Research Progress of Traditional Chinese Medicine in the Treatment of Acute Respiratory Distress Syndrome

Mengqi YAO, Shuyan FU, Ziqiang ZHOU, Fangyun SUN

Department of Medicine, Xizang Minzu University/Engineering Research Center for Tibetan Medicine Testing Technology of the Ministry of Education, Xianyang 712082, China

Abstract Based on the modern pathological research mechanism of ARDS, this paper summarizes the clinical therapeutic effect of traditional Chinese medicine on ARDS from the aspects of reducing inflammatory mediators, cells and factors, regulating signal pathway, regulating aquaporin, anticoagulation and so on. The purpose is to provide new theoretical basis and ideas for scholars in the future, and to improve the internationalization process of traditional Chinese medicine in the treatment of acute respiratory distress syndrome.

Key words Acute respiratory distress syndrome, Acute lung injury, Traditional Chinese medicine, Inflammation, Cytokines, Aquaporin

1 Introduction

Acute respiratory distress syndrome (ARDS) refers to the diffuse damage of pulmonary capillary endothelial cells and alveolar epithelial cells caused by cytokine storms. At present, the main ways of Western medicine to treat ARDS are auxiliary mechanical ventilation, control of body fluid exchange and anti-infection, but its clinical fatality rate is still high. In addition, some corticosteroids and other drugs are used, and there is a certain therapeutic effect, but the side effects do great harm to the human body, so that we can not achieve the desired effect. In recent years, with the continuous development of traditional Chinese medicine, certain results have been achieved in the prevention and treatment of ARDS.

The clinical symptoms of ARDS are fever, cough, expectoration,etc., of which the serious one is dyspnea, because the disease progresses rapidly, resulting in lung insufficiency, patients will develop serious symptoms such as respiratory failure in a short period of time, and the fatality rate is as high as 50%[1]. In the early stage of the lesion, the blood vessels of the alveolar wall are dilated and congested, and fluid exudation can be seen in the alveolar cavity, and in severe cases, it develops into pulmonary consolidation. When it develops to the later stage, the body liquifies and absorbs or coughs up the alveolar contents, causing pulmonary interstitial fibrosis and fibrous hyperplasia of the pulmonary membrane, resulting in alveolar fibrous occlusion. The concepts of acute lung injury (ALI) and ARDS were put forward in the 1994 American-European Consensus Conference (AECC). At this meeting, it is considered that ALI and ARDS are two different stages in the pathogenesis of the same disease. ALI represents the early stage, while ARDS represents the later stage of the disease, and 55% of ALI will further become ARDS within three days. Subsequently, in the Berlin definition published in theJournaloftheAmericanMedicalAssociation(JAMA) in 2012, it decided to cancel the naming of ALI and referred to them as ARDS[2].

2 The theory of traditional Chinese medicine

Matthayetal.[3]believed that ARDS is actually high permeability pulmonary edema caused by diffuse alveolar capillary injury and increased pulmonary capillary permeability. Since ancient times, there is no record of ALI/ARDS in traditional Chinese medicine, but it is classified as "wheezing" and "sudden dyspnea" because of its fever, expectoration, cough and dyspnea. Li Yanruetal.[4]believed that the impaired diffusion and downbearing of the lung and the imbalance of body fluid transfusion and excretion are the important causes of ALI/ARDS, which are caused by poor blood circulation and poor blood gas flow due to trauma or infection. In recent years, with the in-depth study of the action mechanism of traditional Chinese medicine and its active components, it has been more and more widely accepted by the public because of its safety, effectiveness and low price, and has become a new class of widely used anti-inflammatory drugs. With the increasing number of studies on traditional Chinese medicine through multi-target, multi-component treatment of ARDS, certain results have been achieved in the prevention and treatment of ARDS.

3 Treatment aiming at inflammatory mediators, cells and factors

ARDS is a diffuse injury of pulmonary capillary endothelial cells and alveolar epithelial cells caused by the release of various cytokines and inflammatory cells (macrophages, neutrophils and vascular endothelial cells) triggered by inflammatory factor storm. Therefore, to effectively and quickly control the release of cytokines and inflammatory cells is an important means to inhibit inflammatory response.

