Under the background of the Healthy China strategy， the integration of traditional Chinese medicine （TCM） into the public health emergency response system has become an important measure to enhance the capacity for coping with public health emergencies. In recent years， the role of TCM in responding to such emergencies has become increasingly prominent. Taking major emerging epidemics as an example， TCM has developed a rich theoretical system and practical experience in epidemic prevention and treatment over thousands of years， and has played a significant role in successive outbreaks with its unique advantages. Based on the concept of ''preventing disease before its onset'' and the theoretical framework of treatment based on syndrome differentiation， TCM has achieved remarkable results through early intervention and full participation in the integrated model of TCM and Western medicine， from severe acute respiratory syndrome （SARS） to corona virus disease-2019 （COVID-19）， in improving clinical symptoms and outcomes， reducing adverse reactions， and promoting recovery. From the perspective of the Healthy China strategy， this paper systematically reviews the historical development of TCM in epidemic prevention and treatment， with particular attention to recent epidemics such as SARS， influenza A （H1N1）， and COVID-19. It further examines the similarities and differences between TCM and Western medicine in responding to major emerging epidemics， as well as relevant policies related to TCM in epidemic prevention and control. In addition， it summarizes the existing problems in TCM's role in the prevention and treatment of major emerging epidemics， and explores measures to improve its rapid response capacity under the Healthy China strategy. This study not only provides a ''Chinese solution'' for the prevention and control of newly emerging infectious diseases worldwide， but also offers theoretical and practical references for strengthening the public health emergency response system， carrying strategic significance for promoting the modernization and internationalization of TCM.

Objective:To evaluate the effect of irisin on the alveolar macrophage polarization in a rat model of ventilator-induced lung injury (VILI).Methods:Thirty SPF healthy adult male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 3 groups ( n=10 each) using a random number table method: control group (group C), VILI group (group V) and irisin group (group I). The rats were mechanically ventilation (tidal volume 20 ml/kg, respiratory rate 80 times/min, inhaled oxygen concentration 21%, inspiratory/expiratory ratio 1∶2, positive end-expiratory pressure 0) for 4 h to develop VILI model.Group C kept spontaneous breathing for 4 h. Irisin 1 μg/kg was injected via the tail vein at 30 min before tracheal intubation in group I, while the equal volume of normal saline was given instead in the other groups.The rats were sacrificed at 4 h of mechanical ventilation, the lung tissues were removed for examination of pathological changes which were scored and for determination of wet to dry weight ratio (W/D ratio), and bronchoalveolar lavage fluid (BALF) was collected for determination of concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) and IL-10 (by enzyme-linked immunosorbent assay), expression of inducible nitric oxide synthase (iNOS), argininase 1 (Arg-1), and phosphorylated nuclear factor kappa B (p-NF-κB) p65 and p-NF-κB p50 in alveolar macrophages (by Western blot), and percentage of M1 and M2 alveolar macrophages and M1/M2 ratio (by flow cytometry). Results:Compared with group C, the W/D ratio, lung injury score, and concentrations of IL-6, TNF-α and IL-10 in BALF were significantly increased, the expression of iNOS, Arg-1, p-NF-κB p65 and p-NF-κB p50 was up-regulated, and the percentage of M1 and M2 alveolar macrophages and M1/M2 ratio were increased in group V and group I ( P<0.05). Compared with group V, the W/D ratio, lung injury score, and concentrations of IL-6 and TNF-α in BALF were significantly decreased, the expression of iNOS and p-NF-κB p65 was down-regulated, the percentage of M1 alveolar macrophages and M1/M2 ratio were decreased ( P<0.05), and no significant change was found in levels of IL-10 and Arg-1 in BALF, percentage of M2 alveolar macrophages and expression of p-NF-κB p50 in group I ( P>0.05). Conclusions:The mechanism by which irisin reduces VILI may be related to inhibition of NF-κB signaling pathway activation and reduction of alveolar macrophage polarization to M1 phenotype in rats.

