ObjectiveTo investigate the mechanisms by which Renshentang treats atherosclerosis （AS） in mice， focusing on the regulation of endothelial inflammatory responses mediated by transient receptor potential vanilloid subtype 1 （TRPV1）. MethodsAn AS model was established in apolipoprotein E knockout （ApoE^-/-） mice fed a high-fat diet. The mice were randomly divided into a simvastatin group （0.02 g·kg^-1·d^-1） and low-， medium-， and high-dose Renshentang groups （1.77， 3.54， 7.08 g·kg^-1·d^-1）， with 12 mice in each group. ApoE^-/- mice were fed a high-fat diet and treated simultaneously. C57BL/6J mice fed a normal diet served as the normal group （n=9）. After continuous administration for 12 weeks， mice were anesthetized and the aortas were collected. Oil Red O staining was used to observe lipid plaque formation in the aorta. Hematoxylin-eosin （HE） staining was performed to examine pathological changes in the aortic root. Immunohistochemistry was used to analyze the levels of pro-inflammatory factors tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β）， as well as the expression of TRPV1， phosphorylated phosphoinositide 3-kinase （p-PI3K）， and phosphorylated protein kinase B （p-Akt） in the aortic root. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect endothelial nitric oxide synthase （eNOS） mRNA expression in the aorta， and Western blot was used to detect TRPV1 protein expression. ResultsCompared with the normal group， the model group showed a significant increase in aortic plaque formation （P<0.01） and significantly elevated levels of TNF-α and IL-1β in the aortic root （P<0.01）. The expression levels of TRPV1， p-PI3K， and p-Akt were decreased （P<0.05， P<0.01）， and eNOS mRNA expression was reduced （P<0.05， P<0.01）. Compared with the model group， all Renshentang groups significantly reduced aortic plaque formation （P<0.01）， significantly decreased TNF-α and IL-1β levels （P<0.01）， and markedly increased the expression levels of TRPV1， p-PI3K， p-Akt， and eNOS mRNA （P<0.05， P<0.01）. ConclusionRenshentang may inhibit endothelial inflammation and suppress the formation of AS by increasing TRPV1 protein expression and up-regulating the PI3K/Akt/eNOS signaling pathway， which may be one of the molecular mechanisms underlying its therapeutic effect against AS.

ObjectiveTo investigate the mechanism of Huangqi Gegentang （HGT） in the treatment of type 2 diabetes mellitus （T2DM） through the application of proteomic techniques. MethodsThe rat model of T2DM was established by streptozotocin combined with a high-fat， high-sugar diet. Thirty-two male SD rats were randomized into four groups： blank， model， HGT （8.10 g·kg^-1·d^-1）， and positive control （metformin hydrochloride， 76.5 mg·kg^-1·d^-1）. After 6 weeks of drug intervention， the fasting blood glucose level was measured， and an oral glucose tolerance test （OGTT） was performed. The area under the curve （AUC） was calculated. Enzyme-linked immunosorbent assay was performed to assess the level of glycated hemoglobin （GHbA1c） in the serum. The limulus amebocyte lysate assay was employed to measure the serum level of lipopolysaccharide （LPS）. Pathological changes in the colon were observed by hematoxylin-eosin staining. The mRNA levels of pro-inflammatory cytokines including tumor necrosis factor （TNF）-α， interleukin （IL）-6， and IL-1β in the colon tissue were quantified via Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. Additionally， the protein and mRNA levels of zonula occludens-1 （ZO-1）， Occludin， and Claudin-1 in the colon tissue were assessed by Western blot and Real-time PCR， respectively. Label-free quantitative proteomics was employed to identify the differentially expressed proteins between the colon tissue samples from the blank， model， and HGT groups. Key proteins identified were subsequently validated by Western blot and Real-time PCR. Finally， bioinformatics analysis was conducted on the differentially expressed proteins. ResultsCompared with the blank group， the model group