Objective To identify factors affecting and key environmental factors of the Oncomelania hupensis snail density in the Yangtze River Delta region using machine learning methods. Methods Administrative village-level O. hupensis snail survey data in the Yangtze River Delta (including Shanghai Municipality, Jiangsu Province, Zhejiang Province and Anhui Province) from 2011 to 2021 were retrieved from the Information Management System for Parasitic Disease Control of Chinese Center for Disease Control and Prevention. Environmental factor data were captured from the Google Earth Engine platform, including elevation, slope, terrain, normalized difference vegetation index (NDVI), vegetation type, soil type, total petroleum hydrocarbon (TPH), ammonium nitrogen, inorganic nitrogen, dissolved oxygen, pH of water, chemical oxygen demand (COD) and inorganic phosphorus, and climatic factor data in the study region were retrieved from the Copernicus Climate Data Store, including annual precipitation, aridity index and annual mean temperature (AMT). O. hupensis snail survey data in the Yangtze River Delta region from 2011 to 2021 were randomly divided into a training set (70%) and a test set (30%), and five machine learning models were selected for machine learning model construction and comparative analysis of the O. hupensis snail density using the software R 4.3.0, including random forest (RF), eXtreme gradient boosting (XGBoost), support vector machine (SVM), gradient boosting machine (GBM) and neural network (NN). The XGBoost model was employed to construct a predictive model for the O. hupensis snail density, and the impact of each environmental factor on O. hupensis snail distribution was quantified. The SHapley Additive exPlanations (SHAPs) values were calculated to estimate the average contribution of each variable to the model prediction, and the core environmental factors affecting the O. hupensis snail population density were screened. Results Among the five machine learning models, the XGBoost model exhibited the optimal comprehensive performance, with the coefficient of determination (R²) of 0.855, mean squared error (MSE) of 0.188, root mean squared error (RMSE) of 0.434 and mean absolute error (MAE) of 0.155, respectively. Analysis of factors affecting the O. hupensis snail density with the XGBoost model showed that among the 16 environmental factors, the top four high-impact factors ranked by SHAPs values included annual precipitation, elevation, aridity index and NDVI, with cumulative SHAPs contributions of 75%, which was higher than that of other environmental factors. If NDVI was higher than 0.6, the O. hupensis snail density increased with NDVI and peaked if NDVI was 0.8 (1.60 snails/0.1 m²). The O. hupensis snail density increased with elevation if the elevation ranged from 14 to 40 m, and slowly rose if the annual precipitation ranged from 900 to 1 300 mm, and then increased rapidly to the peak (1.52 snails/0.1 m²) if the annual precipitation ranged from 1 300 to 1 500 mm. In addition, the O. hupensis snail density increased rapidly to the maximum (1.60 snails/0.1 m²) if the aridity index ranged from 0.8 to 1.1, and decreased gradually if the aridity index exceeded 1.1. Conclusions The XGBoost model shows excellent performance in prediction of the O. hupensis snail density and identification of key environmental factors in the Yangtze River Delta region. Annual precipitation, elevation, aridity index and NDVI are key environmental factors affecting the distribution and density of O. hupensis snails in the Yangtze River Delta region.