Objective:To evaluate the effect of irisin on ventilator-induced lung injury (VILI) in rats and the relationship with expression of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasomes.Methods:Thirty-six SPF-grade healthy adult male Sprague-Dawley rats, aged 6-8 weeks, weighing 220-300 g, were divided into 3 groups ( n=12 each) using a random number table method: control group (group C), group VILI and irisin group (group I). All the groups underwent tracheotomy and intubation, group C kept spontaneous breathing for 4 h, and the animals were mechanically ventilated for 4 h in VILI and I groups.Irisin 1 μg/kg was injected via the tail vein at 30 min before tracheal intubation in group I, and the equal volume of normal saline mixture (normal saline∶phosphate buffer solution containing 5% trehalose=1∶9) were given in the other 2 groups via the tail vein.The rats were mechanically ventilated with the tidal volume of 20 ml/kg, respiratory rate 80 breaths/min, inspiratory/expiratory ratio 1∶1, inspired oxygen fraction ratio 21% and positive end-expiratory pressure 0.Blood samples from left femoral artery were collected before tracheal intubation and at the end of mechanical ventilation for detection of PaO 2.The animals were sacrificed and the lung tissue samples and bronchoalveolar lavage fluid (BALF) were then collected for examination of the pathological changes (under the light microscope), and for determination of wet to dry weight (W/D) ratio and the concentrations of total protein in BALF and interleukin-1β (IL-1β) and IL-18 in BALF and serum (by enzyme-linked immunosorbent assay), level of reactive oxygen species (ROS) in alveolar macrophages in BALF (by DCFH-DA) and the expression of NLRP3, apoptosis-associated speck-like protein (ASC) and caspase-1 protein and mRNA in lung tissues (by Western blot and by quantitative reverse transcription polymerase chain reaction). The pathological changes of the lung were scored. Results:Compared with group C, PaO 2 was significantly decreased at the end of mechanical ventilation, lung injury score and W/D ratio were increased, concentration of total protein and ROS level in alveolar macrophages in BALF and concentrations of BALF, IL-1β and IL-18 in serum were increased, and the expression of NLRP3, ASC and caspase-1 protein and mRNA in lung tissues was up-regulated in group VILI and group I ( P<0.01). Compared with group VILI, PaO 2 was significantly increased at the end of mechanical ventilation, lung injury score and W/D ratio were decreased, concentration of total protein and ROS level in alveolar macrophages in BALF and concentrations of BALF, IL-1β and IL-18 in serum were decreased, and the expression of NLRP3, ASC and caspase-1 protein and mRNA in lung tissues was down-regulated in group I ( P<0.05). Conclusion:Irisin can reduce VILI, and the mechanism is related to inhibiting activation of NLRP3 inflammasome and reducing inflammatory response in rats.

Objective:To investigate the effect of irisin on pyroptosis in rats with ventilator-induced lung injury.Methods:Thirty-six healthy clean-grade male Sprague-Dawley rats, weighing 200-250 g, aged 6-8 weeks, were divided into 3 groups ( n=12 each) using a random number table method: control group (group C), ventilator-induced lung injury group (group V) and ventilator-induced lung injury plus irisin group (group V+ I). In group V+ I, irisin 1 μg/kg was injected via the tail vein before mechanical ventilation.The animals were mechanically ventilated (tidal volume of 40 ml/kg, respiratory rate 60 breaths/min, inspiratory/expiratory ratio 1∶2, positive end expiratory pressure 0 and inspired oxygen fraction ratio 21%.Blood samples were then taken from the femoral artery for blood gas analysis, and PaO 2 was recorded.Bronchoalveolar lavage fluid (BALF) was collected, the total protein concentrations in BALF were measured, and the concentrations of BALF and serum interleukin-1β (IL-1β) and IL-18 were measure by enzyme-linked immunosorbent assay.The lung tissues were obtained for determination of the pathological changes after HE staining which were scored, wet to dry weight (W/D) ratio, expression of pyroptosis-related proteins N-terminal gasdermin D (GSDMD-N) and caspase-1 protein and mRNA (by Western blot or using real-time polymerase chain reaction). Results:Compared with group C, the lung injury score and W/D ratio were significantly increased, PaO 2 and OI were decreased, the total protein concentrations in BALF, concentrations of IL-1β and IL-18 in BALF and serum were increased, and the expression of caspase-1 and GSDMD-N protein and mRNA was up-regulated in group V ( P<0.01). Compared with group V, the lung injury score and W/D ratio were significantly decreased, PaO 2 and OI were increased, the total protein concentrations in BALF, concentrations of serum IL-1β and IL-18 in BALF and serum were decreased, and the expression of caspase-1 and GSDMD-N protein and mRNA was down-regulated in group V+ I ( P<0.01). Conclusion:The mechanism by which irisin reduces ventilator-induced lung injury is probably related to inhibiting pyroptosis in rats.