3.1 Inflammatory mediators

3.1.1Nitric oxide (NO). NO is a substance mainly produced by vascular endothelial cells and usually exists in the form of free radicals in the body. Usually, as one of the important gases needed by the human body, NO plays an important role in relaxing blood vessels and regulating blood pressure. During lung injury, a large number of inflammatory factors TNF-α and IL-6 are produced, and a large amount of nitric oxide synthase is induced by alveolar macrophages and alveolar epithelial cells, which makes NO produced in large quantities, increases vascular permeability, and leads to pulmonary edema and respiratory disorders in ARDS. When the inducible nitric oxide synthase (iNOS) is overexpressed, it will lead to the production of a large amount of NO, and it is also combined with superoxides, which aggravates the degree of lung injury. Zhou Mengjing[5]believed that the use of pulsatilla saponin B4 can reduce the level of NO in the supernatant of RAW264.7 cells and reduce the synthesis and release of inflammatory cytokines. Guo Meietal.found that[6]ligustrazine can reduce the level and activity of iNOS in serum of ALI in rats induced by LPS, reduce vascular permeability and maintain stable blood pressure. Geng Yunetal.[7]found that Xianxiongtaocheng decoction combined with Shenmai injection significantly decreased the content of NO in serum of ARDS rats compared with the model group, and reduced the degree of lung injury and hypoxemia to some extent. Gu Yanetal.[8]found that the use of self-made Qingfei decoction can also reduce the serum NO of ALI/ARDS patients, reduce the degree of pulmonary edema, and play a certain role in prevention and treatment. At the same time, Chen Jianrongetal.[9]found that the level and activity of iNOS and the content of NO in serum of patients with ARDS treated with Qingfei decoction were down-regulated to a certain extent, and the effect on pulmonary edema was alleviated obviously.

3.1.2Vascular endothelial growth factor (VEGF). VEGF is a regulatory medium that binds to specific receptors of vascular endothelial cells and has the function of regulating vascular permeability. Under normal circumstances, the content of VEGF in the human body is very low, and it is relatively rich only in the lung tissue compared with other human organs. However, when dyspnea, hypoxia, pregnancy and tumor occur, VEGF will be highly expressed in the body, which will increase alveolar capillary permeability and cause pulmonary edema, which is one of the important factors leading to lung injury. The increase of plasma VEGF level can lead to the increase of pulmonary capillary permeability and the aggravation of pulmonary edema. At the same time, when the patient has ARDS, the concentration of VEGF in serum will increase over time, which not only leads to the increase of alveolar capillary permeability, but also leads to the increase of vascular permeability of damaged organs. Therefore, down-regulation of VEGF expression is one of the keys to the treatment of ARDS. Yang Linjiangetal.[10]used Tanreqing injection to treat dozens of patients with ARDS, and found that Tanreqing injection could reduce the expression of serum inflammatory mediator VEGF, reduce vascular permeability, maintain blood pressure and reduce the degree of pulmonary edema in patients with ARDS. Xue Leixietal.[11]found that Xuebijing can down-regulate the content of VEGF-A in serum of patients with ALI/ARDS, reduce the vascular permeability of lung tissue and reduce pulmonary edema. Meng Lingetal.[12]found that the use ofR.kirilowiiinjection can also reduce the content of VEGF-A in serum and protect the lung tissue of patients. Liu Xuanetal.[13]found thatAstragalusextract could significantly down-regulate the content of VEGF in serum of experimental ARDS rats, reduce the vascular permeability of lung tissue, and play a positive role in the prevention and treatment of pulmonary edema.

3.1.3Serum endothelin-1 (ET-1). ET-1 is a polypeptide composed of multiple amino acids. ET-1 is mainly found in endothelial cells, cardiomyocytes, fibroblasts and neurons. It can contract the coronary artery and increase the blood pressure of the whole body. Under normal circumstances, the content of ET-1 in lung tissue in the body is the highest. Endothelin is a physiologically regulatory hormone, which is involved in the occurrence of many diseases, such as shock, stroke, myocardial ischemia, and infection. Gu Yanetal.[14]used self-made Qingfei decoction, which has the effects of detoxification, clearing heat, relieving asthma and so on, to treat patients with ARDS. The content of ET-1 in serum of the treatment group was significantly lower than that of the normal treatment group, and it inhibited the synthesis and release of ET-1, and successfully treated 26 patients, playing the role of treating ARDS. He Lanetal.[15]found that Xuebijing injection combined with high-dose ambroxol significantly decreased the content of plasma ET-1 in patients with severe pneumonia complicated with acute respiratory distress syndrome, and improved the respiratory function of the patients. Li Zhongetal.[16]found that Danggui Buxue decoction significantly decreased the content of ET-1 in plasma of rats with acute radiation-induced lung injury, alleviated the degree of pulmonary edema and improved lung injury.

