ObjectiveTo explore the mechanism by which Banxia Xiexin Tang （BXT） regulates the advanced glycation end products （AGE）/receptor for advanced glycation end products （RAGE） signaling pathway to reduce neuroinflammatory responses and ameliorate cognitive dysfunction in the rat model of vascular dementia （VD）. MethodsThe components of BXT were detected by ultra performance liquid chromatography-quadrupole -orbitrap-tandem mass spectrometry（UPLC-Q-Orbitrap-MS/MS）， and the core components and key action pathways were screened out by network pharmacology and molecular docking. Sixty SPF-grade male SD rats were randomly allocated into the sham and modeling groups by the random number table method. The VD model was replicated by the modified bilateral occlusion of the common carotid arteries （2-VO） method. The successfully modeled rats were randomly allocated into the model， low-， medium-， and high-dose （3.748 5， 7.497， 14.994 g·kg^-1） BXT （BXT-L， BXT-M， and BXT-H）， and nimodipine （NMP， 0.002 7 g·kg^-1） groups according to the random number table method. The rats in the drug intervention groups were administrated with corresponding drugs by gavage， and the sham and model groups received the same amount of normal saline for 14 consecutive days. The Morris water maze， Y-maze， and new object recognition experiments were conducted to evaluate the cognitive dysfunction of rats. Hematoxylin-eosin （HE） staining was used to evaluate the histopathological changes of the hippocampal tissue in rats. The mRNA levels of AGE， RAGE， and phosphorylated nuclear factor-kappa B p65 （p-NF-κB p65） in the hippocampal tissue of rats were determined by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. The expression of related proteins in the AGE/RAGE pathway in the hippocampal tissue of rats was determined by Western blot and immunohistochemistry （IHC）. The levels of neurotransmitters and inflammatory mediators in the rat serum were measured by enzyme-linked immunosorbent assay （ELISA）. ResultsThe chemical components of BXT were detected by UPLC-Q-Orbitrap-MS/MS. Network pharmacology and molecular docking identified the AGE/RAGE pathway as the key pathway. The results of the water maze， Y maze， and novel object recognition tests showed that compared with the sham group， the model group demonstrated prolonged successful latency and decreases in number of platform crossings， alternation rate， number of entries into the new arm， preference index， and discrimination index （P0.01）. Compared with the model group， the BXT-H and BXT-M groups showed shortened successful latency （P0.01） and increases in number of platform crossings （P0.05）， alternation rate （P0.01）， number of entries into the new arm （P0.05）， preference index （P0.01）， and discrimination index （P0.01）. HE results showed that compared with the sham group， the cells of model rats were loosely and disorderly arranged， and the nuclei were condensed. Compared with the model group， the pathological changes of the hippocampus in the BXT group were mitigated. Real-time PCR results showed that compared with the sham group， the model group presented up-regulated mRNA levels of AGE， RAGE， and p-NF-κB p65 in the hippocampus （P0.01）， and compared with the model group， the BXT-H and BXT-M groups showcased down-regulated mRNA levels of AGE， RAGE， and p-NF-κB p65 （P0.01）. Western blot results showed that compared with the sham group， the model group presented up-regulated expression of AGE， RAGE， p-NF-κB p65， and tumor necrosis factor-α （TNF-α） （P0.05）， and compared with the model group， the BXT-H group presented down-regulated expression of AGE， RAGE， p-NF-κB p65， and TNF-α （P0.05）. IHC results showed that compared with the sham group， the model group had increased expression of RAGE （P0.01）， and compared with the model group， the BXT-H and BXT-M groups had reduced expression of RAGE （P0.01）. ELISA results showed that compared with the sham group， the model group exhibited elevated levels of TNF-α and Interleukin-1β （IL-1β） and declined levels of acetylcholine （ACh） and dopamine （DA） in the serum （P0.01）. Compared with the model group， the BXT-L， BXT-M， and BXT-H groups showed lowered levels of TNF-α and IL-1β in the serum （P0.05） and elevated levels of ACh and DA （P0.05）. ConclusionBXT may ameliorate cognitive dysfunction in the rat model of VD by down-regulating the AGE/RAGE signaling pathway， reducing neuroinflammatory responses， and regulating neurotransmitter levels.

