Background: Influenza A virus (IAV) is a negative-sense RNA virus of the Orthomyxoviridae family and is the etiological agent of a highly contagious acute respiratory disease that can lead to acute lung injury. Objective: To elucidate the molecular mechanisms of IAV infection, an integrative research approach combining gene expression profiling, multinetwork analysis, and in vivo experimental validations was employed. Methods: First, a series of network-based analyses were performed, including protein-protein interaction network construction, weighted gene co-expression network analysis, and subsequent gene set enrichment analysis, to identify the major underlying mechanisms of IAV infection. Following gene expression analysis, core targets, both direct and indirect regulators, were screened. An IAV (H1N1) strain A/PR/8/34-induced acute lung injury mouse model was constructed for in vivo validations. Batch one included two groups to evaluate findings from the multi-network analysis: Mock (n = 10; 5 males and 5 females) and IAV (n = 10; 5 males and 5 females). Batch two included three groups to assess the role of toll-like receptor 3 (TLR3) in IAV infection: Mock (n = 6; 3 males and 3 females), IAV (n = 6; 3 males and 3 females), and TLR3 inhibitor (n = 6; 3 males and 3 females). Body weight was measured on days 0, 3, and 5 after infection. On day 5, lung tissues were collected to assess viral load and histopathological changes. Key targets were examined using enzyme-linked immunosorbent assay, Western blotting, and immunofluorescence staining, both in sera and lung tissues. Results: IAV infection was significantly associated with dysregulation of the immune-inflammation system, such as the LTR, nucle-otide-binding oligomerization domain-(NOD) like receptor, retinoic acid-inducible gene I-like receptor, and nuclear factor kappa-B signaling pathways. Gene set enrichment analysis further indicated that the TLR and necroptosis signaling pathways played crucial roles in the progression of IAV infection (TLR signaling pathway normalized enrichment score = 2.3941, P = 1.00 × 10 ⁻¹⁰; necroptosis normalized enrichment score = 1.9421, P = 6.21 × 10 ⁻⁷). Among the core targets, TLR3 and mixed lineage kinase domain-like protein (MLKL) may regulate gene expression at the transcriptional level (all P < 0.05). In vivo validation using an IAV (PR8) infected acute lung injury mouse model demonstrated increased viral load and lung index, alveolar structural damage, and inflammatory cell infiltration. Immunofluorescence staining exhibited large gaps in Lamin B1 staining and breaches in Emerin signals following IAV-PR8 infection. Expression levels of TLR3, p-receptor-interacting serine/threonine-protein kinase 3 (RIPK3)/RIPK3, and p-mixed lineage kinase domain-like protein (MLKL)/MLKL proteins in lung tissues, as well as proinflammatory factors and mediators in sera, were significantly elevated after IAV infection. Moreover, enhanced neutrophil infiltration (myeloperoxidase) and citrullinated histone H3 (a neutrophil extracellular trap-specific marker), both established indicators of neutrophil extracellular trap formation, were observed. Notably, treatment with a TLR3 inhibitor significantly ameliorated IAV-induced acute lung injury by regulating necroptosis-related targets. Conclusion: Our study provides network-based in vivo evidence that TLR3-receptor-interacting serine/threonine-protein kinase 3-MLKL-mediated necroptosis may underlie IAV-induced acute lung injury and could serve as a potential therapeutic target in severe influenza cases.

Objective: To develop a convenient, direct, and highly sensitive method for screening trace chemical additives in complex Chinese patent medicines, thereby addressing core technological bottlenecks in pharmaceutical analysis and quality control. Methods: A brush ionization probe device was independently designed and constructed, and an efficient detection method was established through systematic optimization of key parameters. Twenty-three Chinese patent medicine samples, representing 6 dosage forms (capsules, tablets, pills, granules, powders, and liquid preparations), were analyzed using 10 common chemical additives as target analytes. Results: All samples were successfully analyzed without complex pretreatment, and 5 chemical additives were detected in 7 Chinese patent medicines. The brush ionization probe device exhibited cost-effectiveness (~0.2 USD per probe), operational simplicity, rapid analysis (~10s per sample), high efficiency, and minimal reagent consumption (~10 μL per sample). Conclusion: This advancement is expected to provide an innovative scientific tool for improving the generality and convenience of on-site quality control, while promoting technological progress in disciplines such as pharmacology and traditional Chinese medicine.