3.1.4Serum prostaglandin-E2 (PGE2). PGE2 belongs to adipose hormone. It exists in all organs of the body, among which the content of lung tissue is the highest. It can stimulate kidney to produce erythropoietin (EPO), dilate blood vessels, relax airway, and protect gastric mucosa. Gu Yanetal.[14]used Qingfei decoction, a self-made traditional Chinese medicine, to treat ARDS patients, and found that the serum PGE2 content in the treatment group was significantly lower than that in the normal treatment group, and the oxygenation index (PaO2/FiO2) of ARDS patients was improved to reduce the mortality of ARDS. Zhang Huietal.[17]found that the content of PGE2 in bronchoalveolar lavage fluid of ALI in mice induced by LPS was significantly lower than that of the model group, and the respiratory function of lung tissue was improved.

3.1.5Triggering receptors expressed on myeloid cell-1 (TREM-1). TREM-1 is a kind of immunoglobulin mainly expressed on the surface of neutrophils and mature monocytes. TREM-1 can amplify the inflammatory response and promote the secretion of various inflammatory cytokines. TREM-1 also plays an important role in the inflammatory response induced by ARDS. It is conceivable that if it can down-regulate the synthesis and release of TREM-1, it can protect the lung tissue of the body. The study of Yu Hairongetal.[18]showed that compoundS.flavescenscould reduce the content of TREM-1 in lung tissue of rabbit with ARDS induced by LPS, reduce the occurrence of inflammatory reaction, down-regulate the synthesis and release of pro-inflammatory cytokines, and significantly improve respiratory function.

3.1.6Intercellular adhesion molecule-1 (ICAM-1). Intercellular adhesion molecule-1 (ICAM-1) is a special substance that mediates intracellular cells and extracellular matrix. ICAM-1 is a member of the immunoglobulin superfamily (IGSF) on vascular endothelial cells. Under normal conditions, ICAM-1 shows low expression in vascular endothelial cells, but when pro-inflammatory factors IL-1β, IL-6 and IL-8 are highly expressed, the expression of ICAM-1 will be significantly up-regulated, resulting in a large number of white blood cells gathering in lung tissue, causing lung parenchyma injury and continuous expression of pro-inflammatory factors. Jiang Longetal.[19]found that when using astragalus polysaccharides (APS) extracted from the dried rhizome of Radix Astragali to treat ALI induced by LPS in rats, the expression of ICAM-1 in serum in the treatment group was significantly lower than that in the model group, and the degree of lung injury was significantly improved. Fu Xuelinetal.[20]found that when rhubarb combined with ulinastatin was used to treat ARDS patients, the expression of serum ICAM-1 was significantly down-regulated, alleviating lung injury and further aggravation of inflammatory reaction. Hu Yananetal.[21]found that curcumin could significantly down-regulate the content of ICAM-1 in serum of rats with bleomycin-induced acute lung injury and reduce inflammatory reaction in the treatment of lung injury. Liu Xiaofangetal.[22]found that the content of ICAM-1 in serum of patients with acute lung injury treated with Shenmai injection decreased significantly, which played a protective role in lung injury.

