Objective: To characterize perioperative dynamic changes in immune-cell phenotypes and inflammatory cytokines in patients undergoing CPB (cardiopulmonary bypass) cardiac surgery, and to explore their associations with postoperative outcomes. Methods: In this prospective cohort study, 120 adult patients who underwent elective cardiac surgery under CPB at West China Hospital from May 2022 to March 2023 were enrolled. Perioperative immune-cell phenotypes and concentrations of 40 inflammation-related cytokines were measured. The primary outcomes were the sequential organ failure assessment (SOFA) score at 24 h after surgery and ΔSOFA (the peak SOFA score within 48 h after surgery minus the preoperative SOFA score). Secondary outcomes included major adverse cardiovascular events (MACE), acute kidney injury (AKI), respiratory failure, severe liver injury, and infection. Results: The mean age of enrolled patients was 57±10 years. Of these, 52% (62/120) were male and 90% (108/120) underwent valve surgery. During the rewarming to the end of CPB, neutrophil counts rapidly increased (7.39×10 /L vs preoperative 3.07×10 /L, P<0.001), with significant upregulation of CD11b (7.30×10 /L vs preoperative 3.05×10 /L, P<0.001) and CD54 (7.15×10 /L vs preoperative 2.99×10 /L, P<0.001). Lymphocyte counts increased at the end of CPB (1.75×10 /L vs preoperative 1.12×10 /L, P<0.001) but decreased significantly at 24 h after surgery (0.59×10 /L vs preoperative 1.12×10 /L, P<0.001). Plasma analysis showed that multiple pro-inflammatory cytokines increased during CPB and remained elevated up to 24 h after surgery; five chemokines and the anti-inflammatory cytokine IL-10 peaked at the end of CPB. The SOFA score increased from 1 (1, 2) preoperatively to 7 (5, 10) at 24 h after surgery, with a ΔSOFA of 6 (4, 8). Within 30 days after surgery, 48 patients (40.0%) developed AKI, 17 (14.2%) developed infection, 4 (3.3%) developed severe liver injury, 3 (2.5%) developed respiratory failure, and 3 (2.5%) experienced MACE. During the 2-year follow-up, 8 patients (6.7%) experienced MACE and 5 (4.2%) died. Conclusion: Multi-organ dysfunction is common after cardiac surgery under CPB (median ΔSOFA, 6), accompanied by perioperative activation of multiple immune-cell subsets and upregulation of pro-inflammatory, anti-inflammatory, and chemotactic mediators. This study provides data-driven evidence and research clues for further investigation of the associations between CPB-related immune perturbations and postoperative organ dysfunction and clinical outcomes.

Background Lead smelting workers are exposed to mixed heavy metals such as lead (Pb) and cadmium (Cd). However, the specific associations and molecular mechanisms by which their combined exposure induces genetic damage remain unclear. Objective To clarify the association between combined Pb-Cd exposure and genetic damage and to explore the possible biological mechanisms through occupational epidemiological investigations and animal experiments. Methods (1) Population study: A cross-sectional study was conducted on 374 lead smelting workers in northern China. Inductively coupled plasma mass spectrometry (ICP-MS) was used to detect urinary levels of 8 metals including Pb and Cd, and graphite furnace atomic absorption spectroscopy (GFAAS) was used to quantify blood levels of Pb and Cd. The cytokinesis-block micronucleus assay (CBMN) was used to assess genetic damage. Poisson regression was used to analyze the association between metal exposure and micronucleus rates. (2) In vivo experiment: Thirty SD rats were randomly assigned to five groups: control (pure water), Pb (300 mg·L⁻¹ lead acetate), Cd (50 mg·L⁻¹ cadmium chloride), combined exposure (Pb + Cd), and resveratrol intervention (Pb + Cd + 50 mg·L⁻¹ resveratrol). After 8 weeks of ad libitum drinking water exposure, liver pathology, oxidative stress indicators [reactive oxygen species (ROS), reduced glutathione (GSH), oxidized glutathione (GSSG), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD)], genetic damage (Comet assay and γ-H2AX) were evaluated. Furthermore, cell cycle distribution, apoptosis rates, and mRNA expression of DNA damage response (DDR), DNA repair, and apoptosis-related genes were measured. Results (1) The geometric mean (GM, 95%CI) of urinary Pb and Cd were 14.69 (13.14, 16.51) µg·L⁻¹ and 2.11 (1.90, 2.33) µg·L⁻¹, respectively; the blood Pb and Cd levels were 117.10 (105.59, 129.87) µg·L⁻¹ and 4.55 (4.23, 4.89) µg·L⁻¹, respectively among the 374 workers. The mean