ObjectiveTo explore the mechanism by which Banxia Xiexin Tang （BXT） regulates the advanced glycation end products （AGE）/receptor for advanced glycation end products （RAGE） signaling pathway to reduce neuroinflammatory responses and ameliorate cognitive dysfunction in the rat model of vascular dementia （VD）. MethodsThe components of BXT were detected by ultra performance liquid chromatography-quadrupole -orbitrap-tandem mass spectrometry（UPLC-Q-Orbitrap-MS/MS）， and the core components and key action pathways were screened out by network pharmacology and molecular docking. Sixty SPF-grade male SD rats were randomly allocated into the sham and modeling groups by the random number table method. The VD model was replicated by the modified bilateral occlusion of the common carotid arteries （2-VO） method. The successfully modeled rats were randomly allocated into the model， low-， medium-， and high-dose （3.748 5， 7.497， 14.994 g·kg^-1） BXT （BXT-L， BXT-M， and BXT-H）， and nimodipine （NMP， 0.002 7 g·kg^-1） groups according to the random number table method. The rats in the drug intervention groups were administrated with corresponding drugs by gavage， and the sham and model groups received the same amount of normal saline for 14 consecutive days. The Morris water maze， Y-maze， and new object recognition experiments were conducted to evaluate the cognitive dysfunction of rats. Hematoxylin-eosin （HE） staining was used to evaluate the histopathological changes of the hippocampal tissue in rats. The mRNA levels of AGE， RAGE， and phosphorylated nuclear factor-kappa B p65 （p-NF-κB p65） in the hippocampal tissue of rats were determined by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. The expression of related proteins in the AGE/RAGE pathway in the hippocampal tissue of rats was determined by Western blot and immunohistochemistry （IHC）. The levels of neurotransmitters and inflammatory mediators in the rat serum were measured by enzyme-linked immunosorbent assay （ELISA）. ResultsThe chemical components of BXT were detected by UPLC-Q-Orbitrap-MS/MS. Network pharmacology and molecular docking identified the AGE/RAGE pathway as the key pathway. The results of the water maze， Y maze， and novel object recognition tests showed that compared with the sham group， the model group demonstrated prolonged successful latency and decreases in number of platform crossings， alternation rate， number of entries into the new arm， preference index， and discrimination index （P<0.01）. Compared with the model group， the BXT-H and BXT-M groups showed shortened successful latency （P<0.01） and increases in number of platform crossings （P<0.05）， alternation rate （P<0.01）， number of entries into the new arm （P<0.05）， preference index （P<0.01）， and discrimination index （P<0.01）. HE results showed that compared with the sham group， the cells of model rats were loosely and disorderly arranged， and the nuclei were condensed. Compared with the model group， the pathological changes of the hippocampus in the BXT group were mitigated. Real-time PCR results showed that compared with the sham group， the model group presented up-regulated mRNA levels of AGE， RAGE， and p-NF-κB p65 in the hippocampus （P<0.01）， and compared with the model group， the BXT-H and BXT-M groups showcased down-regulated mRNA levels of AGE， RAGE， and p-NF-κB p65 （P<0.01）. Western blot results showed that compared with the sham group， the model group presented up-regulated expression of AGE， RAGE， p-NF-κB p65， and tumor necrosis factor-α （TNF-α） （P<0.05）， and compared with the model group， the BXT-H group presented down-regulated expression of AGE， RAGE， p-NF-κB p65， and TNF-α （P<0.05）. IHC results showed that compared with the sham group， the model group had increased expression of RAGE （P<0.01）， and compared with the model group， the BXT-H and BXT-M groups had reduced expression of RAGE （P<0.01）. ELISA results showed that compared with the sham group， the model group exhibited elevated levels of TNF-α and Interleukin-1β （IL-1β） and declined levels of acetylcholine （ACh） and dopamine （DA） in the serum （P<0.01）. Compared with the model group， the BXT-L， BXT-M， and BXT-H groups showed lowered levels of TNF-α and IL-1β in the serum （P<0.05） and elevated levels of ACh and DA （P<0.05）. ConclusionBXT may ameliorate cognitive dysfunction in the rat model of VD by down-regulating the AGE/RAGE signaling pathway， reducing neuroinflammatory responses， and regulating neurotransmitter levels.

