Highly variable magmatic accretion at the ultraslow-spreading Gakkel Ridge.

Crustal accretion at mid-ocean ridges governs the creation and evolution of the oceanic lithosphere. Generally accepted models1-4 of passive mantle upwelling and melting predict notably decreased crustal thickness at a spreading rate of less than 20 mm year-1. We conducted the first, to our knowledge, high-resolution ocean-bottom seismometer (OBS) experiment at the Gakkel Ridge in the Arctic Ocean and imaged the crustal structure of the slowest-spreading ridge on the Earth. Unexpectedly, we find that crustal thickness ranges between 3.3 km and 8.9 km along the ridge axis and it increased from about 4.5 km to about 7.5 km over the past 5 Myr in an across-axis profile. The highly variable crustal thickness and relatively large average value does not align with the prediction of passive mantle upwelling models. Instead, it can be explained by a model of buoyant active mantle flow driven by thermal and compositional density changes owing to melt extraction. The influence of active versus passive upwelling is predicted to increase with decreasing spreading rate. The process of active mantle upwelling is anticipated to be primarily influenced by mantle temperature and composition. This implies that the observed variability in crustal accretion, which includes notably varied crustal thickness, is probably an inherent characteristic of ultraslow-spreading ridges.

Dysregulated RNA editing of EIF2AK2 in polycystic ovary syndrome: clinical relevance and functional implications.

BACKGROUND: Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder affecting women of reproductive ages. Our previous study has implicated a possible link between RNA editing and PCOS, yet the actual role of RNA editing, its association with clinical features, and the underlying mechanisms remain unclear. METHODS: Ten RNA-Seq datasets containing 269 samples of multiple tissue types, including granulosa cells, T helper cells, placenta, oocyte, endometrial stromal cells, endometrium, and adipose tissues, were retrieved from public databases. Peripheral blood samples were collected from twelve PCOS and ten controls and subjected to RNA-Seq. Transcriptome-wide RNA-Seq data analysis was conducted to identify differential RNA editing (DRE) between PCOS and controls. The functional significance of DRE was evaluated by luciferase reporter assays and overexpression in human HEK293T cells. Dehydroepiandrosterone and lipopolysaccharide were used to stimulate human KGN granulosa cells to evaluate gene expression. RESULTS: RNA editing dysregulations across multiple tissues were found to be associated with PCOS in public datasets. Peripheral blood transcriptome analysis revealed 798 DRE events associated with PCOS. Through weighted gene co-expression network analysis, our results revealed a set of hub DRE events in PCOS blood. A DRE event in the eukaryotic translation initiation factor 2-alpha kinase 2 (EIF2AK2:chr2:37,100,559) was associated with PCOS clinical features such as luteinizing hormone (LH) and the ratio of LH over follicle-stimulating hormone. Luciferase assays, overexpression, and knockout of RNA editing enzyme adenosine deaminase RNA specific (ADAR) showed that the ADAR-mediated editing cis-regulated EIF2AK2 expression. EIAF2AK2 showed a higher expression after dehydroepiandrosterone and lipopolysaccharide stimulation, triggering changes in the downstrean MAPK pathway. CONCLUSIONS: Our study presented the first evidence of cross-tissue RNA editing dysregulation in PCOS and its clinical associations. The dysregulation of RNA editing mediated by ADAR and the disrupted target EIF2AK2 may contribute to PCOS development via the MPAK pathway, underlining such epigenetic mechanisms in the disease.

A functional mechanism for a non-coding variant near AGTR2 associated with risk for preterm birth.

BACKGROUND: Preterm birth (PTB), defined as delivery before 37 gestational weeks, imposes significant public health burdens. A recent maternal genome-wide association study of spontaneous PTB identified a noncoding locus near the angiotensin II receptor type 2 (AGTR2) gene. Genotype-Tissue Expression data revealed that alleles associated with decreased AGTR2 expression in the uterus were linked to an increased risk of PTB and shortened gestational duration. We hypothesized that a causative variant in this locus modifies AGTR2 expression by altering transcription factor (TF) binding. METHODS: To investigate this hypothesis, we performed bioinformatics analyses and functional characterizations at the implicated locus. Potential causal single nucleotide polymorphisms (SNPs) were prioritized, and allele-dependent binding of TFs was predicted. Reporter assays were employed to assess the enhancer activity of the top PTB-associated non-coding variant, rs7889204, and its impact on TF binding. RESULTS: Our analyses revealed that rs7889204, a top PTB-associated non-coding genetic variant is one of the strongest eQTLs for the AGTR2 gene in uterine tissue samples. We observed differential binding of CEBPB (CCAAT enhancer binding protein beta) and HOXA10 (homeobox A10) to the alleles of rs7889204. Reporter assays demonstrated decreased enhancer activity for the rs7889204 risk "C" allele. CONCLUSION: Collectively, these results demonstrate that decreased AGTR2 expression caused by reduced transcription factor binding increases the risk for PTB and suggest that enhancing AGTR2 activity may be a preventative measure in reducing PTB risk.

