISL increases the protein levels of insulin receptor substrate (IRS) 1 and IRS2 and enhances the phosphorylation of protein kinase B (Akt), thereby improving insulin sensitivity. In conclusion, ISL is able to alleviate T2DM associated symptoms by improving abnormal ERS and enhancing insulin sensitivity.

AIM To investigate the impact of varying dosages of Supplemented Wendan Decoction on the PI3K/Akt/FOXO1 glycolipid metabolic pathway in 3T3-L1 adipocytes.METHODS The CCK-8 assay was used to determine the concentration of Supplemented Wendan Decoction-medicated serum.The mature adipocytes differentiated from 3T3-L1 preadipocytes after induction were further divided into the blank control group,the model group,the rosiglitazone group(10 mg/L),and the Supplemented Wendan Decoction groups(5％,10％,and 20％),followed by the sample collections after 48 hours of treatment.Oil red O staining quantified lipid accumulation in 3T3-L1 adipocytes;extracellular glucose levels were measured using glucose oxidase(GOD)assay;RT-qPCR analyzed mRNA expressions of IRS-1,PI3K,Akt,GLUT4,IL-6,TNF-α and IL-1β;Western blot assessed protein expressions of INSR,IRS-1,PI3K-p85,Akt,FOXO1 and GLUT4.RESULTS No significant changes in cell viability(P＞0.05)were observed in 3T3-L1 preadipocytes exposed to serum containing supplemented Wendan Decoction at different concentrations for 24,48,or 72 hours.The 3T3-L1 preadipocytes held the capacity to differentiate into mature adipocytes within a 14-day induction period.Compared to the model group,all supplemented Wendan Decoction groups exhibited reduced lipid accumulation in adipocytes and downregulated mRNA expression of IRS-1,IL-6,TNF-α and IL-1β(P＜0.01);the low-dose group demonstrated increased mRNA expressions of PI3K and GLUT4(P＜0.05,P＜0.01),alongside elevated protein expressions of INSR,IRS-1,PI3K-p85,Akt and GLUT4(P＜0.05,P＜0.01);the medium-dose group showed enhanced GLUT4 mRNA expression,and upregulated protein expressions of INSR and FOXO1(P＜0.01).After 24 hours intervention,the high-dose Supplemented Wendan Decoction group exhibited increased glucose consumption in adipocytes(P＜0.01),and elevated protein expression of INSR,Akt and FOXO1(P＜0.05,P＜0.01).CONCLUSION Supplemented Wendan Decoction reduces lipid accumulation in adipocytes,regulates glucose and lipid metabolism,and promotes metabolic homeostasis through PI3K/Akt/FOXO1 signaling pathway.

Chronic hepatitis B（CHB）is one of the major challenges in the global public health field. As of 2022，approximately 254 million people worldwide were infected with the hepatitis B virus（HBV）. CHB is one of the main causes of liver cirrhosis and hepatocellular carcinoma（HCC）. Nucleos（t）ide analogs（NAs）and interferon therapy can delay the progression of liver fibrosis by inhibiting viral replication，but they cannot completely avoid the problem of heterogeneous treatment responses. Some patients are in a state of low-level viremia（LLV）during treatment. The persistent LLV state can induce chronic inflammation and the progression of liver fibrosis，ultimately increase the risk of HCC. In patients with poor treatment responses，the continuous active viral replication can induce immune disorders，accelerate the evolution of fibrosis to the decompensated stage of liver cirrhosis，and increase the risk of patient death. This article aims to review the definition，mechanisms，and impact on treatment outcomes of LLV and suboptimal response based on the latest research，provide a basis for optimizing antiviral therapy for CHB.

Objective Investigate the clinical efficacy and application value of gasless trans-subclavian approach endoscopic surgery(GTAES)for the treatment of primary hyperparathyroidism(PHPT).Methods 55 PHPT patients who underwent unilateral parathyroid adenoma resection from January 2023 to October 2024 were absorbed.Based on surgical approaches,31 patients were divided into the traditional low-collar arc incision open surgery group(open group)and 24 patients were divided into gasless trans-subclavian approach endoscopic surgery group(endoscopic group).The perioperative data,anterior neck function recovery,and incision healing were compared between two groups.Results There were no significant differences in operation time,intraoperative blood loss,postoperative drainage volume and postoperative hospital stay between the two groups(P＞0.05).The preoperative blood calcium levels of the endoscopic group and the open group were(2.68±0.10)mmol/L and(2.63±0.16)mmol/L,respectively.The blood calcium levels on the first day after surgery were(2.39±0.12)mmol/L and(2.36±0.16)mmol/L,respectively.Preoperative parathyroid hormone(PTH)was 27.55(110.05,155.75)pg/ml in endoscopic group and 137.00(107.00,210.30)pg/ml in open group,respectively.PTH on the first day after surgery was 18.98(12.64,23.53)pg/ml and 13.85(7.36,23.23)pg/ml,respectively.Blood calcium and PTH in each group 1 day after surgery decreased compared with that before surgery,and the difference was statistically significant(P＜0.05).There were no postoperative complications such as hoarseness,bleeding and incision infection in both groups.Postoperative hand and foot numbness:5 cases(20.8％)in endoscopic group and 8 patients(25.8％)in the open group,there was no significant difference between the two groups(P=0.667).There was no significant difference in the score of neck pain 3 days after surgery between the two groups(P＞0.05).The score of swallowing tension[(1.92±1.06)points compared with(2.77±1.38)points,P=0.015]and the score of anterior neck discomfort[(1.63±0.88)points compared with(2.35±1.33)points,P=0.018]in the endoscopic group one month after surgery were better than those in the open group.There was no significant difference in the score of neck scar scale between the two groups 3 months after surgery(P＞0.05).VAS score of incision satisfaction was(9.08±0.88)in endoscopic group and(8.19±1.30)in open group,and the endoscopic group was better than the open group,the difference was statistically significant(P=0.004).Conclusion For PHPT patients caused by unilateral parathyroid adenoma confirmed through preoperative localization examination,GTAES is a safe and effective surgical approach,which offers unique advantages in intraoperative lesion identification,cosmetic outcomes of the incision,and preservation of anterior neck function,providing a new surgical option for PHPT patients.