Objective:To investigate the neurorestorative effect of basic fibroblast growth factor (bFGF) on neurological function recovery in rats with spinal cord injury and its potential mechanisms.Methods:Ninety adult SD rats were selected and randomly divided into 6 groups using a random number table: sham-operated group ( n=24), spinal cord injury group ( n=24), bFGF group ( n=24), bFGF autophagy pathway validation group ( n=6), bFGF+rapamycin group ( n=6), and bFGF+MHY1485 group ( n=6). A spinal cord injury model was established by impacting the T 10 spinal cord segment using a self-made Allen′s weight-drop impactor. The sham-operated group underwent a 3 cm midline dorsal incision without spinal cord injury; the bFGF group received immediate intrathecal injection of 100 μl bFGF solution (20 μg/L) after injury; the sham surgery group and spinal cord injury group received an equal volume of saline after injury; the bFGF autophagy pathway validation group received the identical treatment as the bFGF group; the bFGF+rapamycin group received the same treatment as the bFGF group with additional intraperitoneal injection of rapamycin (4 mg·kg -1·d -1); the bFGF+MHY1485 group received the identical bFGF treatment plus intraperitoneal injection of MHY1485 (10 mg·kg -1·d -1). At 28 days after injury, the rats were sacrificed and the spinal cord tissue was collected at 5 mm from the injury epicenter for HE staining and pathological observation. At 7, 14, 21, and 28 days after injury, BBB scoring was used to assess hindlimb motor function; P wave latency and P1-N1 wave amplitude were recorded to evaluate neuroelectrophysiological changes; Western blot analysis was performed to detect the expression levels of phosphorylated mammalian target of rapamycin (p-mTOR)/mammalian target of rapamycin (mTOR) and microtubule-associated protein light chain 3-II (LC3-II) and evaluate changes in mTOR signaling pathway and autophagy activity. At 28 days after injury, behavioral alterations, neuroelectrophysiological changes, and auctophagy-related protein expression levels were assessed in the bFGF autophagy pathyway validation group, bFGF+rapamycin group and bFGF+MHY1485 group. Results:At 28 days after injury, the sham-operated group exhibited regular nuclear morphology, while the spinal cord injury group showed disordered cell structures and the bFGF group displayed relatively normal nuclear morphology. At 7, 14, 21, and 28 days after injury, the BBB scores in both the spinal cord injury group and bFGF group were lower than those in the sham-operated group ( P<0.01), with higher scores in the bFGF group than those in the spinal cord injury group ( P<0.01). At 7, 14, 21, and 28 days after injury, P-wave latency was longer and P1-N1 wave amplitude was lower in both the spinal cord injury group and bFGF group compared to those in the sham-operated group ( P<0.01), with shorter P-wave latency and higher P1-N1 wave amplitude in the bFGF group compared to those in the spinal cord injury group ( P<0.01). Western blot results indicated that at 7, 14, 21, and 28 days after injury, in the spinal cord injury group, p-mTOR/mTOR levels were lower than those in both the sham-operated group and bFGF group ( P<0.01), while LC3-II expression levels were higher ( P<0.01); in the bFGF group, p-mTOR/mTOR levels were higher than those in the spinal cord injury group but lower than those in the sham-operated group ( P<0.01), and LC3-II expression levels were lower than those in the spinal cord injury group but higher than those in the sham-operated group ( P<0.01). At 28 days after injury, the BBB scores were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher scores in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). P-wave latency was shorter in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with shorter P-wave latency in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). P1-N1 wave amplitude was lower in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than that in the bFGF+rapamycin group ( P<0.01), with lower P1-N1 wave amplitude in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). The p-mTOR/mTOR levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher p-mTOR/mTOR levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). The LC3-II expression levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher LC3-II expression levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). Conclusion:bFGF can improve the pathological state, motor behavior, and neuroelectrophysiological function in rats with spinal cord injury, for which the mechanism of action may involve downregulating cellular autophagy function by activating the mTOR pathway, thereby inhibiting excessive autophagy to promote neuronal regeneration and repair.

Objective To explore the changes in neural activity in patients with type 2 diabetes mellitus(T2DM)and their corre-lation with executive function,and to analyze the neural mechanisms underlying the decline in executive function in T2DM patients.Methods Thirty-one T2DM patients(T2DM group)and thirty-two healthy controls(HC)(HC group)matched for body mass index(BMI)underwent resting-state functional magnetic resonance imaging(rs-fMRI)scans and N-back task tests were included.Differ-ences in the amplitude of low-frequency fluctuation(ALFF),regional homogeneity(ReHo),and seed-based functional connectivity(FC)between the two groups were compared,and partial correlation analyses were performed between the difference results and N-back task performance.Results The T2DM group showed prolonged reaction time(RT)in the 1-back and 2-back tasks.T2DM patients exhibited increased ALFF in the bilateral caudate nucleus,left medial superior frontal gyrus,and right postcentral gyrus,as well as elevated ReHo in the right putamen.FC analysis revealed significant alterations in FC between the caudate nucleus,putamen,and multiple brain regions in T2DM patients,with some of these FC changes significantly correlated with RT and accuracy(ACC)in the N-back task.Conclusion The decline in executive function in T2DM patients may be associated with abnormal neural activity in brain regions such as the striatum,salience network,and frontoparietal control network.FC further decreases under increased cognitive load.These findings provide evidence for the study of the neural mechanisms of executive function impairment in T2DM patients.