Objective: To understand the current status of short video addiction among vocational nursing students in higher vocational colleges (hereinafter referred to as "nursing students") and its related factors, so as to provide a reference for formulating online education programs in colleges. Methods: From March to May 2025, a stratified random sample of 2 223 nursing students from four vocational colleges in Henan Province was selected. Short Video Addiction Scale for College Students, Short form Egna Minnen av Barndoms Uppfostran for Chinese, Peer Rejection Scale, and University of California at Los Angels Loneliness Scale were used for investigation. Chi square test and multivariate Logistic regression analysis were used to explore the related factors of short video addiction among nursing students. Results: The detection rate of short video addiction of higher vocational nursing students was 26.95%, and the scores for avoidance, loss of control, inefficiency and withdrawal were (8.05±2.97) (10.24±3.09) (4.99±1.88) and (11.97±4.10), respectively. Multivariate Logistic regression analysis showed that sophomore year 2 ( OR=1.83, 95%CI =1.39-2.40), higher maternal education level (secondary school/vocational college: OR =1.34, 95% CI =1.06-1.68; college/undergraduate: OR =1.38, 95% CI =1.05-1.82), paternal overprotection ( OR=1.59, 95%CI =1.27-2.00), high peer rejection ( OR=1.40, 95%CI =1.19-1.66), and strong loneliness ( OR=1.57, 95%CI =1.07-2.28) were associated with a higher risk of short video addiction among nursing students (all P <0.05). Paternal affectionate and warm rearing style ( OR=0.82, 95%CI = 0.71- 0.95) was associated with a lower risk of short video addiction ( P <0.05). Conclusions The detection rate of short video addiction among nursing students is relatively high. Short video addiction is related to the nursing students grade, maternal education level, paternal overprotection and affectionate rearing style, peer rejection, and loneliness.

Hydrogenases, as a class of highly efficient and reversible biological catalysts, can catalyze the reduction of protons to molecular hydrogen, thus demonstrating great potential in a wide range of fields such as renewable energy production and green chemistry. Despite their significant potential, the large-scale industrial application of hydrogenases has long been constrained by several inherent limitations, including high sensitivity to molecular oxygen, the challenges in the in vitro reconstitution and maturation of their catalytic centers, and the inefficiency and instability of the natural electron transfer pathways. To overcome these limitations and enhance the catalytic performance of hydrogenases, researchers have developed various strategies, among which enzyme molecular engineering, photo-driven modification, and enzyme immobilization techniques are the most common exploration directions. Particularly, enzyme immobilization technology is widely used to improve the reusability of hydrogenases, but traditional immobilization methods often come with disadvantages in practical applications, such as complex multi-step procedures and insufficient biocompatibility of the immobilization materials. In recent years, bioencapsulation technology has emerged as a promising alternative strategy to enhance the catalytic performance of hydrogenases. This method utilizes biologically derived encapsulation materials to construct physically confined and precisely defined chemical microenvironments around the enzyme molecules, offering simpler self-assembly processes and superior biocompatibility. With these biomimetic constructs, bioencapsulation technology not only provides better oxygen tolerance but also helps to create a local microenvironment conducive to sustained catalytic function. This article systematically reviews the latest research progress of two main bioencapsulation strategies for hydrogenases: one is the encapsulation technology based on protein-based nanocages; the other is the engineering strategy for whole-cell hydrogenase expression. In the nanocage-based systems, this article focuses on the structural and functional characteristics of virus-like capsids and carboxysome protein shells, which serve as efficient enzyme encapsulation scaffolds, not only providing a stable physical barrier to prevent oxygen diffusion but also enabling high-density enzyme loading, thereby promoting substrate channeling effects and electron transfer kinetics. This article also discusses whole-cell encapsulation systems, which achieve hydrogenase compartmentalization within engineered cellular structures or by using external natural polysaccharide-based encapsulation matrices to wrap whole-cell catalysts. Bioencapsulation strategies can bring multiple synergistic benefits: they can effectively protect hydrogenases from oxygen-mediated inactivation, significantly delay the decline of catalytic activity over time, and enhance the hydrogen production rate by increasing the local concentration of active enzyme molecules and optimizing the electron transfer efficiency from redox partners to the catalytic center.Despite the significant progress made, several technical challenges remain to be addressed. The main obstacles include limited enzyme loading and encapsulation efficiency, insufficient long-term stability of encapsulation materials under operating conditions, and the need to improve the matching of the photo-biological interface in systems integrating light-harvesting components with enzymatic catalysis. Future efforts can focus on the integration of multiple technological approaches, such as using computer-aided protein design to optimize encapsulation structures, developing engineered electron transfer pathways to enhance catalytic conversion efficiency, and designing composite multifunctional materials with both structural stability and functional adaptability. These directions collectively aim to achieve efficient, stable, and scalable hydrogen production applications of bioencapsulated hydrogenase systems.