3.2 Inflammatory cellsAfter being infected with ARDS, the body will produce a large number of inflammatory factors and mediators, which promote the accumulation of inflammatory cells in lung tissue, such as neutrophils, macrophages, and lymphocytes. Inflammatory cells activated by inflammatory response lead to the unique "respiratory burst" of ARDS, and produce a series of chain reactions, resulting in a large number of oxygen free radicals, which make the inflammatory response more serious. Excessive inflammatory reaction can lead to damage of alveolar capillary endothelial cells and alveolar epithelial cells, increase vascular permeability and form microthrombus; a large amount of body fluid permeates into pulmonary interstitium and alveoli to form pulmonary edema, resulting in the formation of hyaline membrane in alveoli, atelectasis and pulmonary interstitial fibrosis. Dachengqi decoction, a famous prescription in Treatise on Febrile Diseases written by Zhang Zhongjing in the Eastern Han Dynasty, is composed of rhubarb, magnolia, mirabilite andF.Aurantii. It can play a therapeutic role with multiple components and multiple targets, and has a broad application prospect in the treatment of ALI/ARDS. The experimental study of Li Yumeietal.[23]found that the use of Dachengqi decoction can prevent the accumulation of polymorphonuclear leukocytes (PMN) in lung tissue and inhibit its activation, thus protecting pulmonary capillary endothelial cells and alveolar epithelial cells, reducing vascular permeability and alleviating the degree of pulmonary edema. Zhou Mengjingetal.[24]found that pulsatilla saponin B4 could significantly reduce the number of BALF neutrophils in LPS-induced mouse ALI model, and the number of leukocytes in BALF also had a certain downward trend, reducing the occurrence of "respiratory burst" and a series of subsequent chain reactions, so as to achieve the effect of prevention and treatment of ARDS.

3.3 Inflammatory cytokines

3.3.1Pro-inflammatory cytokines. Studies have shown that pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and interleukin-8 (IL-8) play an important role in the pathogenesis of ARDS disease. When a large number of inflammatory factors and mediators are produced, it will promote the accumulation of inflammatory cells in the lung tissue, including macrophages, and TNF-α is mainly produced by activated macrophages. And TNF-α is the most important cytokine and initiator of inflammatory response caused by ARDS, and it is also an important factor to activate the cascade of inflammatory factors. When a large amount of TNF-α is released, it will cause aggregation and activation of IL-1β, IL-6, IL-8, platelet activating factor (PAF), prostaglandin (PG), NO and endothelin[25]. First of all, it binds to specific receptors on pulmonary capillary endothelial cells and alveolar epithelial cells, and produces a large number of oxygen free radicals leading to increased vascular permeability and microthrombosis[26]; at the same time, TNF-α reacts to stimulate macrophages to produce NO, increase vascular permeability, lead to pulmonary edema, dilate blood vessels and lead to falling blood pressure. IL-1β is mainly produced by activated monocytes-macrophages. IL-1β can release bone marrow neutrophils into the blood, activate them, and make them accumulate to aggravate the effect of lung injury. IL-6 is a cytokine produced by activated T cells and fibroblasts. When inflammation occurs, PMN can accumulate in the lung tissue and aggravate the degree of pulmonary edema. IL-6 has become the key node of some cytokine storm syndrome (CSS). IL-8 is mainly produced by a variety of inflammatory cells such as neutrophils, macrophages, lymphocytes, pulmonary capillary endothelial cells and alveolar epithelial cells. It is also through the chemotaxis of neutrophils to gather in the lung tissue, which aggravates pulmonary edema. Jiang Longetal.[19]found that when using astragalus polysaccharides (APS) to treat LPS-induced ALI in rats, the serum TNF-α and IL-6 level in the treatment group was significantly lower than that in the model group, regulating the inflammatory response of the body, thus achieving the function of protecting rat lung tissue. Li Yumeietal.[27]found that Dachengqi decoction can inhibit the synthesis and release of TNF-α, IL-1β, IL-6 and IL-8, eliminate excessive pro-inflammatory cytokines, reduce the damage of ARDS to lung tissue, and make the immune function of patients play a normal function. Mao Yiminetal.[28]found that ginsenosides from stems and leaves can reduce the content of TNF-α in lung tissue and inhibit the expression of IL-8 in lung tissue of ALI rats, which can play a role in the prevention and treatment of ARDS. Liu Enshunetal.[29]found that when treating ALI/ARDS rats with Tongfu Xiefei prescription, it could reduce the expression of inflammatory factors TNF-α, IL-6, IL-10 and IL-1β in serum, reduce inflammatory reaction and protect lung tissue. In the treatment of patients with acute lung injury with traditional Chinese medicine combined with Western medicine, Xu Shunguietal.[30]found that the levels of TNF-α and IL-1β in serum of patients in the combined treatment group decreased significantly, and it down-regulated the expression of inflammatory factors and reduced the inflammatory reaction. Zhang Zhilinetal.[31]found that when treating ALI rats with integrated traditional Chinese and Western medicine, Tanreqing injection was used in the traditional Chinese medicine group and ulinastatin in the Western medicine group, the levels of TNF-α and IL-6 in the traditional Chinese medicine group and the Western medicine group were significantly lower than those in the model group, and there was no significant difference between the traditional Chinese medicine group and the Western medicine group, indicating that Tanreqing injection could inhibit the expression of inflammatory factors. Chen Yanetal.[32]found that compared with the Western medicine treatment group, the levels of TNF-α, IL-1β, IL-8 and mortality decreased significantly with ginseng, astragalus, gecko,Ophiopogonjaponicusand other drugs as prescriptions.