exhibited increased fasting blood glucose， AUC， and GHbA1c levels （P<0.01）， damaged colonic mucosal epithelial structure and inflammatory cell infiltration， up-regulated mRNA levels of TNF-α， IL-6， and IL-1β in the colon and an increase in serum LPS content （P<0.05， P<0.01）， and down-regulated protein and mRNA levels of ZO-1， Occludin， and Claudin-1 in the colon （P<0.01）. Compared with the model group， the HGT group showed reductions in fasting blood glucose， AUC， and GHbA1c （P<0.01）， alleviated damage to the colonic mucosal epithelium， down-regulated mRNA levels of TNF-α， IL-6， and IL-1β in the colon， a reduction in serum LPS content （P<0.05， P<0.01）， and up-regulated protein and mRNA levels of ZO-1， Occludin， and Claudin-1 in the colon （P<0.05， P<0.01）. Proteomics analysis identified 70 differentially expressed proteins that exhibited a downward trend in the model group relative to the blank group and an upward trend in the HGT group relative to the model group. These findings were corroborated by Western blot and Real-time PCR， which confirmed that the protein and mRNA levels of mucin 2 （Muc2） and transforming growth factor （TGF）-beta receptor 1 （Tgfbr1） in the colon tissue were consistent with the proteomic data. Bioinformatics analysis showed that these 70 differentially expressed proteins identified were significantly enriched in multiple signaling pathways， among which the TGF-β and advanced glycation endproduct （AGE）/receptor for advanced glycation endproduct （RAGE） signaling pathways were closely associated with damage to the intestinal mucosal barrier. This suggests that HGT may ameliorate intestinal mucosal barrier damage by regulating these pathways. ConclusionHGT potentially exerts anti-T2DM effects by influencing AGE/RAGE and TGF-β signaling pathways， thereby contributing to the restoration of the intestinal mucosal barrier.

ObjectiveTo explore the effects of Renshentang on atherosclerosis （AS） in mice based on the role of transient receptor potential vanilloid1 （TRPV1） in regulating cholesterol metabolism in foam cells. MethodsNine SPF-grade 8-week-old C57BL/6J mice were set as a normal group， and 60 ApoE^-/- mice were randomized into model， positive drug （simvastatin， 0.02 g·kg^-1·d^-1）， and low-， medium-， and high-dose （1.77， 3.54， 7.08 g·kg^-1·d^-1， respectively） Renshentang groups （n=12） according to body weight. The normal group was fed with a normal diet， and the other groups were fed with a high-fat diet and given corresponding drugs by oral gavage for the modeling of AS. The mice were administrated with corresponding drugs once a day for 12 weeks. After the last administration and fasting for 12 h， the aorta was collected. Plaque conditions， pathological changes， levels of total cholesterol （TC）， triglcerides （TG）， low-density lipoprotein-cholesterol （LDL-C）， and high-density lipoprotein-cholesterol （HDL-C）， and the expression of TRPV1， liver X receptor （LXR）， inducible degrader of the low-density lipoprotein receptor （IDOL）， and low-density lipoprotein receptor （LDLR） in the aortic tissue were observed and detected by gross oil red O staining， HE staining， Western blot， immunohistochemistry， and real-time PCR. ResultsCompared with the normal group， the model group presented obvious plaque deposition in the aorta， raised levels of TC， TG， and LDL-C in the serum （P<0.01）， up-regulated expression level of LDLR in the aorta （P<0.01）， lowered level of HDL-C in the serum， and down-regulated expression levels of TRPV1， LXR， and IDOL in the aorta （P<0.05， P<0.01）. Compared with the model group， the positive drug and Renshentang at different doses alleviated AS， elevated the levels of HDL-C， TRPV1， LXR， and IDOL （P<0.05， P<0.01）， while lowering the levels of TC， TG， LDL-C， and LDLR （P<0.05， P<0.01）. ConclusionRenshentang has a lipid-lowering effect on AS mice. It can effectively reduce lipid deposition， lipid levels， and plaque area of AS mice by activating TRPV1 expression and regulating the LXR/IDOL/LDLR pathway.