Objective:To evaluate the role of protein kinase C-delta (PKC-δ) in ventilator-induced lung injury (VILI) and the relationship with NLR family CARD domain-containing protein 4 (NLRC4) in rats.Methods:Thirty-six clean-grade healthy adult male Sprague-Dawley rats, weighing 200-250 g, were divided into 3 groups ( n=12 each) using a random number table method: control group (group C), VILI group (group V) and VILI plus KAI 9803 group (group VK). In V and VK groups, tracheal tubes were placed for mechanical ventilation after tracheotomy, ventilator settings were adjusted with a tidal volume of 40 ml/kg, respiratory rate of 60 breaths/min, and inspiratory/expiratory ratio of 1∶2, and air was inhaled.Group C received no mechanical ventilation after tracheal intubation.Immediately after completion of intubation, PKC-δ specific inhibitor KAI 9803 200 μg/kg was intratracheally injected in group VK, and the equal volume of phosphate buffer saline was given instead in the other two groups.Blood samples were taken from the femoral artery at 4 h of mechanical ventilation to record PaO 2.The chest was opened at the end of mechanical ventilation, lung tissues were removed, and the left lung tissues were lavaged to collect bronchoalveolar lavage fluid (BALF). The pathological changes of lung tissues were examined with a light microscope and scored.Enzyme-linked immunosorbent assay was used to detect the concentrations of interleukin-1beta (IL-1β) and IL-18 in BALF, Western blot was used to detect the expression of NLRC4, caspase-1 and PKC-δ in the right lower lobe of the lung, and the expression of NLRC4 mRNA in the right lower lobe of the lung was determined by real-time polymerase chain reaction, and the wet/dry weight ratio (W/D ratio) of the right middle lobe of the lung was calculated. Results:Compared with group C, the pathological score and W/D ratio were significantly increased, PaO 2 was decreased, the concentrations of IL-1β and IL-18 in BALF were increased, and the expression of NLRC4, caspase-1 and NLRC4 mRNA was up-regulated in V and VK groups, and the expression of PKC-δ was significantly up-regulated ( P<0.01), and a large amount of edema fluid was seen in the alveolar space, with inflammatory cell infiltration in group V ( P<0.01). Compared with group V, the pathological score and W/D ratio were significantly decreased, PaO 2 was increased, the concentrations of IL-1β and IL-18 in BALF were decreased, the expression of NLRC4, caspase-1, PKC-δ and NLRC4 mRNA was down-regulated ( P<0.05), and fluid exudation in the alveolar space and the degree of inflammatory cell infiltration were significantly attenuated in group VK. Conclusion:PKC-δ is involved in VILI, which is related to inhibiting NLRC4 expression in rats.

Objective:To evaluate the obesity factor on ventilator-induced lung injury (VILI) in rats.Methods:Forty-five clean-grade male Sprague-Dawley rats, aged 6-8 weeks, were divided into 3 groups ( n = 15 each)according to the body weight: normal weight control group (group C), normal weight VILI group (group CV) and obese VILI group (group FV). The body weight was 233-267 g in C and CV groups and 288-332 g in FV group.In group C, the tidal volume (V T) was 10 ml/kg.In CV and FV groups, the rats were ventilated for 4 h with the V T set at 40 ml/kg, respiratory rate 40 breaths/min, inspiratory/expiratory ratio 1∶2, PEEP 0 mmHg, and fraction of inspired oxygen 21% to establish the VILI model.The arterial blood samples were collected immediately before tracheal intubation and at 4 h of mechanical ventilation for blood gas analysis and PaO 2 recording.The remaining blood samples were used for plasma collection.The rats were sacrificed after blood collection at 4 h of ventilation, and the bilateral lung tissues were isolated to collect the bronchoalveolar lavage fluid (BALF). The concentrations of leptin in plasma and tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and interleukin-6 (IL-6) in plasma and BALF were detected by enzyme-linked immunosorbent assay.The wet/dry weight (W/D) ratio of lung tissues was measured.The pathological changes of lung tissues were observed after HE staining, and the lung injury score was evaluated.The expression of NF-κB p65 in lung tissues was detected by Western blot. Results:Compared with group C and group CV, the plasma leptin concentration was significantly increased in group FV( P<0.01). Compared with group C, the concentrations of TNF-α, IL-6 and IL-1β in plasma and BALF were significantly increased, PaO 2 was decreased, the lung injury score and W/D ratio of lung tissues were increased, and NF-κB p65 expression was up-regulated at 4 h of ventilation in CV and FV groups ( P<0.01). Compared with group CV, the concentrations of TNF-α, IL-6 and IL-1β in plasma and BALF were significantly decreased, PaO 2 was increased, the lung injury score and W/D ratio of lung tissues were decreased, and NF-κB p65 expression was down-regulated at 4 h of ventilation in group FV ( P<0.05). Conclusion:Obesity factor can reduce VILI in rats, and the mechanism may be related to the increase in plasma leptin levels.