Bio-based Carbon dots Loaded with 5-Fu: A Multifunctional drug Delivery System.

In the present work, a simple and efficient stirring method was used to successfully synthesize a novel multifunctional carbon dots-drug delivery system AMP-CDs@5-Fu in the form of intertwined filaments. The results showed that AMP-CDs@5-Fu had the highest final release in the medium mimicking the physiological environment of the human small intestine compared to that of 5-Fu and that the drug release behaviors followed a zero-grade drug release within the first 3 h. The results also showed that AMP-CDs@5-Fu could be used to reduce the toxicity of 5-Fu while significantly improving the anticancer ability. In vitro hemolysis and anticancer assays showed that AMP-CDs@5-Fu could significantly improve the anticancer ability while decreasing the toxicity of 5-Fu, and the hemolysis rate of AMP-CDs@5-Fu was significantly lower than that of 5-Fu; their IC50 against 4T1 cancer cells were 201.63 ± 8.94 µg 5-Fu/mL and 241.24 ± 11.05 µg 5- Fu/mL. In addition, AMP-CDs@5-Fu allowed clear cell imaging. Therefore, AMP-CDs@5-Fu is expected to improve the bioavailability of 5-Fu as a novel oral agent with fluorescent properties and very promising as a novel fluorescence tracking drug loading system, which is expected to be used in the field of anticancer targeted therapy and fluorescence tracking to monitor the distribution of drugs.

Synthesis, characterization, biological activity, and in vitro digestion of selenium nanoparticles stabilized by Antarctic ice microalgae polypeptide.

A new type of uniformly dispersed selenium nanoparticles (SeNPs) was prepared using Antarctic ice microalgae polypeptides (AIMP) as the stabilizer and dispersant. Different characterization techniques and tests show that the SeNPs are effectively combined with AIMP through physical adsorption and hydrogen bonding to form a more stable structure. Orange-red, zero-valence, amorphous, and spherical AIMP-SeNPs with a diameter of 52.07 ± 1.011 nm and a zeta potential of -41.41 ± 0.882 mV were successfully prepared under the optimal conditions. The AIMP-SeNPs had significantly higher DPPH, ABTS and hydroxyl radicals scavenging abilities compared with AIMP and Na2SeO3, and prevented the growth of both Gram-negative and Gram-positive bacteria by disrupting the integrity of cell walls, cell membranes and mitochondrial membranes. The AIMP-SeNPs had higher gastrointestinal stability compared with SeNPs. Thus, this research highlights the crucial role of AIMP as a biopolymer framework in the dispersion, stabilization, and size management of SeNPs and concludes that AIMP-SeNPs can be exploited as a potent antioxidant supplement and antibacterial substance in foods and medicine.

Effect of Ultrasonic Treatment on Structure, Antibacterial Activity of Sugarcane Leaf Polysaccharides.

This study investigated the impact of ultrasonic extraction (UE) on the structure and in vitro antibacterial activity of polysaccharides from sugarcane leaves (SLW). Native sugarcane leaf polysaccharides were treated with ultrasound (480 W) for 3 h to yield sugarcane leaf polysaccharides (SLU). Compared to SLW (33.59 kDa), the molecular weight of SLU (13.08 kDa) was significantly decreased, while the monosaccharide composition of SLU was unchanged. The results of SEM and XRD indicated that UE significantly changed the surface morphology of SLW and destroyed its inner crystalline structure. In vitro experiments showed that SLU had stronger antibacterial activity. These findings revealed that UE treatment could alter the tertiary structure of SLW but had no impact on its primary structure. Furthermore, the antibacterial activity of SLW could be greatly enhanced after UE treatment. As a bioactive additive, SLU has great application potential in functional foods, cosmetics, and pharmaceuticals.