Based on network pharmacology,molecular docking,and experimental validation,this study explored the mechanism by which Hypericum japonicum Thunb-Prunella vulgaris treat liver injury.Mice were randomly divided into four groups:a control group(CON),a model group(CCl4),a high-dose drug group(TXD-H),and a low-dose drug group(TXD-L).A mouse liver in-jury model was established using CCl4 induction.The pathological morphology of liver tissue was observed,and the serum levels of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)were measured.Active ingredients of traditional Chinese medicine and targets related to these medicines and diseases were obtained from databases such as TCMSP,PubChem,Swiss Tar-get Prediction,GeneCards,and DisGeNET.The intersection of these targets was used to identify potential drug targets.A network diagram illustrating the relationships between"drug-active com-ponent-intersection target"was constructed using Cytoscape.Potential targets were analyzed using the STRING database for protein-protein interaction(PPI)analysis and the DAVID database for Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis.Molecular docking validation was performed using AutoDock Tools software.Subsequently,key target genes,including those related to the NLRP3 inflammasome and pyroptosis,were detected to validate the molecular docking results.Animal experimental results showed that compared to the CON group,serum AST and ALT activities in the CCl4 group mice were significantly increased(P＜0.01),while in the TXD-L group,serum AST and ALT activities were significantly decreased(P＜0.05)compared to the CCl4 group,and in the TXD-H group,AST and ALT activities were significantly decreased(P＜0.01).Through network pharmacology,135 potential targets were i-dentified,with key components found to be tetramethoxyluteolin,quercetin,kaempferol,luteolin and morin based on degree values,and key targets including TNF,SRC,AKT1,EGFR and ESR1.GO enrichment analysis yielded 304 entries,while KEGG enrichment analysis identified 91 biologi-cal pathways.Molecular docking results demonstrated strong binding between the main compo-nents of Hypericum japonicurn Thunb-Prunella vulgaris and key targets.qPCR results showed that compared to the CON group,the CCl4 group exhibited upregulated relative expression levels of SRC,EGFR,TNF-α,AKT1,and IL-18 mRNA,with significant increases in MyD88,NF-κB,IL-1β,NLRP3,Caspase-1,and ASC mRNA(P＜0.05),and significant upregulation of TLR4 and GS-DMD mRNA(P＜0.01).Compared to the CCl4 group,the TXD-H group displayed significant downregulation of EGFR,AKT1,TLR4,IL-1β,and GSDMD mRNA(P＜0.01),significant decrea-ses in TNF-α,MyD88,NF-κB,NLRP3,and ASC mRNA(P＜0.05),while SRC,IL-18,and Caspase-1 mRNA showed a downward trend.In conclusion,Hypericum japonicum Thunb-Prunel-la vulgaris exerts hepatoprotective effects through multiple components and pathways,among which inhibition of the NF-κB-NLRP3 pathway to reduce hepatocyte pyroptosis may be one of the important pathways for its protective effects.