Objective:To evaluate the effect of rapamycin on the activity of NOD-like receptor C4 (NLRC4) inflammasomes in the rats with ventilator-induced lung injury (VILI).Methods:Thirty-six healthy clean-grade male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 3 groups ( n=12 each) using a random number table method: control group (group C), VILI group and rapamycin group (group RAPA). In group RAPA, rapamycin 4 mg·kg -1·d -1 was intraperitoneally injected once a day for 3 consecutive days before establishing the model, while the equal volume of normal saline was given instead in group C and group VILI.The patients were mechanically ventilated for 4 h (tidal volume 20 ml/kg, respiratory rate 80 breaths/min, inspiratory/expiratory ratio 1∶1, fraction of inspired oxygen 21%) in VILI and RAPA groups.Blood samples were collected from the femoral artery after the end of ventilation for blood gas analysis and for determination of serum interleukin-1β (IL-1β) and interleukin-18 (IL-18) concentrations (by enzyme-linked immunosorbent assay), and PaO 2 was recorded.The bronchoalveolar lavage fluid (BALF) was collected for determination of the neutrophil count and IL-1β and IL-18 concentrations by enzyme-linked immunosorbent assay.The lung tissues were obtained for examination of the pathological changes (under the light microscope) after HE staining which were scored and for determination of wet to dry weight (W/D) ratio, and expression of mammalian target of rapamycin (mTOR), NLRC4 and caspase-1 (by Western blot) and expression of NLRC4 mRNA (by real-time polymerase chain reaction). Results:Compared with group C, the W/D ratio, lung injury score, neutrophil counts in BALF, and concentrations of IL-1β and IL-18 in serum and BALF were significantly increased, PaO 2 was decreased, and the expression of mTOR, NLRC4, caspase-1 and NLRC4 mRNA was up-regulated in group VILI and group RAPA ( P<0.01). Compared with group VILI, the W/D ratio, lung injury score, neutrophil counts in BALF, and concentrations of IL-1β and IL-18 in serum and BALF were significantly decreased, PaO 2 was increased, and the expression of mTOR, NLRC4, caspase-1 and NLRC4 mRNA was down-regulated in group RAPA ( P<0.05). Conclusion:The mechanism by which rapamycin alleviates VILI may be related to inhibiting activation of mTOR signaling pathway and inhibiting the activity of NLRC4 inflammasomes in rats.