To explore the advantages of traditional Chinese medicine （TCM） and integrative TCM-Western medicine approaches in the treatment of diabetic microvascular complications （DMC）， refine key pathophysiological insights and treatment principles， and promote academic innovation and strategic research planning in the prevention and treatment of DMC. The 38th session of the Expert Salon on Diseases Responding Specifically to Traditional Chinese Medicine， hosted by the China Association of Chinese Medicine， was held in Beijing， 2024. Experts in TCM， Western medicine， and interdisciplinary fields convened to conduct a systematic discussion on the pathogenesis， diagnostic and treatment challenges， and mechanism research related to DMC， ultimately forming a consensus on key directions. Four major research recommendations were proposed. The first is addressing clinical bottlenecks in the prevention and control of DMC by optimizing TCM-based evidence evaluation systems. The second is refining TCM core pathogenesis across DMC stages and establishing corresponding "disease-pattern-time" framework. The third is innovating mechanism research strategies to facilitate a shift from holistic regulation to targeted intervention in TCM. The fourth is advancing interdisciplinary collaboration to enhance the role of TCM in new drug development， research prioritization， and guideline formulation. TCM and integrative approaches offer distinct advantages in managing DMC. With a focus on the diseases responding specifically to TCM， strengthening evidence-based support and mechanism interpretation and promoting the integration of clinical care and research innovation will provide strong momentum for the modernization of TCM and the advancement of national health strategies.

Objective: To investigate the association between sleep duration and depressive symptoms in children and adolescents, so as to provide scientific evidence for promoting mental health and preventing depression among relevant populations. Methods: A total of 2 192 children and adolescents aged 10-17 years with complete data from the 2018 China Family Panel Studies Database were included. Eight item Center for Epidemiologic Studies Depressive Scale(CES-D8) was used to assess participants depressive levels, and sleep duration was assessed via questionnaire. Multivariate Logistic regression model was used to analyze the association between different sleep duration categories and depressive symptom occurrence among children and adolescents. A restricted cubic spline(RCS) model analyzed the dose response relationship between sleep duration and the risk of depressive symptoms occurrence and segmented Logistic regression models to identify dose response effects. Results: Among the surveyed children and adolescents, 524(23.91%) exhibited depressive symptoms. Compared to those with sufficient sleep, children aged 10-12 years had a higher risk of depressive symptoms on average per day( OR =1.66, 95% CI =1.19-2.33) and during weekdays( OR =1.76, 95% CI =1.26-2.46), as well as in adolescents aged 13-17 years on a daily basis( OR =1.40，95% CI =1.06-1.85) and during weekdays( OR = 1.48，95% CI =1.12-1.95), and excessive sleep in adolescents on rest days was also significantly associated with higher risk of depressive symptoms( OR =1.65，95% CI =1.11-2.43)(all P <0.05). RCS analysis results indicate that children s sleep duration exhibits a linear negative correlation with the risk of depressive symptoms(all P nonlinear >0.05), while adolescents sleep duration showed a U shaped association with depressive symptoms(all P nonlinear <0.05) on a daily basis, during weekdays and weekends, with potential threshold effects at 10.00, 9.88, and 9.60 hours, respectively. Conclusions Sleep duration among children and adolescents is associated with depressive symptoms, with notable age related differeneces. It is recommended to develop targeted age specific interventions to reduce the risk of depressive symptoms in children and adolescents.