ObjectiveTo explore the effects of Renshentang on atherosclerosis （AS） in mice based on the role of transient receptor potential vanilloid1 （TRPV1） in regulating cholesterol metabolism in foam cells. MethodsNine SPF-grade 8-week-old C57BL/6J mice were set as a normal group， and 60 ApoE^-/- mice were randomized into model， positive drug （simvastatin， 0.02 g·kg^-1·d^-1）， and low-， medium-， and high-dose （1.77， 3.54， 7.08 g·kg^-1·d^-1， respectively） Renshentang groups （n=12） according to body weight. The normal group was fed with a normal diet， and the other groups were fed with a high-fat diet and given corresponding drugs by oral gavage for the modeling of AS. The mice were administrated with corresponding drugs once a day for 12 weeks. After the last administration and fasting for 12 h， the aorta was collected. Plaque conditions， pathological changes， levels of total cholesterol （TC）， triglcerides （TG）， low-density lipoprotein-cholesterol （LDL-C）， and high-density lipoprotein-cholesterol （HDL-C）， and the expression of TRPV1， liver X receptor （LXR）， inducible degrader of the low-density lipoprotein receptor （IDOL）， and low-density lipoprotein receptor （LDLR） in the aortic tissue were observed and detected by gross oil red O staining， HE staining， Western blot， immunohistochemistry， and real-time PCR. ResultsCompared with the normal group， the model group presented obvious plaque deposition in the aorta， raised levels of TC， TG， and LDL-C in the serum （P<0.01）， up-regulated expression level of LDLR in the aorta （P<0.01）， lowered level of HDL-C in the serum， and down-regulated expression levels of TRPV1， LXR， and IDOL in the aorta （P<0.05， P<0.01）. Compared with the model group， the positive drug and Renshentang at different doses alleviated AS， elevated the levels of HDL-C， TRPV1， LXR， and IDOL （P<0.05， P<0.01）， while lowering the levels of TC， TG， LDL-C， and LDLR （P<0.05， P<0.01）. ConclusionRenshentang has a lipid-lowering effect on AS mice. It can effectively reduce lipid deposition， lipid levels， and plaque area of AS mice by activating TRPV1 expression and regulating the LXR/IDOL/LDLR pathway.

Objective: To analyze the impact of maternal metal exposure during early pregnancy on the physical development of offspring at 1 and 3 years of age, so as to provide scientific evidence for reducing the adverse effects of heavy metals on their health. Methods: From 2024 to 2018, a total of 1 588 mother child pairs from the Jiangsu Birth Cohort (JBC) were included in this study. Multiple linear regression models, generalized estimating equations (GEE), and weighted quantile sum (WQS) regression models were used to assess the associations between 24 urinary metal mass concentrations (adjusted for specific gravity, SG) during early pregnancy and offspring growth outcomes, including length/height for age Z score(HAZ), weight for age Z score(WAZ), weight for length/height Z score(WHZ), and head circumference for age Z score(HCAZ) at 1 and 3 years of age. Results: After adjusting for confounders, GEE analysis revealed that each natural log unit increase in maternal urinary concentrations of vanadium, tin, cerium, lead, and uranium during early pregnancy was associated with an average reduction in HCAZ by 14.29%, 4.82%, 2.62 %, 5.04 %, and 8.33%, respectively, at 1 and 3 years of age (FDR- P <0.05). Multiple linear regression analysis revealed that increased urinary vanadium concentration was associated with reduced HAZ at 1 year of age, while increased urinary concentrations of vanadium, chromium, tin, antimony, and uranium were associated with reduced HCAZ at 1 year of age (FDR- P <0.05). In the WQS regression model, each unit increase in the WQS index was associated with a 22.64% reduction in HCAZ at 1 year of age, with tin (22.2%) contributing the highest weight, followed by uranium (16.2%), lead (11.5%), vanadium (10.0%), arsenic (6.5%), and chromium (5.0%). Conclusions Prenatal exposure to specific metals and their mixtures may significantly impact the physical development of offspring at 1 and 3 years of age, particularly head circumference. These findings highlight the need to enhance monitoring of maternal metal exposure during early pregnancy to reduce the potential health risks posed by environmental metal pollution to infants and young children.