IRAK1 Is a Critical Mediator of Inflammation-Induced Preterm Birth.

Preterm birth (PTB) is a major cause of neonatal mortality and morbidity, often triggered by chorioamnionitis or intrauterine inflammation (IUI) with or without infection. Recently, there has been a strong association of IL-1 with PTB. We hypothesized that IL-1R-associated kinase 1 (IRAK1), a key signaling mediator in the TLR/IL-1 pathway, plays a critical role in PTB. In human fetal membranes (FM) collected immediately after birth from women delivering preterm, p-IRAK1 was significantly increased in all the layers of FM with chorioamnionitis, compared with no-chorioamnionitis subjects. In a preterm rhesus macaque model of IUI given intra-amniotic LPS, induction of p-IRAK1 and downstream proinflammatory signaling mediators were seen in the FM. In a C57BL/6J wild-type PTB mouse model of IUI given intrauterine LPS, an IRAK1 inhibitor significantly decreased PTB and increased live birth in a dose-dependent manner. Furthermore, IRAK1 knockout mice were protected from LPS-induced PTB, which was seen in wild-type controls. Activation of IRAK1 was maintained by K63-mediated ubiquitination in preterm FM of humans with chorioamnionitis and rhesus and mouse IUI models. Mechanistically, IRAK1 induced PTB in the mouse model of IUI by upregulating expression of COX-2. Thus, our data from human, rhesus, and mouse demonstrates a critical role IRAK1 in IUI and inflammation-associated PTB and suggest it as potential therapeutic target in IUI-induced PTB.

A single blood sample for stimulated LH assayed by ICMA is useful for monitoring the treatment efficacy of triptorelin depot in girls.

BACKGROUND: There is still no consensus on the optimal monitoring method to evaluate the hypothalamic-pituitary-gonadal axis (HPGA) inhibition. METHODS: There were 124 girls treated with triptorelin depot due to puberty disorders, including 77 central precocious puberty and 47 early puberty. After treatment, triptorelin stimulation tests were performed, and blood samples were collected at 0, 20, 40 and 60 min. Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured by immunochemiluminometric assay (ICMA). RESULTS: Peak LH (PLH), peak FSH and estradiol in 124 girls were significantly decreased after treatment, while 2 cases had inadequate treatment efficacy. Areas under the receiver operating characteristic curves (AUC) of PLH and peak FSH after stimulation for the diagnosis of HPGA suppression were 0.984 and 0.121. When the cut-off value of PLH was ≤ 2.25 IU/L, the sensitivity was 96.7% and specificity was 100.0%. There was no difference in AUC between PLH and a single LH at 20, 40, or 60 min (p > 0.05). When LH were ≤ 2.34 IU/L, ≤ 2.21 IU/L and ≤ 2.00 IU/L at 20, 40 and 60 min, respectively, the sensitivity were 99.1%, 96.7% and 98.4%, and the specificity were all 100.0%. The correlation coefficients between PLH and LH at 20, 40 or 60 min were 0.947, 0.975 and 0.961. CONCLUSION: A single blood sample for stimulated LH at 20 min, 40 min, or 60 min assayed by ICMA during triptorelin stimulation test is useful for monitoring the treatment efficacy of triptorelin depot in girls with puberty disorders.

Inhibition of IRAK1 Ubiquitination Determines Glucocorticoid Sensitivity for TLR9-Induced Inflammation in Macrophages.

Inflammatory responses are controlled by signaling mediators that are regulated by various posttranslational modifications. Recently, transcription-independent functions for glucocorticoids (GC) in restraining inflammation have emerged, but the underlying mechanisms are unknown. In this study, we report that GC receptor (GR)-mediated actions of GC acutely suppress TLR9-induced inflammation via inhibition of IL-1R-associated kinase 1 (IRAK1) ubiquitination. ß-TrCP-IRAK1 interaction is required for K48-linked ubiquitination of IRAK1 at Lys134 and subsequent membrane-to-cytoplasm trafficking of IRAK1 interacting partners TNFR-associated factor 6 and TAK1 that facilitates NF-κB and MAPK activation. Upon costimulation of macrophages with GC and TLR9-engaging ligand, GR physically interacts with IRAK1 and interferes with protein-protein interactions between ß-TrCP and IRAK1. Ablation of GR in macrophages prevents GC-dependent suppression of ß-TrCP-IRAK1 interactions. This GC-mediated suppression of IRAK1 activation is unique to TLR9, as GC treatment impairs TLR9 but not TLR4 ligand-induced K48-linked IRAK1 ubiquitination and trafficking of IRAK1 interacting partners. Furthermore, mutations in IRAK1 at Lys134 prevent TLR9 ligand-induced activation of inflammatory signaling mediators and synthesis of proinflammatory cytokines to an extent comparable to GC-mediated inhibition. Collectively, these findings identify a transcription-independent, rapid, and nongenomic GC suppression of TLR9 ligand-mediated IRAK1 ubiquitination as a novel mechanism for restraining acute inflammatory reactions.