[摘 要] 目的：探究纺锤体蛋白1（SPIN1）促进胃腺癌细胞迁移与侵袭的分子机制。方法: 通过TCGA数据库数据分析胃腺癌组织中SPIN1 mRNA表达与上皮间质转化（EMT）评分、血管生成评分间的相关性。收集2018年8月至2021年11月期间山东第一医科大学附属省立医院手术切除的52例胃腺癌患者的癌组织制成组织芯片，每例均包含胃腺癌组织、对应癌旁组织及淋巴结转移灶，通过免疫组织化学法检测胃腺癌组织中SPIN1与STAT3的蛋白表达水平及相关性。通过Transwell实验研究干扰SPIN1对胃腺癌细胞侵袭与迁移的影响。使用GEPIA2网站分析SPIN1基因与Janus-激酶/信号转导和转录激活因子（JAK/STAT）通路相关因子在胃腺癌中的表达相关性。通过qPCR法、WB法检测干扰SPIN1后JAK/STAT通路相关mRNA和蛋白的表达变化。结果: TCGA数据库数据分析结果显示，SPIN1表达与EMT评分和血管生成评分呈正相关（均P < 0.05）。SPIN1与STAT3在胃腺癌组织和淋巴结转移灶中表达升高（均P < 0.05），在癌旁胃黏膜组织中阴性表达。SPIN1与STAT3的表达显著正相关（P < 0.05）。干扰SPIN1后胃腺癌细胞的迁移、侵袭能力明显降低（P < 0.05或P < 0.01）。GEPIA2网站分析结果显示，SPIN1基因与JAK1、JAK2、STAT1、STAT2及STAT3表达均呈显著正相关（均P < 0.05）。干扰SPIN1后JAK2、STAT3的mRNA水平下降，而JAK1、STAT1、STAT2的mRNA水平变化不明显。WB法实验结果表明，干扰SPIN1后JAK2、STAT3、p-JAK2及p-STAT3的蛋白表达均显著降低（均P < 0.01），过表达SPIN1后JAK2、STAT3、p-JAK2及p-STAT3的蛋白表达均显著升高（均P < 0.01）。结论: SPIN1可通过参与JAK2/STAT3信号通路促进胃腺癌细胞迁移与侵袭。

Objective To systematically analyze the characteristics of the disease burden of hypertensive heart disease (HHD) in the elderly (≥60 years) globally and in China from 1990 to 2021, and to predict its future trends from 2022 to 2040, with the aim of providing data support for optimizing comprehensive prevention and control strategies for HHD. Methods Based on the Global Burden of Disease (GBD) 2021 database, the number of prevalent cases and disability-adjusted life years (DALYs) of HHD in the elderly were extracted for the world, China, and five regions categorized by sociodemographic index (SDI). Joinpoint regression was used to analyze the temporal trends of age-standardized prevalence rate and age-standardized DALYs rate of HHD in the elderly. A three-factor decomposition method was applied to evaluate the relative contributions of aging, population growth, and epidemiological changes to the variations in the elderly HHD burden. Additionally, a Bayesian age-period-cohort model was used to predict the elderly HHD burden from 2022 to 2040. Results In 2021, the number of prevalent elderly HHD cases reached 10 283 000 globally and 3 412 400 in China, representing increases of 179.20% and 159.20% respectively, compared with 1990. The DALYs of elderly HHD were 18 812 700 person-years globally and 4 731 400 person-years in China, rising by 76.08% and 29.45% respectively from 1990. Meanwhile, the growth rates of the number of prevalent cases and DALYs of elderly HHD varied across different SDI regions. From 1990 to 2021, the age-standardized prevalence rate of elderly HHD in China, as well as the age-standardized DALYs rate of elderly HHD both globally and in China, showed significant downward trends (all average annual percentage changes<0, all P<0.001). In 2021, the 70-74 years age group accounted for the highest proportion of prevalent cases and DALYs of elderly HHD, both globally and in China. Decomposition analysis revealed that population growth was the dominant factor driving the increase in the elderly HHD burden across all regions. The prediction model results indicated that the number of prevalent cases and DALYs of elderly HHD would continue to rise globally and in China from 2022 to 2040, with the growth rate of the elderly HHD burden in China between 2021 and 2040 expected to exceed the global average. Conclusion Over the past 32 years, although the age-standardized disease rates of elderly HHD have mainly shown a downward trend globally and in China, the absolute number of the disease burden has increased substantially. The projection model indicates a continued upward trajectory, with the growth rate in China higher than the global average. Therefore, there is an urgent need to implement precise prevention and control strategies to effectively mitigate the disease burden of elderly HHD.