Objective:To investigate the neurorestorative effect of basic fibroblast growth factor (bFGF) on neurological function recovery in rats with spinal cord injury and its potential mechanisms.Methods:Ninety adult SD rats were selected and randomly divided into 6 groups using a random number table: sham-operated group ( n=24), spinal cord injury group ( n=24), bFGF group ( n=24), bFGF autophagy pathway validation group ( n=6), bFGF+rapamycin group ( n=6), and bFGF+MHY1485 group ( n=6). A spinal cord injury model was established by impacting the T 10 spinal cord segment using a self-made Allen′s weight-drop impactor. The sham-operated group underwent a 3 cm midline dorsal incision without spinal cord injury; the bFGF group received immediate intrathecal injection of 100 μl bFGF solution (20 μg/L) after injury; the sham surgery group and spinal cord injury group received an equal volume of saline after injury; the bFGF autophagy pathway validation group received the identical treatment as the bFGF group; the bFGF+rapamycin group received the same treatment as the bFGF group with additional intraperitoneal injection of rapamycin (4 mg·kg -1·d -1); the bFGF+MHY1485 group received the identical bFGF treatment plus intraperitoneal injection of MHY1485 (10 mg·kg -1·d -1). At 28 days after injury, the rats were sacrificed and the spinal cord tissue was collected at 5 mm from the injury epicenter for HE staining and pathological observation. At 7, 14, 21, and 28 days after injury, BBB scoring was used to assess hindlimb motor function; P wave latency and P1-N1 wave amplitude were recorded to evaluate neuroelectrophysiological changes; Western blot analysis was performed to detect the expression levels of phosphorylated mammalian target of rapamycin (p-mTOR)/mammalian target of rapamycin (mTOR) and microtubule-associated protein light chain 3-II (LC3-II) and evaluate changes in mTOR signaling pathway and autophagy activity. At 28 days after injury, behavioral alterations, neuroelectrophysiological changes, and auctophagy-related protein expression levels were assessed in the bFGF autophagy pathyway validation group, bFGF+rapamycin group and bFGF+MHY1485 group. Results:At 28 days after injury, the sham-operated group exhibited regular nuclear morphology, while the spinal cord injury group showed disordered cell structures and the bFGF group displayed relatively normal nuclear morphology. At 7, 14, 21, and 28 days after injury, the BBB scores in both the spinal cord injury group and bFGF group were lower than those in the sham-operated group ( P<0.01), with higher scores in the bFGF group than those in the spinal cord injury group ( P<0.01). At 7, 14, 21, and 28 days after injury, P-wave latency was longer and P1-N1 wave amplitude was lower in both the spinal cord injury group and bFGF group compared to those in the sham-operated group ( P<0.01), with shorter P-wave latency and higher P1-N1 wave amplitude in the bFGF group compared to those in the spinal cord injury group ( P<0.01). Western blot results indicated that at 7, 14, 21, and 28 days after injury, in the spinal cord injury group, p-mTOR/mTOR levels were lower than those in both the sham-operated group and bFGF group ( P<0.01), while LC3-II expression levels were higher ( P<0.01); in the bFGF group, p-mTOR/mTOR levels were higher than those in the spinal cord injury group but lower than those in the sham-operated group ( P<0.01), and LC3-II expression levels were lower than those in the spinal cord injury group but higher than those in the sham-operated group ( P<0.01). At 28 days after injury, the BBB scores were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher scores in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). P-wave latency was shorter in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with shorter P-wave latency in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). P1-N1 wave amplitude was lower in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than that in the bFGF+rapamycin group ( P<0.01), with lower P1-N1 wave amplitude in the bFGF+MHY1485 group than that in the bFGF autophagy pathway validation group ( P<0.01). The p-mTOR/mTOR levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher p-mTOR/mTOR levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). The LC3-II expression levels were higher in both the bFGF autophagy pathway validation group and bFGF+MHY1485 group than those in the bFGF+rapamycin group ( P<0.01), with higher LC3-II expression levels in the bFGF+MHY1485 group than those in the bFGF autophagy pathway validation group ( P<0.01). Conclusion:bFGF can improve the pathological state, motor behavior, and neuroelectrophysiological function in rats with spinal cord injury, for which the mechanism of action may involve downregulating cellular autophagy function by activating the mTOR pathway, thereby inhibiting excessive autophagy to promote neuronal regeneration and repair.

Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome is characterized by congenital vaginal hypoplasia and primordial uterus caused by Müllerian anomalies. Case reports concerning adenomyosis associated with MRKH syndrome are limited, and the formation and intervention of adenomyosis without endometrium are unclear. Here, we present the case of a patient with MRKH syndrome complicated with adenomyosis without endometrium, a hypoechoic solid mass next to the right ovary. According to the intraoperative observation and histopathological examination findings, the mass were diagnosed as adenomyosis of the primordial uterus. Moreover, our report provides insights about its mechanism of occurrence and interventions in MRKH syndrome combined with adenomyosis without endometrium.