ObjectiveMitochondria are not only the central organelles responsible for cellular energy metabolism but also play essential roles in regulating cell cycle progression and cytoskeletal dynamics. In recent years, accumulating evidence has demonstrated that mitochondrial homeostasis is closely associated with mitotic progression and cytokinesis. Schizosaccharomyces pombe serves as a classical and well-established model organism. Because its cell cycle regulatory mechanisms are highly conserved throughout evolution, its genetic background is clearly defined, and experimental manipulation is efficient and convenient, it has been extensively applied in studies of cell growth, division, and reproductive mechanisms. The SPBC1604.04 gene encodes a previously uncharacterized mitochondrial carrier protein in Schizosaccharomyces pombe. This gene is located on chromosome II and spans 1 018 base pairs in length. It encodes a protein consisting of 238 amino acids with a predicted molecular mass of approximately 31.03 ku. Bioinformatic analysis predicts that this protein is responsible for the transport of thiamine pyrophosphate (TPP) into mitochondria. However, the effects of SPBC1604.04 gene deletion on mitotic cell dynamics under different temperature conditions have not been fully elucidated. MethodsThe SPBC1604.04 deletion strain of Schizosaccharomyces pombe was used as the experimental model. Fluorescent protein markers were constructed in the deletion background to label mitochondria, microtubules, actin, myosin, the nuclear envelope, and chromosomes. Live-cell imaging was performed using a TCS-SP8 laser scanning confocal microscope under normal temperature conditions (25℃) and heat stress conditions (37℃). Time-lapse microscopy was applied to dynamically monitor mitochondrial morphology and distribution, spindle assembly and elongation, chromosome segregation, as well as the formation and constriction of the actomyosin ring during cytokinesis. ImageJ software was used for quantitative measurements, including microtubule length during mitosis, spindle length at different mitotic stages, mitochondrial fluorescence intensity as an indicator of mitochondrial content, actomyosin ring length, nuclear envelope area, and chromosome segregation timing. Statistical analyses were conducted to compare phenotypic differences between the wild-type and SPBC1604.04 deletion strains at both temperature conditions. Through these analyses, we systematically investigated the impact of SPBC1604.04 deletion on mitotic cell dynamics in fission yeast under both normal physiological conditions and temperature stress. ResultsAt 25℃, compared with wild-type cells, the SPBC1604.04Δ strain exhibited a pronounced tendency toward mitochondrial fragmentation, accompanied by abnormal mitochondrial content and a significant reduction in mitochondrial fluorescence intensity. These observations suggest impaired mitochondrial homeostasis under normal growth conditions. In addition, the constriction time of actomyosin ring during cytokinesis was markedly prolonged, indicating that deletion of SPBC1604.04 affects the dynamics of the contractile machinery. However, no obvious defects were observed in spindle assembly, spindle elongation, or chromosome segregation. Under heat stress at 37℃, mitochondrial morphology in the SPBC1604.04Δ strain showed a tendency to recover toward a continuous tubular network structure. Mitochondrial content was restored, fluorescence intensity increased, and the constriction time of the actomyosin ring returned to levels comparable to those of wild-type cells. These results indicate that the mitotic defects observed at normal temperature are partially or fully alleviated under heat stress conditions. ConclusionThis study demonstrates that deletion of the SPBC1604.04 gene leads to abnormal mitochondrial content in Schizosaccharomyces pombe. The mitochondrial carrier protein SPBC1604.04 participates in regulating actomyosin ring constriction during mitosis but does not appear to be directly involved in the regulation of spindle dynamics or chromosome segregation. Our findings provide key experimental evidence for understanding the functional link between the SPBC1604.04 gene, mitochondrial homeostasis, and mitotic regulation.