Electrically tuned whispering gallery mode microresonator based on Kagomé photonic crystal fibers infiltrated with nematic liquid crystals.

In this study, an electrically tunable whispering gallery mode (WGM) microresonator based on Kagomé hollow-core photonic crystal fiber (HC-PCF) is proposed by infiltrating the cross-sectional air holes with nematic liquid crystals (NLCs). Experimental results indicate that the LC molecules turn out in planar alignment. As the applied electric field strength gradually increases, the WGM resonance wavelengths shift toward the longer-wavelength region. The Freedericksz transition threshold of the proposed Kagomé HC-PCF microresonator is experimentally proved to be around 1.2 V µm-1. The electrically tunable microresonator, integrated with NLCs, is anticipated to find potential applications in optical filtering, all-optical switching, and electrically controlled micro-optics devices.

Serum microRNA181a: Correlates with the intracellular cytokine levels and a potential biomarker for acute graft-versus-host disease.

The aim of this study was to investigate the clinical relevance of lymphocyte-related serum miRNAs to the pathogenesis of acute graft-versus-host disease (aGVHD) and evaluate the predictive and prognosis value of miRNAs. Consecutive patients who received allogeneic peripheral blood stem cell transplantation (allo-PBSCT) in General Hospital of Jinan Military District were enrolled. aGVHD patients were diagnosed and graded clinically, and divided into the training set and the testing set. Blood samples were collected, total RNA was isolated, and RT-PCR was performed for miRNA expression (miR-181a-3p, miR-214-3p and miR-326). Intracellular cytokines levels were assayed by flow cytometry, and the disease specificity assay of miRNAs for aGVHD was detected. A total of 120 patients were admitted. Serum level of miR-181a in aGVHD patients was highly increased and associated with the severity of aGVHD, but not miR-214 and miR-326. Levels of cytokines including IL-2, IL-22, and IL-17a were positively correlated with miR-181a level, while serum IL-13 level was negatively correlated with miR-181a level in aGVHD patients. Moreover, increased miR-181a level was not detected in patients with acute rejection after kidney transplantation or sepsis patients. MiR-181a level was sensitively and specifically increased, especially in severe aGVHD patients. MiR-181a may be a potential biomarker for the identification, diagnosis, and prognosis of aGVHD patients.

Nanostructured lipid carriers as novel drug delivery system for lung cancer gene therapy.

CONTEXT: Nanostructured lipid carriers (NLC) are potentially good colloidal drug carriers for gene delivery. They are advised to be the second lifetime of lipid nanocarriers. OBJECTIVE: The aim of this study is to develop novel modified NLC as nanomedicine for delivery of plasmid-containing enhanced green fluorescence protein (pEGFP). This system could target the lung cancer cells through receptor-mediated pathways to increase the nuclear uptake of genetic materials. METHODS: In the present study, pEGFP-loaded NLC (NLC/pEGFP) were prepared. Transferrin (Tf) containing ligands were used for the surface coating of the vectors. In vitro transfection efficiency of the modified vectors was evaluated in human alveolar adenocarcinoma cell line (A549 cells) and in vivo transfection efficiency of the modified vectors was evaluated on mice bearing A549 cells model. RESULTS: Tf-modified NLC/pEGFP (Tf-NLC/pEGFP) has a particle size of 157 nm, and ∼ 82% of gene loading quantity. Tf-NLC/pEGFP displayed remarkably higher transfection efficiency than non-modified NLC/pEGFP both in vitro and in vivo. CONCLUSION: The results demonstrate that the novel NLC gene delivery system offers an effective strategy for lung cancer gene therapy.

Transforming growth factor-ß-activated kinase 1 resistance limits glucocorticoid responsiveness to Toll-like receptor 4-mediated inflammation.