3.3.2Anti-inflammatory cytokines. Studies have shown that anti-inflammatory cytokines such as interleukin-4 (IL-4) and interleukin-10 (IL-10) play an important role in the development of ARDS disease. IL-4 and IL-10 are mainly derived from the immune regulation involving lymphocytes and macrophages and play a key role in humoral and cellular immunity. IL-4 and IL-10 can inhibit the synthesis and release of pro-inflammatory cytokines and reduce the inflammatory response. However, during the occurrence of ARDS, these anti-inflammatory cytokines are significantly reduced, which is also one of the reasons for the serious inflammatory response in ARDS. Some studies have shown that Li Yumeietal.[27]used Dachengqi decoction to up-regulate the synthesis and release of IL-4 and IL-10. At the same time, these anti-inflammatory factors acted on pro-inflammatory factors, and reduced inflammatory reaction, to achieve the role of prevention and treatment of ARDS. Ji Yuhongetal.[33]found that the pretreatment of IL-10 in serum of ALI rats with ginsenosides can play a role of up-regulation, improve the release of anti-inflammatory factors and reduce inflammatory reaction.

4 Regulating TLR4-NF-κB signal pathway

First of all, the key pro-inflammatory cytokine in this pathway is HMGB1, which is the core of initiating and maintaining "respiratory bursts". Some studies have shown that when the lung tissue is seriously damaged, HMGB1 will actively participate in tissue remodeling and the formation of pulmonary hypertension. At the same time, HMGB1 is the upstream regulatory factor of TLR4, and inflammatory response can be induced by a variety of mechanisms. TLR4 can promote the activation and release of neutrophils and pro-inflammatory cytokines, and aggravate the inflammatory response of ARDS. The activation of TLR4 will cause a series of cascade reactions, which can promote the activation of NF-κB. NF-κB will further release a large number of inflammatory factors, which will cause inflammatory reaction again and aggravate the degree of lung injury in ARDS. Liu Shiyongetal.[34]found that resveratrol can down-regulate the content of NF-κB in lung tissue of mice with LPS-induced ALI, reduce the release of inflammatory factors in the cascade reaction, and alleviate the inflammatory reaction. Guo Tingting[35]found that vanillin can significantly reduce the protein expression of inflammatory cytokines by regulating NF-κB, thus reducing the inflammatory response. Gu Zhilongetal.[36]found that curcumin had a protective effect on ALI induced by LPS in mice, and the main mechanism may be related to the inhibition of LPS-TLR4 and activation of MyD88-NF-κB signal transduction pathway. Li Xinetal.[37]found that Yiqi Huayu Jiedu prescription can protect ARDS rats by inhibiting NF-κB/p38MAPK pathway, reduce inflammatory reaction and slow down the release of subsequent inflammatory factors. Xiang Hong[38]found that the aqueous extract of R. Hedysari can treat rats with ALI induced by endotoxin by inhibiting the expression of NF-κBp65 signal pathway, reduce the expression of TNF-α, and play a certain role in prevention and treatment. Ruan Qiongetal.[39]found that Xuanfei Tongfu prescription can protect the lung tissue of ALI rats by reducing the expression of NF-κB protein, and reduce the expression of serum inflammatory factors TNF-α, IL-6, IL-10, IL-1β, and reduce the injury of lung tissue. Su Zhonghaoetal.[40]used Xuanbai Chengqi decoction to study the relationship between lipopolysaccharide binding protein (LBP) and TLR4 in lung tissue of rats with ALI induced by LPS. It was found that the expression level of TLR4mRNA in Xuanbai Chengqi decoction treatment group was lower than that in model group, and it had a protective effect on lung injury by reducing the expression of TLR4. Zhou Enetal.[41]found that Qingwen Baidu Yin had a certain protective effect on LPS-induced acute lung injury in rats, and the degree of lung tissue injury in the treatment group was significantly lower than that in the model group, and it was concluded that one of the key causes of acute lung injury was the activation of NF-κB.