Hydrogenases, as a class of highly efficient and reversible biological catalysts, can catalyze the reduction of protons to molecular hydrogen, thus demonstrating great potential in a wide range of fields such as renewable energy production and green chemistry. Despite their significant potential, the large-scale industrial application of hydrogenases has long been constrained by several inherent limitations, including high sensitivity to molecular oxygen, the challenges in the in vitro reconstitution and maturation of their catalytic centers, and the inefficiency and instability of the natural electron transfer pathways. To overcome these limitations and enhance the catalytic performance of hydrogenases, researchers have developed various strategies, among which enzyme molecular engineering, photo-driven modification, and enzyme immobilization techniques are the most common exploration directions. Particularly, enzyme immobilization technology is widely used to improve the reusability of hydrogenases, but traditional immobilization methods often come with disadvantages in practical applications, such as complex multi-step procedures and insufficient biocompatibility of the immobilization materials. In recent years, bioencapsulation technology has emerged as a promising alternative strategy to enhance the catalytic performance of hydrogenases. This method utilizes biologically derived encapsulation materials to construct physically confined and precisely defined chemical microenvironments around the enzyme molecules, offering simpler self-assembly processes and superior biocompatibility. With these biomimetic constructs, bioencapsulation technology not only provides better oxygen tolerance but also helps to create a local microenvironment conducive to sustained catalytic function. This article systematically reviews the latest research progress of two main bioencapsulation strategies for hydrogenases: one is the encapsulation technology based on protein-based nanocages; the other is the engineering strategy for whole-cell hydrogenase expression. In the nanocage-based systems, this article focuses on the structural and functional characteristics of virus-like capsids and carboxysome protein shells, which serve as efficient enzyme encapsulation scaffolds, not only providing a stable physical barrier to prevent oxygen diffusion but also enabling high-density enzyme loading, thereby promoting substrate channeling effects and electron transfer kinetics. This article also discusses whole-cell encapsulation systems, which achieve hydrogenase compartmentalization within engineered cellular structures or by using external natural polysaccharide-based encapsulation matrices to wrap whole-cell catalysts. Bioencapsulation strategies can bring multiple synergistic benefits: they can effectively protect hydrogenases from oxygen-mediated inactivation, significantly delay the decline of catalytic activity over time, and enhance the hydrogen production rate by increasing the local concentration of active enzyme molecules and optimizing the electron transfer efficiency from redox partners to the catalytic center.Despite the significant progress made, several technical challenges remain to be addressed. The main obstacles include limited enzyme loading and encapsulation efficiency, insufficient long-term stability of encapsulation materials under operating conditions, and the need to improve the matching of the photo-biological interface in systems integrating light-harvesting components with enzymatic catalysis. Future efforts can focus on the integration of multiple technological approaches, such as using computer-aided protein design to optimize encapsulation structures, developing engineered electron transfer pathways to enhance catalytic conversion efficiency, and designing composite multifunctional materials with both structural stability and functional adaptability. These directions collectively aim to achieve efficient, stable, and scalable hydrogen production applications of bioencapsulated hydrogenase systems.

ObjectiveMitochondria are not only the central organelles responsible for cellular energy metabolism but also play essential roles in regulating cell cycle progression and cytoskeletal dynamics. In recent years, accumulating evidence has demonstrated that mitochondrial homeostasis is closely associated with mitotic progression and cytokinesis. Schizosaccharomyces pombe serves as a classical and well-established model organism. Because its cell cycle regulatory mechanisms are highly conserved throughout evolution, its genetic background is clearly defined, and experimental manipulation is efficient and convenient, it has been extensively applied in studies of cell growth, division, and reproductive mechanisms. The SPBC1604.04 gene encodes a previously uncharacterized mitochondrial carrier protein in Schizosaccharomyces pombe. This gene is located on chromosome II and spans 1 018 base pairs in length. It encodes a protein