Through molecular docking and experimental validation,24 SPF male KM mice were ran-domly divided into four groups:the control group(CON),model group(LPS),high-dose Yang Shuhua group(YSH-H),which was gavaged with drug solution containing 1 g/mL crude Yang Shuhua,and the low-dose Yang Shuhua group(YSH-L),which was gavaged with drug solution containing 0.5 g/mL crude Yang Shuhua for a 17-day experimental period.Mouse body weight was recorded during the experiment,and fecal scoring was done 1 h after intraperitoneal injection of LPS.At the end of the experiment,histopathological changes in the jejunum tissue were examined,and the expression of tight junction protein-related genes was detected.Compared to the CON group,mice in the LPS group showed significant decreases in villus height,villus height/crypt depth(V/C)ratio(P＜0.01),and significant increase in crypt depth(P＜0.01).The mRNA ex-pression levels of ZO-1 and claudin-1 were significantly decreased(P＜0.01).Compared to the LPS group,mice in the YSH-H group showed significant decrease in crypt depth(P＜0.05),significant increase in villus height(P＜0.05),and significant increase in V/C ratio(P＜0.01).The YSH-L group showed a significant increase in V/C ratio(P＜0.05),a trend of decreased crypt depth,and an increasing trend of villus height.The mRNA expression of ZO-1 in the YSH-H group showed a significant increase(P＜0.05)and claudin-1 showed an increasing trend.Luteolin,quercetin,kaempferol,eriodictyol,and the top 5 potential key targets TP53,IL-1β,TNF,AKT1,and IL-10 exhibited molecular docking scores less than-20.95 kJ/mol,indicating strong activity.GO and KEGG enrichment analysis suggested that Yang Shuhua compounds might act on enteritis through the TNF signaling pathway,IL-17 signaling pathway,and PI3K-Akt signaling pathway.The qPCR results showed an upward trend in the mRNA expression levels of TLR4 and AKT1,significant in-crease in Caspase-1 and ASC(P＜0.05),and significantly increased expression of NF-κB and NL-RP3(P＜0.01).The mRNA expression level of AKT1,TLR4,NLRP3,ASC,Caspase-1,and NF-κB decreased compared to the LPS group,with significant differences in Caspase-1 and NF-κB(P＜0.05).This study suggests that Yang Shuhua exerts anti-enteritis effects through multiple compo-nents and pathways,with blockade of the TLR4-AKT-NF-κB pathway possibly being a key thera-peutic mechanism for treating enteritis.

Objective To explore the changes in neural activity in patients with type 2 diabetes mellitus(T2DM)and their corre-lation with executive function,and to analyze the neural mechanisms underlying the decline in executive function in T2DM patients.Methods Thirty-one T2DM patients(T2DM group)and thirty-two healthy controls(HC)(HC group)matched for body mass index(BMI)underwent resting-state functional magnetic resonance imaging(rs-fMRI)scans and N-back task tests were included.Differ-ences in the amplitude of low-frequency fluctuation(ALFF),regional homogeneity(ReHo),and seed-based functional connectivity(FC)between the two groups were compared,and partial correlation analyses were performed between the difference results and N-back task performance.Results The T2DM group showed prolonged reaction time(RT)in the 1-back and 2-back tasks.T2DM patients exhibited increased ALFF in the bilateral caudate nucleus,left medial superior frontal gyrus,and right postcentral gyrus,as well as elevated ReHo in the right putamen.FC analysis revealed significant alterations in FC between the caudate nucleus,putamen,and multiple brain regions in T2DM patients,with some of these FC changes significantly correlated with RT and accuracy(ACC)in the N-back task.Conclusion The decline in executive function in T2DM patients may be associated with abnormal neural activity in brain regions such as the striatum,salience network,and frontoparietal control network.FC further decreases under increased cognitive load.These findings provide evidence for the study of the neural mechanisms of executive function impairment in T2DM patients.