Objective To evaluate the effect of penehyclidine hydrochloride on the expression of airway mucin 5AC(MUC5AC)during ventilator-induced lung injury(VILI)and the relationship with Toll-like receptor 4/myeloid differentiation factor 88(TLR4/MyD88)signaling pathway in rats.Methods Thir-ty-six clean-grade healthy male Sprague-Dawley rats,aged 6-8 weeks,weighing 200-250 g,were divided into 3 groups(n＝12 each)using a random number table method: sham operation group(group S),VILI group(group VILI),and penehyclidine hydrochloride group(group P).The rats were tracheotomized in group S.The rats were tracheotomized,connected to a small animal ventilator and mechanically ventilated for 4 h with the tidal volume of 20 ml/kg,respiratory rate 80 breaths/min,inspiratory/expiratory ratio 1 ∶1,and inspired oxygen fraction ratio 21％in VILI and P groups.At 30 min before mechanical ventilation,penehyclidine hydrochloride 2 mg/kg was injected via the tail vein in group P,and the equal volume of nor-mal saline was given instead in S and VILI groups.At 4 h of mechanical ventilation,the arterial blood sam-ples were taken for measurement of PaO2.The rats were then sacrificed,and broncho-alveolar lavage fluid(BALF)was collected for determination of interleukin-1β(IL-1β),IL-6 and tumor necrosis factor-α(TNF-α)concentrations by enzyme-linked immunosorbent assay.The lung specimens were collected for calculation of the wet/dry weight ratio(W/D ratio),for examination of pathological changes which were scored after haematoxylin and eosin staining(under a light microscope),and for determination of the ex-pression of MUC5AC(by immunohistochemistry),expression of TLR4,MyD88,p38 mitogen-activated protein kinase(p38MAPK)and nuclear factor-kappa B(NF-κB)in lung tissues(by Western blot),and expression of MUC5AC mRNA in lung tissues(by real-time polymerase chain reaction).Results Com-pared with group S,PaO2 was significantly decreased,the W/D ratio and lung injury score were increased,the expression of MUC5AC protein and mRNA was up-regulated,the concentrations of IL-1β,IL-6 and TNF-α in BALF were increased,and the expression of TLR4,p38MAPK,MyD88 and NF-κB was up-reg-ulated in VILI and P groups(P＜0.01).Compared with group VILI,PaO2 was significantly increased,the W/D ratio and lung injury score were decreased,the expression of MUC5AC protein and mRNA was down-regulated,the concentrations of IL-1β,IL-6 and TNF-α in BALF were decreased,and the expression of TLR4,p38MAPK,MyD88 and NF-κB was down-regulated in group P(P＜0.05).Conclusion Penehy-clidine hydrochloride can decrease the expression of airway MUC5AC during VILI,and the mechanism may be related to inhibiting activation of TLR4/MyD88 signaling pathway in rats.

Objective: To evaluate the effect of penehyclidine hydrochloride on the expression of airway mucin 5AC (MUC5AC) during ventilator-induced lung injury (VILI) and the relationship with Toll-like receptor 4/myeloid differentiation factor 88 (TLR4/MyD88) signaling pathway in rats. Methods: Thirty-six clean-grade healthy male Sprague-Dawley rats, aged 6-8 weeks, weighing 200-250 g, were divided into 3 groups (n=12 each) using a random number table method: sham operation group (group S), VILI group (group VILI), and penehyclidine hydrochloride group (group P). The rats were tracheotomized in group S. The rats were tracheotomized, connected to a small animal ventilator and mechanically ventilated for 4 h with the tidal volume of 20 ml/kg, respiratory rate 80 breaths/min, inspiratory/expiratory ratio 1∶1, and inspired oxygen fraction ratio 21% in VILI and P groups.At 30 min before mechanical ventilation, penehyclidine hydrochloride 2 mg/kg was injected via the tail vein in group P, and the equal volume of normal saline was given instead in S and VILI groups.At 4 h of mechanical ventilation, the arterial blood samples were taken for measurement of PaO₂.The rats were then sacrificed, and broncho-alveolar lavage fluid (BALF) was collected for determination of interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) concentrations by enzyme-linked immunosorbent assay.The lung specimens were collected for calculation of the wet/dry weight ratio (W/D ratio), for examination of pathological changes which were scored after haematoxylin and eosin staining (under a light microscope), and for determination of the expression of MUC5AC (by immunohistochemistry), expression of TLR4, MyD88, p38 mitogen-activated protein kinase (p38MAPK) and nuclear factor-kappa B (NF-κB) in lung tissues (by Western blot), and expression of MUC5AC mRNA in lung tissues (by real-time polymerase chain reaction). Results: Compared with group S, PaO₂ was significantly decreased, the W/D ratio and lung injury score were increased, the expression of MUC5AC protein and mRNA was up-regulated, the concentrations of IL-1β, IL-6 and TNF-α in BALF were increased, and the expression of TLR4, p38MAPK, MyD88 and NF-κB was up-regulated in VILI and P groups (P<0.01). Compared with group VILI, PaO₂ was significantly increased, the W/D ratio and lung injury score were decreased, the expression of MUC5AC protein and mRNA was down-regulated, the concentrations of IL-1β, IL-6 and TNF-α in BALF were decreased, and the expression of TLR4, p38MAPK, MyD88 and NF-κB was down-regulated in group P (P<0.05). Conclusion Penehyclidine hydrochloride can decrease the expression of airway MUC5AC during VILI, and the mechanism may be related to inhibiting activation of TLR4/MyD88 signaling pathway in rats.