micronucleus rate was (1.64±0.081) ‰, with significantly higher rates in males (1.65±0.083) ‰ than females (1.53±0.334) ‰ (U=4.166, P=0.041). All Pb and Cd biomarkers were positively correlated with micronucleus rate (FR>1, P<0.05), with a significant interaction effect observed between Pb and Cd (FR>1, P<0.05). (2) In rats, co-exposure to Pb and Cd caused liver tissue damage and inflammatory infiltration. Significant increases were observed in lymphocyte ROS; GSSG and MDA in lung tissue increased, while GSH and CAT activity decreased. Comet assay indicators and γ-H2AX levels were significantly elevated. Co-exposure induced S-phase arrest and increased apoptosis. mRNA levels of DDR (ATM, ATR, Chk2, and P53) and pro-apoptotic genes (Bax and Caspase-3) were upregulated, while the anti-apoptotic gene Bcl-2 and DNA repair genes (BRCA1, BRCA2, RAD51, RAD52, and CtIP) were downregulated. Two-way ANOVA confirmed synergistic effects on GSSG, Comet assay indicators, and ATR/Chk2 mRNA expression. Conclusion Occupational co-exposure to Pb and Cd synergistically induces genetic damage. This damage is mediated by oxidative stress and DNA damage, which activates the DDR pathway and inhibits the expression of DNA repair genes, ultimately leading to cell cycle arrest and apoptosis.

Background Lead smelting workers are exposed to mixed heavy metals such as lead (Pb) and cadmium (Cd). However, the specific associations and molecular mechanisms by which their combined exposure induces genetic damage remain unclear. Objective To clarify the association between combined Pb-Cd exposure and genetic damage and to explore the possible biological mechanisms through occupational epidemiological investigations and animal experiments. Methods (1) Population study: A cross-sectional study was conducted on 374 lead smelting workers in northern China. Inductively coupled plasma mass spectrometry (ICP-MS) was used to detect urinary levels of 8 metals including Pb and Cd, and graphite furnace atomic absorption spectroscopy (GFAAS) was used to quantify blood levels of Pb and Cd. The cytokinesis-block micronucleus assay (CBMN) was used to assess genetic damage. Poisson regression was used to analyze the association between metal exposure and micronucleus rates. (2) In vivo experiment: Thirty SD rats were randomly assigned to five groups: control (pure water), Pb (300 mg·L⁻¹ lead acetate), Cd (50 mg·L⁻¹ cadmium chloride), combined exposure (Pb + Cd), and resveratrol intervention (Pb + Cd + 50 mg·L⁻¹ resveratrol). After 8 weeks of ad libitum drinking water exposure, liver pathology, oxidative stress indicators [reactive oxygen species (ROS), reduced glutathione (GSH), oxidized glutathione (GSSG), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD)], genetic damage (Comet assay and γ-H2AX) were evaluated. Furthermore, cell cycle distribution, apoptosis rates, and mRNA expression of DNA damage response (DDR), DNA repair, and apoptosis-related genes were measured. Results (1) The geometric mean (GM, 95%CI) of urinary Pb and Cd were 14.69 (13.14, 16.51) µg·L⁻¹ and 2.11 (1.90, 2.33) µg·L⁻¹, respectively; the blood Pb and Cd levels were 117.10 (105.59, 129.87) µg·L⁻¹ and 4.55 (4.23, 4.89) µg·L⁻¹, respectively among the 374 workers. The mean micronucleus rate was (1.64±0.081) ‰, with significantly higher rates in males (1.65±0.083) ‰ than females (1.53±0.334) ‰ (U=4.166, P=0.041). All Pb and Cd biomarkers were positively correlated with micronucleus rate (FR>1, P<0.05), with a significant interaction effect observed between Pb and Cd (FR>1, P<0.05). (2) In rats, co-exposure to Pb and Cd caused liver tissue damage and inflammatory infiltration. Significant increases were observed in lymphocyte ROS; GSSG and MDA in lung tissue increased, while GSH and CAT activity decreased. Comet assay indicators and γ-H2AX levels were significantly elevated. Co-exposure induced S-phase arrest and increased apoptosis. mRNA levels of DDR (ATM, ATR, Chk2, and P53) and pro-apoptotic genes (Bax and Caspase-3) were upregulated, while the anti-apoptotic gene Bcl-2 and DNA repair genes (BRCA1, BRCA2, RAD51, RAD52, and CtIP) were downregulated. Two-way ANOVA confirmed synergistic effects on GSSG, Comet assay indicators, and ATR/Chk2 mRNA expression. Conclusion Occupational co-exposure to Pb and Cd synergistically induces genetic damage. This damage is mediated by oxidative stress and DNA damage, which activates the DDR pathway and inhibits the expression of DNA repair genes, ultimately leading to cell cycle arrest and apoptosis.