Based on network pharmacology,molecular docking,and experimental validation,this study explored the mechanism by which Hypericum japonicum Thunb-Prunella vulgaris treat liver injury.Mice were randomly divided into four groups:a control group(CON),a model group(CCl4),a high-dose drug group(TXD-H),and a low-dose drug group(TXD-L).A mouse liver in-jury model was established using CCl4 induction.The pathological morphology of liver tissue was observed,and the serum levels of aspartate aminotransferase(AST)and alanine aminotransferase(ALT)were measured.Active ingredients of traditional Chinese medicine and targets related to these medicines and diseases were obtained from databases such as TCMSP,PubChem,Swiss Tar-get Prediction,GeneCards,and DisGeNET.The intersection of these targets was used to identify potential drug targets.A network diagram illustrating the relationships between"drug-active com-ponent-intersection target"was constructed using Cytoscape.Potential targets were analyzed using the STRING database for protein-protein interaction(PPI)analysis and the DAVID database for Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway analysis.Molecular docking validation was performed using AutoDock Tools software.Subsequently,key target genes,including those related to the NLRP3 inflammasome and pyroptosis,were detected to validate the molecular docking results.Animal experimental results showed that compared to the CON group,serum AST and ALT activities in the CCl4 group mice were significantly increased(P＜0.01),while in the TXD-L group,serum AST and ALT activities were significantly decreased(P＜0.05)compared to the CCl4 group,and in the TXD-H group,AST and ALT activities were significantly decreased(P＜0.01).Through network pharmacology,135 potential targets were i-dentified,with key components found to be tetramethoxyluteolin,quercetin,kaempferol,luteolin and morin based on degree values,and key targets including TNF,SRC,AKT1,EGFR and ESR1.GO enrichment analysis yielded 304 entries,while KEGG enrichment analysis identified 91 biologi-cal pathways.Molecular docking results demonstrated strong binding between the main compo-nents of Hypericum japonicurn Thunb-Prunella vulgaris and key targets.qPCR results showed that compared to the CON group,the CCl4 group exhibited upregulated relative expression levels of SRC,EGFR,TNF-α,AKT1,and IL-18 mRNA,with significant increases in MyD88,NF-κB,IL-1β,NLRP3,Caspase-1,and ASC mRNA(P＜0.05),and significant upregulation of TLR4 and GS-DMD mRNA(P＜0.01).Compared to the CCl4 group,the TXD-H group displayed significant downregulation of EGFR,AKT1,TLR4,IL-1β,and GSDMD mRNA(P＜0.01),significant decrea-ses in TNF-α,MyD88,NF-κB,NLRP3,and ASC mRNA(P＜0.05),while SRC,IL-18,and Caspase-1 mRNA showed a downward trend.In conclusion,Hypericum japonicum Thunb-Prunel-la vulgaris exerts hepatoprotective effects through multiple components and pathways,among which inhibition of the NF-κB-NLRP3 pathway to reduce hepatocyte pyroptosis may be one of the important pathways for its protective effects.

Objective To investigate the correlation between insulin resistance and interleukin-6 (IL-6), chemerin, total cholesterol (TC)/high density lipoprotein cholesterol (HDL-C) ratio, triglyceride (TG)/HDL-C ratio, low density lipoprotein cholesterol (LDL-C)/HDL-C ratio and insulin resistance in obese patients with type 2 diabetes mellitus (T2DM), and to provide scientific basis for T2DM prevention and control. Methods A total of 355 obese T2DM patients in Songjiang Hospital Affiliated to Shanghai Jiaotong University School of Medicine were selected from January 2021 to December 2023. IL-6, chemerin and lipids were detected, and the assessment of insulin resistance was conducted through the homeostasis model assessment of insulin resistance (HOMA-IR). Results Among the 355 obese T2DM patients, there were 280 cases of insulin resistance, with the incidence rate of 78.87%. The BMI, IL-6, chemerin, TC/HDL-C, LDL-C/HDL-C, and TG/HDL-C in the insulin resistance group were higher than those in the non-insulin resistance group (P<0.05). The above insulin resistant patients were divided into 4 subgroups by means of insulin resistance, and there were significant differences in BMI, IL-6, chemerin, and TG/HDL-C among the subgroups (P<0.05). IL-6, chemerin, and TG/HDL-C were positively correlated with HOMA-IR in obese T2DM patients (P<0.05), while TC/HDL-C and LDL-C/HDL-C had no significant correlation with HOMA-IR (P>0.05). BMI, IL-6, chemerin, and TG/HDL-C were all influencing factors of insulin resistance in obese T2DM patients (P<0.05). Conclusion IL-6, chemerin and TG/HDL-C are correlated with insulin resistance in obese patients with T2DM and are influencing factors for the occurrence of insulin resistance.