Glucocorticoids (GC) are among the most effective anti-inflammatory drugs, but are often associated with serious adverse effects or inadequate therapeutic responses. Here, we use activation of different Toll-like receptors (TLRs) by their respective ligands to evaluate context-specific GC sensitivity in the macrophage. Recruitment and activation of transforming growth factor-ß-activated kinase 1 (TAK1), downstream of TLR engagement, is crucial in activating multiple inflammatory pathways, and contributes to inflammatory disorders. We hypothesize that GC exert anti-inflammatory effects through regulation of TAK1. Both in vivo and in vitro, in comparison to other TLRs, there was limited GC potency in restricting TLR4 ligand-mediated secretion of interleukin-6, tumour necrosis factor-α and interleukin-12. Also, we found that inactivation of TAK1 both in vivo and in vitro strongly inhibits TLR4-induced inflammation-associated genes beyond the suppressive effects from GC treatment. However, there was no effect of TAK1 inactivation on GC inhibition of TLR3- or TLR9-initiated inflammatory actions. Together, our findings demonstrate that GC resistance for TAK1 activation associated with TLR4 engagement may be an important contributor to GC resistance in inflammatory disorders.

Short communication: Study on the formation of 2-methylimidazole and 4-methylimidazole in the Maillard reaction.

2-Methylimidazole (2-MI) and 4-methylimidazole (4-MI) can be formed via the Maillard reaction during dairy thermal treatment. In this study, different reactions between α-dicarbonyl compounds (methylglyoxal, glyoxal) and aldehydes (formaldehyde, acetaldehyde) in the presence of ammonium sulfate were performed to investigate the formation of 2-MI and 4-MI. Two formation pathways of 2-MI and 4-MI were proposed. One pathway is that α-dicarbonyl compound reacts with equivalent ammonia to form an intermediate, while aldehyde reacts with equivalent ammonia to form another intermediate, then the 2 intermediates react together to generate 2-MI or 4-MI. Alternatively, α-dicarbonyl compound can react with double ammonia to form an intermediate, and subsequently reacts with aldehyde to form 2-MI or 4-MI. Additionally, possible mechanisms were also proposed to explain the phenomenon that the 2-MI content was much lower than 4-MI in Maillard reaction.

Assessment of the use of immunosuppressants combined with cord blood for severe aplastic anemia.

BACKGROUND: The objective of this study was two-fold: 1) to investigate the changes of cytokines concentration in relation to severe aplastic anemia (SAA) when treated with immunosuppressants combined with cord blood (IS + CBI). and 2) to assess the curative effect of umbilical cord blood chimerism engraftment. METHODS: We selected 43 patients with SAA all treated with IS + CBI (newly diagnosed group). Among them, a total of 33 patients were treated effectively (effective group) while 10 cases were treated invalidly (invalid group). An additional 20 healthy individuals were selected as control (control group). The expression levels of IL-17, IL-22 and other cytokines in each group were detected by ELISA. The engraftment of cord blood stem cells was detected by using short tandem repeat-polymerase chain reaction (STR-PCR). RESULTS: 1. IL-17, IL-22 and other cytokines expressions in the newly diagnosed group were significantly higher than in the control group. 2. After six months, the levels in the effective group were significantly lower than pre-therapy levels (P < 0.05). The levels in the invalid group did not differ to those observed prior treatment. 3. After one and three months of treatment, a small amount of engraftment was found in the effective group. However, after six months, transplant rejection was observed in all patients. No effective engraftment was observed in the invalid group. CONCLUSION: 1) Th17 and Th22 producing cells in SAA patients significantly increased indicating a positive correlation between these biomarkers and the progression of SAA. 2) During the IS + CBI treatment the maintenance of a normal hematopoietic function depended on immunesup-pressants. Early umbilical cord blood chimerism engraftment may promote hematopoietic recovery.

Increased immunosuppressive treatment combined with unrelated umbilical cord blood infusion in children with severe aplastic anemia.

A combination treatment of unrelated umbilical cord blood (UCB) and increased immunosuppressive treatment (IST) were investigated to reveal the potentially curative therapy for the severe aplastic anemia (SAA). A total of 36 children (2-17 ages) with SAA who received UCB infusion after an IST were analyzed. The treatment consisted of 100mg/kg cyclophosphamide, 12.5-15 mg/kg antithymocyte globulin and 3mg/kg cyclosporine. After 3 months, the hematologic complete response (CR) rate was 22.2% and partial response (PR) rate was 38.9%. After 6 months, the CR rate and PR rate was 50.4% and 26.3%, respectively. The probability of 3-year survival was 83.3%. There was no difference in the survival rate either between the horse-ATG and rabbit-ATG or between the SAA and VSAA. The results indicated that the increased IST combined with unrelated UCB infusion has an effective therapeutic potential for children with SAA who lack of compatible donor for transplantation.