Alcoholic liver fibrosis is a critical step in the progression of alcoholic liver disease toward liver cirrhosis， yet there is currently still a lack of effective and specific anti-fibrotic therapeutic strategies. Recent studies have shown that as an iron-dependent， lipid peroxidation-driven form of regulated cell death， ferroptosis plays an important role in alcohol-related hepatocellular injury and fibrogenesis. Reactive oxygen species generated during alcohol metabolism can damage hepatocytes， impair their antioxidant defense ability， and lead to disruption of iron homeostasis and accumulation of lipid peroxides， ultimately triggering ferroptosis. Hepatocyte ferroptosis can promote fibrosis by amplifying inflammatory responses and activating hepatic stellate cells， whereas selective induction of ferroptosis in activated hepatic stellate cells may attenuate fibrosis， highlighting the “double-edged sword” effect of ferroptosis. Current interventions against ferroptosis mainly focus on applying antioxidant approaches， reducing iron burden， or blocking the amplification of lipid peroxidation， which have shown preliminary efficacy and a potential clinical value， but there are still limitations such as single-target actions and insufficient cell selectivity. In the future， nanotechnology-based delivery and other targeting strategies may help to realize multi-pathway coordination and cell-specific modulation， thereby improving the anti-fibrotic efficacy of ferroptosis-oriented therapies.

Objective:To explore the impact of adolescent mental health status on smartphone addiction, and construct a predictive model for smartphone addiction based on the eXtreme Gradient Boosting(XGBoost) algorithm and multivariate Logistic regression.Methods:In April 2023, a cross-sectional survey was conducted among 14 666 adolescents.All participants were systematically evaluated using a self-developed general information questionnaire, the middle school student mental health scale(MSSMHS), the adolescents self-harm scale(ASHS), the interaction anxiousness scale(IAS), the mobile phone addiction index(MPAI), the middle school students shame scale(MSSS), the UCLA loneliness scale(UCLA-LS), the multidimensional peer victimization scale(MPVS), and the basic psychological needs scale(BPNS).R software version 4.3.2 was used for data analysis. Participants were randomly divided into training set and validation set at the ratio of 7∶3.The XGBoost model and multivariate logistic regression model were constructed to predict the risk of smartphone addiction, and a nomogram was plotted.Model performance was evaluated using the Hosmer-Lemeshow test, area under the curve(AUC), and accuracy(ACC).Results:(1) A total of 14 036 high school students were included in the study, with 5 069(36.1%) exhibited smartphone addiction.The training set comprised 9 826 students, with 3 549(36.1%) being smartphone addicts.The validation set included 4 210 students, with 1 520(36.1%) being smartphone addicts.(2) The XGBoost model identified shame-proneness and social anxiety as the two main predictors of smartphone addiction.(3) Multivariate Logistic regression analysis revealed that anxiety( B=0.328, OR(95% CI)=1.39(1.07-1.81), P=0.015), interpersonal sensitivity( B=0.311, OR(95% CI)=1.36(1.05-1.77), P=0.018), learning pressure( B=0.606, OR(95% CI)=1.83(1.46-2.31), P<0.001), mood swings( B=0.775, OR(95% CI)=2.17(1.70-2.78), P<0.001), social anxiety( B=0.024, OR(95% CI)=1.02(1.01-1.04), P<0.001), shame-proneness( B=0.049, OR(95% CI)=1.05(1.04-1.06), P<0.001), and peer victimization( B=0.037, OR(95% CI)=1.04(1.02-1.06), P<0.001) were significant predictors of smartphone addiction.(4) The ACC and AUC values of the XGBoost model were 0.890 and 0.929 in the training set, and 0.865 and 0.864 in the validation set, respectively.The multivariate Logistic regression model achieved ACC and AUC values of 0.870 and 0.854 in the training set, and 0.867 and 0.859 in the validation set, respectively. Conclusion:Anxiety, interpersonal sensitivity, learning pressure, mood swings, social anxiety, shame-proneness, and peer victimization are identified risk predictors of smartphone addiction in high school adolescents.