OBJECTIVE To investigate the mechanisms of rutin in alleviating depressive symptoms associated with premenstrual dysphoric disorder （PMDD） characterized by liver qi stagnation syndrome. METHODS Network pharmacology was employed to identify the intersecting targets of action between PMDD and rutin. A protein-protein interaction network was constructed to screen core targets， followed by gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis. Molecular docking simulations validated rutin’s binding affinity to core targets. The bilateral ovaries of female Wistar rats were removed， followed by artificial hormone induction. The rats were then randomly divided into normal group （10 rats） and modeling group （50 rats）. PMDD rat model with liver qi stagnation syndrome was established via restraint stress. The successfully modeled rats were further divided into model group， fluoxetine group （positive control） and rutin group， with 12 rats in each group. The corresponding drug solutions or water were administered by gavage at 9：00 a.m. every day， continuing for two estrous cycles. The open-field test， forced swimming test and Y-maze test were utilized to evaluate the effects of rutin on the behavioral indexes of model rats. Additionally， the density of neuronal dendritic spines in the hippocampal tissues of the rats was observed. Serum brain-derived neurotrophic factor （BDNF） levels and the expressions of BDNF， tyrosine kinase receptor type B （TrkB）， synuclein （Syn）， and postsynaptic density protein 95 （PSD95） in hippocampal tissues were quantified， respectively. RESULTS Network pharmacology and molecular docking revealed the core targets through which rutin ameliorated PMDD characterized by liver qi stagnation syndrome included BDNF， TrkB， PSD65， Syn， etc. The results of experimental validation demonstrated that rutin significantly increased the spontaneous alternation behavior scores of PMDD model rats with liver qi stagnation syndrome during the non-receptive phase， shortened their immobility time during the forced swimming test， and enhanced the density of neuronal dendritic spines in the hippocampal tissues. Additionally， rutin upregulated the levels of serum BDNF and the protein expressions of BDNF， TrkB and Syn in the hippocampal tissues （P＜0.05）. However， it had no significant effect on the above indexes in model rats during the receptive phase （P＞0.05）. CONCLUSIONS Rutin ameliorates depressive symptoms， enhances spatial memory capabilities， and reduces neuronal damage in PMDD model rats with liver qi stagnation syndrome. These effects may be associated with the activation of BDNF/TrkB signaling pathway and upregulation of Syn protein expression.

OBJECTIVE To investigate the effects and potential mechanisms of Xiaoqinglong decoction on airway inflammation in asthma with syndrome of cold retention accumulation in lung based on the metastasis-associated lung adenocarcinoma transcript 1 （MALAT1）. METHODS Forty Wistar rats were randomly divided into blank group， model group， dexamethasone group （positive control， 1 mg/kg）， and Xiaoqinglong decoction group （2.72 g/kg）， with 10 rats in each group. A rat model of asthma with syndrome of cold retention accumulation in lung was established， and the corresponding drugs were administered once daily starting from the second day of modeling for 21 consecutive days. Lung histopathological changes and lung function were evaluated. The levels of superoxide dismutase （SOD）， malondialdehyde （MDA）， interferron-γ （IFN-γ）， tumor necrosis factor α （TNF-α）， and interleukin-13 （IL-13） in serum were measured， and the mRNA expression levels of MALAT1， TNF- α， IL-13， IFN- γ， and transient receptor potential melastatin 2 （TRPM2） in lung tissue were determined. Twenty C57BL/6J wild-type mice and twenty C57BL/6J MALAT1（－/－）mice were randomly divided into wild-type model group， wild-type Xiaoqinglong decoction group， MALAT1 model group， and MALAT1（－/－） Xiaoqinglong decoction group， with 10 mice in each group. The same asthma model was E-mail：yan_peizheng@163.com established， and Xiaoqinglong decoction was administered once daily for 21 days starting from the second day of modeling. The serum levels of SOD， MDA， IFN-γ， TNF-α and IL-13 were measured， along with the mRNA and protein expression levels of TRPM2 in lung tissue. RESULTS The results of the rat experiment showed that， compared with model group， the airway resistance， functional residual capacity， the serum levels of IL- 13， TNF-α and MDA as well as inflammatory infiltration and collagen fiber deposition in lung tissue， and the expressions of IL- 13， TNF-α and TRPM2 in lung tissue were all significantly decreased in the treatment group （P＜0.05 or P＜0.01）. The peak expiratory flow， forced expiratory flow at 50% of forced vital capacity， the serum levels of SOD and IFN-γ， and the expression levels of IFN-γ and MALAT1 in lung tissue were significantly increased （P＜0.05 or P＜0.01）. The results of the mice experiment demonstrated that， compared with the wild-type model group， serum levels of IL-13， TNF-α and MDA in wild-type xiaoqinglong decoction group were significantly reduced （P＜0.05 or P＜0.01）， while serum IFN-γ levels and SOD activity were significantly increased （P＜0.01）. Compared with the wild-type Xiaoqinglong decoction group， the MALAT1（－/－） Xiaoqinglong decoction group showed significantly decreased serum IFN-γ levels and SOD activity （P＜0.01）， along with significantly increased levels of IL-13， TNF-α and MDA （P＜0.05 or P＜0.01）， as well as significantly elevated TRPM2 mRNA and protein expression in lung tissue （P＜0.05）. CONCLUSIONS Xiaoqinglong decoction may alleviate airway inflammation by regulating the expression of MALAT1， modulating oxidative stress， inhibiting TRPM2 activation， and reducing the release of pro-inflammatory cytokines.