consisting of 238 amino acids with a predicted molecular mass of approximately 31.03 ku. Bioinformatic analysis predicts that this protein is responsible for the transport of thiamine pyrophosphate (TPP) into mitochondria. However, the effects of SPBC1604.04 gene deletion on mitotic cell dynamics under different temperature conditions have not been fully elucidated. MethodsThe SPBC1604.04 deletion strain of Schizosaccharomyces pombe was used as the experimental model. Fluorescent protein markers were constructed in the deletion background to label mitochondria, microtubules, actin, myosin, the nuclear envelope, and chromosomes. Live-cell imaging was performed using a TCS-SP8 laser scanning confocal microscope under normal temperature conditions (25℃) and heat stress conditions (37℃). Time-lapse microscopy was applied to dynamically monitor mitochondrial morphology and distribution, spindle assembly and elongation, chromosome segregation, as well as the formation and constriction of the actomyosin ring during cytokinesis. ImageJ software was used for quantitative measurements, including microtubule length during mitosis, spindle length at different mitotic stages, mitochondrial fluorescence intensity as an indicator of mitochondrial content, actomyosin ring length, nuclear envelope area, and chromosome segregation timing. Statistical analyses were conducted to compare phenotypic differences between the wild-type and SPBC1604.04 deletion strains at both temperature conditions. Through these analyses, we systematically investigated the impact of SPBC1604.04 deletion on mitotic cell dynamics in fission yeast under both normal physiological conditions and temperature stress. ResultsAt 25℃, compared with wild-type cells, the SPBC1604.04Δ strain exhibited a pronounced tendency toward mitochondrial fragmentation, accompanied by abnormal mitochondrial content and a significant reduction in mitochondrial fluorescence intensity. These observations suggest impaired mitochondrial homeostasis under normal growth conditions. In addition, the constriction time of actomyosin ring during cytokinesis was markedly prolonged, indicating that deletion of SPBC1604.04 affects the dynamics of the contractile machinery. However, no obvious defects were observed in spindle assembly, spindle elongation, or chromosome segregation. Under heat stress at 37℃, mitochondrial morphology in the SPBC1604.04Δ strain showed a tendency to recover toward a continuous tubular network structure. Mitochondrial content was restored, fluorescence intensity increased, and the constriction time of the actomyosin ring returned to levels comparable to those of wild-type cells. These results indicate that the mitotic defects observed at normal temperature are partially or fully alleviated under heat stress conditions. ConclusionThis study demonstrates that deletion of the SPBC1604.04 gene leads to abnormal mitochondrial content in Schizosaccharomyces pombe. The mitochondrial carrier protein SPBC1604.04 participates in regulating actomyosin ring constriction during mitosis but does not appear to be directly involved in the regulation of spindle dynamics or chromosome segregation. Our findings provide key experimental evidence for understanding the functional link between the SPBC1604.04 gene, mitochondrial homeostasis, and mitotic regulation.

Purpose: Due to the preservation of the entire stomach after endoscopic resection, the occurrence of metachronous gastric cancer (MGC) remains a possibility. In this study, we investigated the incidence and risk factors for MGC in patients with early gastric cancer who underwent endoscopic submucosal dissection (ESD) and successfully eradicatedHelicobacter pylori. Materials and Methods: A retrospective analysis was conducted of 1,191 patients who underwent ESD and successfully eradicated H. pylori at the Affiliated Drum Tower Hospital of Nanjing University. Endoscopic surveillance was performed at 3, 6, and 12 months post-resection, and annually thereafter. MGC was defined as the development of a new cancer at a site other than the primary gastric cancer site, at least 1 year after the initial endoscopic resection. Results: A total of 77 patients were diagnosed with MGC during a median follow-up of 41.5 months. Kaplan-Meier analysis showed a 5-year cumulative incidence of MGC of 9.4% after successful H. pylori eradication. Multivariate analysis of the training set using Cox proportional hazards models identified male sex, severe atrophic gastritis, multiple gastric cancers before H. pylori eradication, and smoking history as independent risk factors for MGC.The nomogram exhibited favorable discrimination, with area under the curves of 0.767 and 0.822 in the training set and 0.724 and 0.745 in the testing set at 3 and 5 years, respectively. Conclusions Patients with gastric cancer who undergo endoscopic resection, even after successful H. pylori eradication, should undergo annual and continuous endoscopic surveillance for MGC.