OBJECTIVES: The diagnostic value of ultrasonographic quantitative indicators of umbilical cord coiling, such as the umbilical coiling index (UCI) and pitch value, in identifying hypercoiling and predicting adverse pregnancy outcomes remains controversial. This study aims to evaluate the predictive value of UCI, pitch value, and the cerebroplacental ratio in pregnancies complicated by umbilical cord hypercoiling. METHODS: Pregnant women with densely coiled umbilical cords identified by routine obstetric ultrasound at Changsha Maternal and Child Health Hospital between November 2022 and November 2024 were enrolled. Complete clinical data, including UCI, pitch value, and cerebroplacental ratio (CPR), were collected. Pregnancy outcome scores were calculated, and newborns were categorized into the normal outcome group (n=177) and adverse outcome group (n=85), with the latter further subdivided into mild (n=51), moderate (n=19), and severe (n=15) subgroups. Differences in baseline data, UCI, pitch value, and incidence of CRP<1 were compared between groups and among subgroups. Correlations between UCI, pitch value, and adverse pregnancy outcomes were analyzed. Receiver operating characteristic (ROC) curve were used to assess the predictive performance of UCI, pitch value, CPR<1, and their combinations. RESULTS: Compared with the normal outcome group, the adverse outcome group had higher age, parity, parity, incidence of CPR<1, and UCI, while gestational age at delivery and pitch values were lower (all P<0.05). The incidence of obesity, gestational diabetes mellitus, and hypertensive disorders of pregnancy did not differ significantly between the 2 groups (all P>0.05). The normal outcome group showed lower UCI and higher pitch values than all 3 adverse outcome subgroups (all P<0.05), while differences among the 3 adverse subgroups were not significant (all P>0.05). UCI was positively correlated with adverse pregnancy outcomes (r_s=0.350, P<0.05), whereas pitch value was negatively correlated (r_s=-0.286, P<0.05). ROC curve analysis showed that the area under the curve (AUC) values for predicting adverse outcomes were 0.837 for UCI, 0.886 for pitch value, and 0.610 for CPR<1, with sensitivities of 77.6%, 82.4%, and 27.1% and specificities of 78.5%, 83.6%, and 94.9%, respectively. The combined UCI+CPR<1 and pitch value+CPR<1 models yielded AUCs of 0.841 and 0.886, with sensitivities of 78.8% and 81.2% and specificities of 78.5% and 84.2%, respectively. No significant differences were found between the AUCs of UCI and pitch value (P>0.05), but both outperformed CPR<1 alone (both P<0.001). The combined models showed no significant improvement over UCI or pitch value alone (both P>0.05), though both were superior to CPR<1 alone (both P<0.001). CONCLUSIONS Most umbilical cord hypercoiling cases had favorable outcomes, with UCI, pitch value, CPR<1 and their combinations demonstrating significant predictive value for adverse pregnancy outcomes.
Humans ; Female ; Pregnancy ; Pregnancy Outcome ; Adult ; Ultrasonography, Prenatal/methods* ; Umbilical Cord/diagnostic imaging* ; Hemodynamics ; Predictive Value of Tests ; Infant, Newborn ; ROC Curve

ObjectiveTo investigate the mechanism and effect of Qingfei Paidu decoction on transient receptor potential vanilloid-1/Transient receptor potential ankyrin1 （TRPV1/TRPA1） based on heat-sensitive channel and inflammatory response. MethodAccording to body weight， 80 8-week-old C57BL/6 mice were randomly divided into the normal group， model group， dexamethasone group （5 mg·kg^-1）， and low-dose， medium-dose， and high-dose groups of Qingfei Paidu decoction （14.865， 29.73， 59.46 g·kg^-1）， with 12 mice in each group. In addition to the normal group， the other groups were administered 20 μL （1×10^-3 g·kg^-1） to each mouse by airway infusion to establish the acute lung injury （ALI） model. In the administration group， the drug was given 1 h after modeling and again after an interval of 24 h. The lung tissue was taken 36 h after modeling. Double lung wet/dry weight ratio（W/D）， hematoxylin-eosin （HE） staining， enzyme-linked immunosorbent assay （ELISA）， and Western blot were used to observe and detect the pathological changes of lung tissue， expression levels of inflammatory cytokine tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6）， and expressions of TRPV1 and TRPA1 proteins in heat-sensitive channel， nuclear factor kappa-B （NF-κB）， inhibitor of NF-κB （IκBα） in inflammatory pathway， and phosphorylated proteins. The phosphorylated protein/total protein ratio was calculated. ResultCompared with that in the normal group， the lung tissue of mice in the model group was seriously damaged， and pulmonary capillary permeability increased. Alveolar capillary congestion and dilation destroyed the complete structure of the alveolar， and the alveolar wall thickened. A large number of inflammatory cells and red blood cells were infiltrated， and pulmonary edema was significantly aggravated. The expressions of TNF-α， IL-6， TRPV1， TRPA1， phosphorylated NF-κB p65/NF-κB p65， and phosphorylated IκBα/IκBα were significantly increased （P<0.01）， and the whole lung W/D was significantly increased （P<0.01）. Compared with the model group， the dexamethasone group and low-dose， medium-dose， and high-dose groups of Qingfei Paidu decoction could significantly improve pulmonary edema. TNF-α， IL-6， TRPV1， TRPA1， lung tissue NF-κB p65， and IκBα phosphorylated protein/total protein ratio decreased significantly （P<0.05， P<0.01）. The whole lung W/D also decreased significantly （P<0.05， P<0.01）. ConclusionQingfei Paidu decoction has anti-inflammatory and protective effects on LPS-ALI mice， which can effectively reduce inflammation， induce diuresis， and alleviate edema. Its mechanism may be related to the regulation of the expression of TRPA1 and TRPV1 and the inhibition of the activation of the NF-κB pathway.