[摘 要] 目的：探究聚丝蛋白（FLG）在黑色素瘤组织中的表达及其与患者临床病理特征、预后的关系。方法：选取2019年6月至2020年8月间山东第一医科大学附属人民医院收治的70例黑色素瘤患者为研究对象，取术中切除的瘤组织及瘤旁组织标本，用免疫组织化学法检测FLG蛋白表达，根据FLG的表达将患者分为阳性组和阴性组，比较瘤组织、瘤旁组织及不同病理特征下黑色素瘤组织中FLG的阳性表达率。随访患者3年，根据患者预后情况将患者分为生存组（n = 43）和死亡组（n = 27），比较两组患者的FLG阳性表达率，采用Kaplan-Meier法绘制生存曲线，比较两组患者生存时间。结果：黑色素瘤组织中FLG表达阳性率显著低于瘤旁组织（P < 0.05）；FLG阳性组肿瘤直径 > 1 cm、Breslow厚度 > 2 mm、局部溃疡、TNM分级Ⅲ～Ⅳ级、淋巴结转移、肿瘤侵袭占比显著低于阴性组（P < 0.05或P < 0.01）；70例患者中死亡27例，生存43例，生存率61.42%，死亡组患者FLG表达阳性率显著低于生存组（P < 0.05），FLG表达阳性患者生存时间显著长于阴性患者（P = 0.010）；多因素Cox回归分析显示，Breslow厚度 > 2 mm、TNM分级Ⅲ～Ⅳ级、淋巴结转移、肿瘤侵袭是影响黑色素瘤患者预后的危险因素（P < 0.01或P < 0.001），FLG表达阳性为保护因素（P < 0.01或P < 0.001）。结论：黑色素瘤组织中FLG显著降低，且与肿瘤Breslow厚度、分期侵袭和淋巴结转移等病理特征及预后有关。

OBJECTIVE To investigate the effects of Ephedra-Cinnamomum couplet medicinals on respiratory function and airway inflammation in rats with asthma of cold-fluid retention in lung syndrome and its mechanism. METHODS Sixty Wistar rats were randomly divided into blank group， model group， dexamethasone group [1 mg/（kg·d）]， and Ephedra-Cinnamomum low-， medium-， high-dose groups [0.234， 0.936， 1.872 g/（kg·d）]， with 10 rats in each group. The model and treatment groups were sensitized by intraperitoneal injection of antigen solution （ovalbumin 100 mg + aluminum hydroxide 100 mg） and challenged with 1% ovalbumin nebulization， along with exposure to a cold environment and ingestion of cold water， to establish the asthma model with cold-fluid retention in lung syndrome. From day 2， rats received corresponding drugs or normal saline intragastrically， once a day， for 21 consecutive days. The general behavioral changes in each group of rats were observed during the experimental process. The lung function parameters [peak expiratory flow （PEF）， airway resistance （Raw）， functional residual capacity （FRC）， expiratory flow at 50% of forced vital capacity （EF50%）] Δ 基金项目 国家自然科学基金青年科学基金项目（No.82004233）； were measured before modeling and after the last medication as well as serum contents of interleukin-6 （IL-6）， IL-13， tumor necrosis factor- α （TNF- α） and interferon-gamma （IFN- γ） after the last medication were determined； the histopathological morphological changes in the lung tissues of rats were also observed； mRNA expressions of IL-6， IL-3， TNF-α， IFN-γ， thymic stromal lymphopoietin （TSLP）， and Toll-like receptor 4 （TLR4）， as well as protein expressions of TSLP and TLR4 were determined in lung tissue. RESULTS Compared with model group， the lung tissue damage of rats was relieved significantly； Raw， FRC， the contents and mRNA expression levels of IL-6， IL-13 and TNF-α， as well as the mRNA and protein expressions of TSLP and TLR4 were significantly decreased （P＜0.05）， while the contents and mRNA expressions of PEF， EF50 % and IFN-γ were significantly increased in the dexamethasone group and Ephedra-Cinnamomum medium- and high-dose groups （P＜0.05）. Moreover， only a few rats in the two groups exhibited typical symptoms of asthma. CONCLUSIONS Ephedra-Cinnamomum couplet medicinals improve respiratory function and ameliorate airway inflammation in asthma rats with cold-fluid retention in lung syndrome， the mechanism of which may be associated with inhibiting TSLP/TLR4 signaling pathway and modulating Th1/Th2 imbalance.