Objectives:To analyze whether there is a causal relationship between plasma proteins and the risk of coronary atherosclerosis(CAS)based on a two-sample Mendelian randomization(MR)analysis and to identify potential therapeutic targets for CAS.Methods:Single nucleotide polymorphisms(SNP)associated with plasma proteins from the UK Biobank Pharmacoproteomics Program(UKB-PPP)database were used as instrumental variables and outcome data were obtained from genome-wide association study databases.The Wald ratio method and inverse variance weighted(IVW)method in two-sample MR were employed as the primary approaches to assess the causal relationship between plasma proteins and CAS.Colocalization analysis was conducted as a sensitivity analysis to ensure the robustness of the MR findings.Results:A total of 132 plasma proteins were found to have causal associations with an increased risk of CAS.Colocalization analysis revealed that 12 plasma proteins shared genetic variants with CAS.Among them,Proprotein convertase subtilise/kexin type 9(PCSK9)(OR=1.23,95%CI:1.15-1.32,P<0.01)and neurocan(NCAN)(OR=1.35,95%CI:1.21-1.52,P<0.01)exhibited posterior probability of hypothesis4(PPH4)values<0.80 in the colocalization analysis,indicating strong support for colocalization and suggesting their potential as primary plasma protein drug targets for CAS.Conclusions:PCSK9 is associated with an increased risk of CAS and is confirmed as a therapeutic target for CAS.NCAN emerges as another potential therapeutic target for CAS.

OBJECTIVE To investigate the effects of the split formulas of Biyuan Heji(BYHJ)on paranasal sinus mucosal in-flammation in rats with acute rhinosinusitis(ARS)based on the pathogenesis of"wind-cold transforming into lung-heat".METHODS Unilateral nasal cavity occlusion combined with nasal dripping of Staphylococcus aureus were performed to establish a rat model of ARS.SD rats were randomly divided into blank,model,BYHJ(wind-cold removal+lung-heat removal),lung-heat removal,wind-cold removal,and positive drug groups,with 6 rats in each group.The rats were treated with the corresponding drugs for 7 d and then the samples were collected.HE staining was used to observe the pathological changes of rat paranasal sinus mucosa tissues,ELISA was employed to determine the levels of interleukin-1β(IL-1β),IL-6,IL-8,IL-9,IL-10,and IL-12 in serum,immunohistochemis-try(IHC)was adopted to measure the protein expression of tumor necrosis factor-α(TNF-α)and intercellular adhesion molecule(ICAM-1)in paranasal sinus mucosa tissues,and Western blot was used to detect the protein expression of phosphorylated p38 mito-gen-activated protein kinase(p38 MAPK),nuclear transcription factor-κB p50(NF-κB p50),and NF-κB p65 in paranasal sinus mucosa tissues.RESULTS The acute sinusitis rat inflammation model was successfully established.Compared with the model group,the water drinking,diet eating,and body weight of rats in the BYHJ group,wind-cold removal,lung-heat removal,and positive drug groups were significantly improved,the aggregation of inflammatory cells in the paranasal sinus mucosal tissue was reduced,and the levels of IL-1β,IL-6,IL-8,IL-9,and IL-12 in the serum were significantly reduced(P<0.01),IL-10 content significantly in-creased(P<0.01),the protein expression of TNF-α,ICAM-1,p38 MAPK,NF-κB p50,and NF-κB p65 in the paranasal sinus mucosa was significantly decreased(P<0.01).The comparison between various traditional Chinese medicine groups showed that the decrease of IL-1β,IL-6,IL-8,IL-9,IL-12,TNF-α,ICAM-1,p38 MAPK,NF-κB p50,and NF-κB p65 and the increase of IL-10 in the BYHJ group were better than those in the split formula groups(P<0.01),and the lung-heat removal group was better than the wind-cold removal group(P<0.01).CONCLUSION BYHJ and its split formulas can effectively inhibit the inflammatory response in rats with ARS.