Objective:To investigate the association of exposure to PM 2.5 and its constituents during pregnancy and fetal growth and to further identify critical windows of exposure for fetal growth. Methods:We included 4 089 mother-child pairs from the Jiangsu Birth Cohort Study between January 2016 and October 2019. Data of general characteristics, clinical information, daily average PM 2.5 exposure, and its constituents during pregnancy were collected. Fetal growth parameters, including head circumference (HC), abdominal circumference (AC), and femur length (FL), were measured by ultrasound after 20 weeks of gestation, and then estimated fetal weight (EFW) was calculated. Generalized linear mixed models were adopted to examine the associations of prenatal exposure to PM 2.5 and its constituents with fetal growth. Distributed lag nonlinear models were used to identify critical exposure windows for each outcome. Results:A 10 μg/m 3 increase in PM 2.5 exposure during pregnancy was associated with a decrease of 0.025 ( β=-0.025, 95% CI: -0.048- -0.001) in HC Z-score, 0.026 ( β=-0.026, 95% CI: -0.049- -0.003) in AC Z-score, and 0.028 ( β=-0.028, 95% CI:-0.052--0.004) in EFW Z-score, along with an increased risk of 8.5% ( RR=1.085, 95% CI: 1.010-1.165) and 13.5% ( RR=1.135, 95% CI: 1.016-1.268) for undergrowth of HC and EFW, respectively. Regarding PM 2.5 constituents, prenatal exposure to black carbon, organic matter, nitrate, sulfate (SO 42-) and ammonium consistently correlated with decreased HC Z-score. SO 42- exposure was also associated with decreased FL Z-scores. In addition, we found that gestational weeks 2-5 were critical windows for HC, weeks 4-13 and 19-40 for AC, weeks 4-13 and 23-37 for FL, and weeks 4-12 and 20-40 for EFW. Conclusions:Our findings demonstrated that exposure to PM 2.5 and its constituents during pregnancy could adversely affect fetal growth and the critical windows for different fetal growth parameters are not completely consistent.

ObjectiveTo investigate the effects of licoflavone A on the proliferation and glycolysis of gastric cancer cells in the hypoxic environment. MethodHuman gastric cancer AGS cells were classified into five groups： Normoxia， hypoxia， and low-， medium-， and high-dose （25， 50， 100 μmol·L^-1， respectively） licoflavone A. The cells in other groups except the normoxia group were cultured in the environment with 5% O₂ for 48 h. The cell counting kit-8 （CCK-8） and colony formation assay were employed to examine the proliferation of AGS cells. Cell migration was detected by the scratch assay. The protein and mRNA levels of hypoxia-inducible factor 1-alpha （HIF-1α）， glucose transporter 1 （GLUT1）， lactate dehydrogenase A （LDHA）， pyruvate kinase M2 （PKM2）， and hexokinase Ⅱ （HK2） in AGS cells were measured by Western blotting and real-time quantitative polymerase chain reaction （Real-time PCR）， respectively. The corresponding kits were used to determine glucose uptake and HK activity. ResultThe CCK-8 results showed that compared with the hypoxia group， the high- and medium-dose licoflavone A groups showed decreased proliferation rate of AGS cells at the time point of 24 h （P<0.01） and all the licoflavone A groups demonstrated decreased proliferation rate at the time point of 48 h （P<0.01）. Compared with the normoxia group， the hypoxia group showed increased number of clone formation of AGS cells （P<0.01）， which was decreased after the treatment with licoflavone A at high， medium， and low doses （P<0.01）. Compared with the normoxia group， the hypoxia group showed increased migration of AGS cells （P<0.01）， which was attenuated by the high， medium， and low doses of licoflavone A （P<0.01）. Compared with the normoxia group， the hypoxia group showed up-regulated mRNA levels of GLUT1， LDHA， PKM2， and HK2 （P<0.05， P<0.01）. Compared with those in the hypoxia group， the mRNA levels of GLUT1， LDHA， PKM2， and HK2 in the high-dose licoflavone A group， GLUT1， LDHA， and HK2 in the medium-dose licoflavone A group， and HK2 in the low-dose licoflavone A group were down-regulated （P<0.05， P<0.01）. The protein levels of HIF-1α， GLUT1， LDHA， PKM2， and HK2 in the hypoxia group were higher than those in the normoxia group （P<0.05， P<0.01）. Compared with those in the hypoxia group， the protein levels of HIF-1α， GLUT1， LDHA， PKM2， and HK2 in the high-dose licoflavone A group and HK2 in the medium- and low-dose licoflavone A groups were down-regulated （P<0.05， P<0.01）. The glucose uptake and HK activity were elevated in the hypoxia group compared with those in the normoxia group （P<0.01）. Compared with the hypoxia group， high-dose licoflavone A decreased the glucose uptake and HK activity， and medium-dose licoflavone A decreased the HK activity （P<0.01）. ConclusionLicoflavone A inhibits the proliferation of AGS cells under hypoxic conditions by regulating glycolysis in gastric cancer.