Serum microRNA155 is increased in patients with acute graft-versus-host disease.

To explore the clinical relevance of three lymphocyte-related serum microRNAs (miR-155, miR-214, and miR-326) to the pathogenesis of graft-versus-host disease (GVHD), 64 subjects who received allogeneic peripheral blood stem cell transplantation (allo-PBSCT) were recruited in this study, of whom 19 subjects did not develop GVHD, 25 subjects were diagnosed with acute GVHD (aGVHD), and 20 subjects were diagnosed with chronic GVHD (cGVHD). Serum miRNAs were determined by real-time RT-PCR. Expression level of miRNAs and the expression signatures of miRNAs as a panel were analyzed among the three groups. The expression level of miR-214 and miR-326 showed no significant difference between GVHD and non-GVHD groups. However, miR-155 was significantly up-regulated in GVHD patients. There was a correlation between the level of miR-155 and the severity of aGVHD. Moreover, serum IFN-gamma, IL-17, and IL-9 levels were higher in aGVHD patients with high miR-155. In conclusion, the expression level of lymphocyte-related miR-155 in serum was significantly increased in aGVHD patients. The miR-155 may be considered as a potential targeted therapy for aGVHD patients.

A promising targeted gene delivery system: folate-modified dexamethasone-conjugated solid lipid nanoparticles.

CONTEXT: Non-viral gene delivery could deliver drugs/genes through cellular membranes and nuclear membranes by some modification of materials. OBJECTIVE: This study develops a kind of vector to target the cells through receptor-mediated pathways. Nuclear localization signal (NLS) was also used to increase the nuclear uptake of genetic materials. MATERIALS AND METHODS: A lipid containing dexamethasone (Dexa) was synthesized as the material of the preparation of solid lipid nanoparticles (SLNs) and folate (Fa)-conjugated PEG-PE (Fa-PEG-PE) ligands were used to modify the SLNs. The in vitro cytotoxicity of the carriers at various concentrations (10, 20, 50, 100, and 200 µg/ml) were evaluated in KB human carcinoma cells (KB cells). In vivo transfection efficiency of the novel modified vectors was evaluated in disseminated peritoneal tumors on mice bearing KB cells. RESULTS: Fa-PEG-PE modified SLNs/enhanced green fluorescence protein plasmid (pEGFP) has a particle size of 258 nm, and the gene loading quantity of the vector was 90%. The in vitro cytotoxicity of Fa-PEG-PE-modified SLNs/pEGFP (Fa-SLNs/pEGFP) was low (cell viabilities were between 80% and 100% compared with controls). Fa-SLNs/pEGFP displayed remarkably higher transfection efficiency (40%) than non-modified SLNs/pEGFP (24%) and the vectors not containing Dexa (30%) in vivo. CONCLUSION: The results demonstrate that Fa and Dexa could function as excellent active targeting ligands to improve the cell targeting and nuclear targeting ability of the carriers and the resulting vectors could be promising active targeting drug/gene delivery systems.

The Novel Insight of Gut Microbiota from Mouse Model to Clinical Patients and the Role of NF-κB Pathway in Polycystic Ovary Syndrome.

Polycystic Ovary Syndrome (PCOS) is a metabolic disorder characterized by hyperandrogenism and related symptoms in women of reproductive age. Emerging evidence suggests that chronic low-grade inflammation plays a significant role in the development of PCOS. The gut microbiota, a complex bacterial ecosystem, has been extensively studied for various diseases, including PCOS, while the underlying mechanisms are not fully understood. This review comprehensively summarizes the changes in gut microbiota and metabolites observed in PCOS and their potential association with the condition. Additionally, we discuss the role of abnormal nuclear factor κB signaling in the pathogenesis of PCOS. These findings offer valuable insights into the mechanisms of PCOS and may pave the way for the development of control and therapeutic strategies for this condition in clinical practice. By bridging the gap between mouse models and clinical patients, this review contributes to a better understanding of the interplay between gut microbiota and inflammation in PCOS, thus paving new ways for future investigations and interventions.