AIM:This study investigated the role of solute carrier family 7 member 11(SLC7A11)in sul-fasalazine(SAS)-induced ferroptosis in acute myeloid leukemia(AML)cells,focusing on the inhibitory effect of nuclear factor E2-related factor 2(NRF2)nuclear translocation-mediated activation of SLC7A11 on ferroptosis and its underlying mechanisms.METHODS:SAS-induced proliferation in AML cell lines,Kasumi-1 and THP-1,was assessed using the MTS assay.Cell death inhibitors were employed to determine the mode of cell death.Lipid reactive oxygen species(ROS)levels were measured by flow cytometry;Fe2+,malonodialdehyde(MDA),glutathione(GSH)levels,and glutathione per-oxidase 4(GPX4)activity were assessed using micromethods.Quantitative PCR(qPCR)was performed to evaluate changes in SLC7A11 mRNA during SAS-induced ferroptosis,while Western blot measured SLC7A11 and GPX4 protein levels.Moreover,Western blot assessed NRF2 nuclear translocation post-SAS treatment.The NRF2 inhibitor ML385 was used to validate these effects.SLC7A11 mRNA and protein levels were then measured following combined SAS and ML385 treatment via qPCR and Western blot.Cell viability and ferroptosis-related indices were evaluated under the same treatment conditions.Furthermore,a shRNA vector targeting SLC7A11 was constructed to assess changes in cell viability and ferroptosis markers after SLC7A11 knockdown with SAS.GPX4 protein levels were examined following SLC7A11 knockdown.RESULTS:SAS significantly inhibited the proliferation of Kasumi-1 and THP-1 cells at 200 μmol/L and 300 μmol/L,respectively(P<0.05).Only ferroptosis inhibitors(Fer-1 and DFO)significantly reversed SAS-induced cy-totoxicity(P<0.01).SAS increased lipid ROS,Fe2+,and MDA levels(P<0.01),while reducing GSH and GPX4 activity(P<0.01).The mRNA and protein expressions of SLC7A11 increased during SAS-induced ferroptosis(P<0.01),where-as GPX4 protein decreased significantly(P<0.01).SAS significantly increased the nuclear-to-cytoplasmic NRF2 ratio(P<0.01),which decreased upon co-treatment with ML385(P<0.05).Following SAS and ML385 co-treatment,both SLC7A11 mRNA and protein levels were downregulated(P<0.01).This combination treatment further reduced AML cell viability(P<0.01),an effect reversed by Fer-1 and DFO(P<0.01).Compared with SAS alone,the combination of SAS and ML385 significantly increased lipid ROS,Fe2+,and MDA while reducing GSH levels and GPX4 activity(P<0.01).SLC7A11 knockdown was successfully achieved.Compared with the NC shRNA group,SLC7A11 knockdown cells showed significantly decreased viability after SAS treatment,which was reversed by Fer-1 and DFO(P<0.01).Lipid ROS,Fe2+,and MDA content were significantly increased(P<0.01),and GSH and GPX4 were substantially decreased(P<0.05).Moreover,GPX4 protein expression was considerably reduced after SLC7A11 knockdown(P<0.01).CONCLUSION:SAS induces ferroptosis in AML cells.It promotes the nuclear translocation of NRF2 protein,which activates SLC7A11 ex-pression.Inhibition of NRF2 or downregulation of SLC7A11 sensitizes AML cells to SAS-induced ferroptosis.