Background Methicillin-resistant Staphylococcus aureus (MRSA) is an important pathogen for both human bloodstream infections and mastitis in cows. However, little attention has been paid to the cross-host transmission of MRSA from cows to high-risk groups in China. Objective To determine the MRSA colonization rates among dairy cows and dairy farm workers in Xinjiang, identify the antibiotic resistance profiles and molecular characteristics of the isolates, and provide scientific evidence for the formulation of targeted infection control strategies. Method A cross-sectional survey combined with laboratory pathogen analysis was conducted. From June to August 2024, large-scale dairy farms in Xinjiang region were selected as study sites. Nasal swabs (n=96) and skin swabs (n=39) were collected from workers, and bovine nasal swab samples (n=109) were collected simultaneously. All samples were subjected to MRSA isolation, cultivation, and identification, followed by antibiotic susceptibility testing to characterize resistance phenotypes. Staphylococcus aureus protein A (Spa) typing was performed to determine strain genotypes and elucidate MRSA colonization rates and molecular epidemiological patterns. Results A total of 35 MRSA strains was successfully isolated from 244 samples. The MRSA colonization rates among dairy farm workers and dairy cows were 20.83% (20/96) and 12.84% (14/109), respectively, with an overall isolation rate of 14.34% (35/244). Among the workers, the nasal colonization rate was 16.67% (16/96), and the skin colonization rate was 12.82% (5/39). One worker exhibited MRSA colonization at multiple body sites. All MRSA strains were resistant to cefoxitin (100%, 35/35). The resistance rates to erythromycin and clindamycin were 42.86% (15/35) and 34.29% (12/35), respectively. Thirteen strains showed a multidrug-resistant phenotype, whereas all strains were susceptible to vancomycin. The MRSA isolates exhibited high genetic diversity, with 13 Spa types identified, among which t441 was the most prevalent (8 strains). Both t441 and t034 types were detected in samples from both the dairy cows and their handlers. These two Spa types also carried and stably inherited specific resistance combinations, including erythromycin–clindamycin–cefoxitin and ciprofloxacin–erythromycin–clindamycin–gentamicin–cefoxitin–tetracycline, and a statistically significant association was also observed between the two resistance profiles and the bacterial types (P < 0.001). In addition, one novel Spa type strain was identified. Conclusion MRSA colonization rates among dairy cows and dairy farm workers in Xinjiang are relatively high, with evidence of multi-site colonization. The isolates exhibit high levels of multidrug resistance and genetic diversity, indicating a potential risk of cross-host transmission.

OBJECTIVE To explore the effects of the Jianpi huatan formula （JPHTF） on polycystic ovary syndrome （PCOS） in rats by regulating the high mobility group box 1 protein （HMGB1）/receptor for advanced glycation end products （RAGE） signaling pathway. METHODS The rats were randomly divided into the normal （Con） group， the PCOS group， the JPHTF-L group （5.54 g/kg）， the JPHTF-H group （11.07 g/kg）， the JPHTF-H+rHMGB1 group （11.07 g/kg of JPHTF+8 μg/kg of rHMGB1）， and metformin group （0.27 g/kg）， with 12 rats in each group. Except for the rats of Con group， which were given 1% sodium carboxymethyl cellulose intragastrically and fed with normal chow， the remaining rats were induced to develop PCOS models by using a high-fat diet combined with letrozole. Af ter successful modeling， rats in each drug group were administered the corresponding drugs by gavage or tail vein injection once a day for 4 consecutive weeks. 24 h after the intervention， body weight and ovarian coefficient were detected. The levels of fasting blood glucose （FBG）， serum levels of fasting insulin （FINS）， follicle stimulating hormone （FSH）， luteinizing hormone （LH）， testosterone （T） and estradiol （E 2 ） were detected. The homeostasis model assessment of insulin resistance （HOMA-IR） was calculated. The levels of tumor necrosis factor-α （TNF-α）， interleukin-18 （IL-18） and IL-1β and the protein expressions of HMGB1， RAGE， phosphorylated nuclear factor-κB （p-NF-κB） and NF-κB in the ovarian tissues of rats were detected. The morphology of ovarian tissue was observed， and the numbers of cystic follicles and corpora lutea were counted. RESULTS Compared with PCOS group， polycystic changes of ovarian tissue in rats showed varying degrees of improvement in the JPHTF-L group， JPHTF-H group， and metformin group； body weight， ovarian coefficient， FBG， the number of cystic follicles， serum levels of FINS， HOMA-IR， T， LH， LH/FSH， the levels of TNF-α， IL-18 and IL-1β and protein expressions of HMGB1 and RAGE in ovarian tissue as well as phosphorylation level of NF-κB protein all significantly decreased； the number of corpora lutea and the serum levels of E 2 and FSH significantly increased （ P ＜0.05）. Compared with JPHTF-H group， above indexes of rats were reversed significantly in JPHTF-H+rHMGB1 group （ P ＜0.05）. CONCLUSIONS JPHTF can reduce the inflammatory response in PCOS rats， mitigate ovarian injury， regulate hormone balance， and improve insulin resistance and follicular development by inhibiting the HMGB1/RAGE signaling pathway.