ObjectiveTo study the effect and mechanism of Linggui Zhugantang in treating chronic bronchitis （CB） induced by exposure to cigarette smoke combined with tracheal instillation of lipopolysaccharide （LPS）. MethodSixty SPF-grade SD rats were randomly divided into normal， model， dexamethasone （1 mg·kg^-1）， and high-， medium-， and low-dose （30.06， 15.03， 7.515 g·kg^-1， respectively） Linggui Zhugantang groups by the body weight stratification method， with 10 rats in each group. Each group was administrated with 200 μL LPS （1 g·L^-1） by tracheal instillation on days 1 and 14， respectively， while the normal group was administrated with an equal volume of normal saline. Except the normal group， the other groups were exposed to cigarette smoke on days 2-13 and 15-30 （10 cigarettes/time/30 min， twice/day） for the modeling of CB. The rats were administrated with corresponding drugs by gavage for 30 consecutive days from day 2 of modeling， and the mental status， behavior， and body weights of the rats were observed and measured. The wet/dry mass ratio （W/D） of the left lung was measured 30 days after modeling. Hematoxylin-eosin staining was employed to observe the pathological changes in the lung and bronchial tissues. The bronchial mucus secretion and goblet cell proliferation were observed by Alcian blue-periodic acid Schiff （AB-PAS） staining. The levels of mucin 5AC （MUC5AC）， interleukin （IL）-13， IL-6， and tumor necrosis factor （TNF）-α in the serum were determined by enzyme-linked immunosorbent assay. The expression of phospholipase A2 （PLA2）， transient receptor potential vanilloid receptor 1 （TRPV1）， and transient receptor potential ankyrin 1 （TRPA1） in the lung tissue was quantitatively analyzed by immunohistochemistry and Western blot. ResultCompared with the normal group， the model group showcased abnormal mental status and behaviors， bloody secretion in the nose and mouth， the mortality rate of 40%， decreased body weight， severe lung bronchial structure damage， a large number of inflammatory mediators and inflammatory cell infiltration in the tube wall， hyperemia， edema， and fibroplasia， massive proliferation of goblet cells， excessive secretion and accumulation of mucus， stenosis and deformation of the lumen， and aggravation of pulmonary edema （P<0.01）. In addition， the model group had higher levels of MUC5AC， IL-13， IL-6， and TNF-α in the serum and higher expression of PLA2 in the lung tissue than the normal group （P<0.01）. Compared with the model group， the medication groups showed normal mental status and behaviors， reduced mortality rate， stable weight gain， reduced lung and bronchial injuries， decreased goblet cell proliferation and mucus secretion， and alleviated pulmonary edema （P<0.01）. Furthermore， Linggui Zhugantang lowered the levels of MUC5AC， IL-13， IL-6， and TNF-α in the serum and down-regulated the protein levels of PLA2， TRPV1， and TRPA1 in the lung tissue （P<0.01）. ConclusionLinggui Zhugantang can reduce the pulmonary inflammation and airway mucus hypersecretion in the rat model of chronic bronchitis. It may exert the effects of reducing inflammation and resolving phlegm by regulating the PLA2-TRPV1/TRPA1 pathway.