Objective:To explore the impact of adolescent mental health status on smartphone addiction, and construct a predictive model for smartphone addiction based on the eXtreme Gradient Boosting(XGBoost) algorithm and multivariate Logistic regression.Methods:In April 2023, a cross-sectional survey was conducted among 14 666 adolescents.All participants were systematically evaluated using a self-developed general information questionnaire, the middle school student mental health scale(MSSMHS), the adolescents self-harm scale(ASHS), the interaction anxiousness scale(IAS), the mobile phone addiction index(MPAI), the middle school students shame scale(MSSS), the UCLA loneliness scale(UCLA-LS), the multidimensional peer victimization scale(MPVS), and the basic psychological needs scale(BPNS).R software version 4.3.2 was used for data analysis. Participants were randomly divided into training set and validation set at the ratio of 7∶3.The XGBoost model and multivariate logistic regression model were constructed to predict the risk of smartphone addiction, and a nomogram was plotted.Model performance was evaluated using the Hosmer-Lemeshow test, area under the curve(AUC), and accuracy(ACC).Results:(1) A total of 14 036 high school students were included in the study, with 5 069(36.1%) exhibited smartphone addiction.The training set comprised 9 826 students, with 3 549(36.1%) being smartphone addicts.The validation set included 4 210 students, with 1 520(36.1%) being smartphone addicts.(2) The XGBoost model identified shame-proneness and social anxiety as the two main predictors of smartphone addiction.(3) Multivariate Logistic regression analysis revealed that anxiety( B=0.328, OR(95% CI)=1.39(1.07-1.81), P=0.015), interpersonal sensitivity( B=0.311, OR(95% CI)=1.36(1.05-1.77), P=0.018), learning pressure( B=0.606, OR(95% CI)=1.83(1.46-2.31), P<0.001), mood swings( B=0.775, OR(95% CI)=2.17(1.70-2.78), P<0.001), social anxiety( B=0.024, OR(95% CI)=1.02(1.01-1.04), P<0.001), shame-proneness( B=0.049, OR(95% CI)=1.05(1.04-1.06), P<0.001), and peer victimization( B=0.037, OR(95% CI)=1.04(1.02-1.06), P<0.001) were significant predictors of smartphone addiction.(4) The ACC and AUC values of the XGBoost model were 0.890 and 0.929 in the training set, and 0.865 and 0.864 in the validation set, respectively.The multivariate Logistic regression model achieved ACC and AUC values of 0.870 and 0.854 in the training set, and 0.867 and 0.859 in the validation set, respectively. Conclusion:Anxiety, interpersonal sensitivity, learning pressure, mood swings, social anxiety, shame-proneness, and peer victimization are identified risk predictors of smartphone addiction in high school adolescents.

OBJECTIVE To investigate the effects of the split formulas of Biyuan Heji(BYHJ)on paranasal sinus mucosal in-flammation in rats with acute rhinosinusitis(ARS)based on the pathogenesis of"wind-cold transforming into lung-heat".METHODS Unilateral nasal cavity occlusion combined with nasal dripping of Staphylococcus aureus were performed to establish a rat model of ARS.SD rats were randomly divided into blank,model,BYHJ(wind-cold removal+lung-heat removal),lung-heat removal,wind-cold removal,and positive drug groups,with 6 rats in each group.The rats were treated with the corresponding drugs for 7 d and then the samples were collected.HE staining was used to observe the pathological changes of rat paranasal sinus mucosa tissues,ELISA was employed to determine the levels of interleukin-1β(IL-1β),IL-6,IL-8,IL-9,IL-10,and IL-12 in serum,immunohistochemis-try(IHC)was adopted to measure the protein expression of tumor necrosis factor-α(TNF-α)and intercellular adhesion molecule(ICAM-1)in paranasal sinus mucosa tissues,and Western blot was used to detect the protein expression of phosphorylated p38 mito-gen-activated protein kinase(p38 MAPK),nuclear transcription factor-κB p50(NF-κB p50),and NF-κB p65 in paranasal sinus mucosa tissues.RESULTS The acute sinusitis rat inflammation model was successfully established.Compared with the model group,the water drinking,diet eating,and body weight of rats in the BYHJ group,wind-cold removal,lung-heat removal,and positive drug groups were significantly improved,the aggregation of inflammatory cells in the paranasal sinus mucosal tissue was reduced,and the levels of IL-1β,IL-6,IL-8,IL-9,and IL-12 in the serum were significantly reduced(P<0.01),IL-10 content significantly in-creased(P<0.01),the protein expression of TNF-α,ICAM-1,p38 MAPK,NF-κB p50,and NF-κB p65 in the paranasal sinus mucosa was significantly decreased(P<0.01).The comparison between various traditional Chinese medicine groups showed that the decrease of IL-1β,IL-6,IL-8,IL-9,IL-12,TNF-α,ICAM-1,p38 MAPK,NF-κB p50,and NF-κB p65 and the increase of IL-10 in the BYHJ group were better than those in the split formula groups(P<0.01),and the lung-heat removal group was better than the wind-cold removal group(P<0.01).CONCLUSION BYHJ and its split formulas can effectively inhibit the inflammatory response in rats with ARS.