5 Regulating aquaporins (AQPs)

The main pathological features of ARDS are diffuse edema and pulmonary parenchyma cell injury, and the increase of vascular permeability leads to the accumulation of a large amount of fluid in the lung tissue. If the excess fluid can be removed and the environment in the alveolar tissue can be kept stable, it will play a positive role in the treatment of ARDS and lung tissue ventilation. Aquaporins are a large family of homologous proteins that selectively and efficiently transport water molecules on the cell membranes of prokaryotes and eukaryotes, and their main role is the transport and absorption of liquids. There are 6 kinds of aquaporins distributed in lung tissues (AQP-1, AQP-3, AQP-4, AQP-5, AQP-8, AQP-9)[42]. AQP-1 is only responsible for transporting water and does not allow any other substance to pass through the endothelial cells. AQP-1 and AQP-5 play a role in clearing water during ARDS, AQP-1 mainly removes the water in the tissue around the bronchus, and AQP-5 removes the water in the alveolar cavity. When aquaporin decreases, it will lead to a decrease in the ability of the lung tissue to reabsorb water, resulting in pulmonary edema and causing it to aggravate the symptoms again. Yu Hairong[18]found that compoundS.flavescenscan up-regulate the content of AQP-1 in lung tissue of rabbits with ARDS induced by LPS, remove excess water in lung tissue, reduce the degree of pulmonary edema and regulate dyspnea. Wu Lipingetal.[43]found that rhubarb can up-regulate the content of AQP-1 and AQP-5 in lung tissue of rabbits with LPS-induced ARDS, and reduce the degree of pulmonary edema. Chen Yietal.[44]found that ligustrazine can increase the content of AQP-1 and AQP-5 in the lung tissue of rats with ALI induced by endotoxin and restore the reabsorption function of water in the lung tissue. The experimental study of Huang Renfaetal.[45]found thatC.sinensishad a positive effect on the expression of AQP-1 in lung tissue, accelerating the reabsorption capacity of lung tissue to water, and protecting the degree of lung injury.

6 Use of anticoagulants

First of all, the activation of coagulation system is closely related to inflammatory reaction. During development of ARDS, a large number of tissue factors are activated and C-reactive protein activity is decreased, which makes the lung tissue become procoagulant and antifibrinolytic. The abnormal state of coagulation and fibrinolysis is accompanied by the whole process of ARDS. Therefore, anticoagulation and fibrinolysis have become an important part of ARDS treatment. Inflammatory cytokines, such as TNF-a, IL-1β, IL-6 and IL-8, can activate the coagulation system through exogenous pathway and make the alveoli become procoagulant and antifibrinolytic. At the same time, LPS can directly act on coagulation factor VII and activate the endogenous coagulation pathway, resulting in hypercoagulable lung tissue. Xu Minetal.[46]found that compoundS.miltiorrhizainjection can down-regulate the expression of PAF in patients with ALI, reduce the hypercoagulable state, slow down the state of intraalveolar fibrinolysis, and achieve the effect of treating ARDS. Jiang Xiaoganetal.[47]found that when Xuebijing injection was used to treat acute respiratory distress syndrome, the prothrombin time (PT) and activated partial prothrombin time (APTT) of patients decreased, which improved coagulation and lung respiratory ability and played a certain therapeutic role in ARDS.

7 Conclusion

To sum up, traditional Chinese medicine and its effective components mainly treat ARDS through anti-inflammatory reaction, anti-oxidant stress, anticoagulation, fibrinolysis, regulation of aquaporin,etc., and achieve good therapeutic effects through multiple targets, multiple components and multiple mechanisms. However, the people’s acceptance of traditional Chinese medicine is not high, and there are few ways to understand it, so it is necessary to strengthen the publicity and development of traditional Chinese medicine, make use of existing science and technology to prepare more perfect Chinese medicine, and improve the treatment rate of ARDS, in order to better face the public and internationalization. ALI/ARDS is a serious injury of lung function caused by a variety of pathogenic factors, and the incidence rate and fatality rate are high. Its pathogenesis has not been fully determined, and many effective chemical components in traditional Chinese medicine are not completely clear, and most of the experiments are still in the experimental animal stage, have not been clinically promoted, so it is necessary to conduct more in-depth research in this area. The research on ALI/ARDS traditional Chinese medicine is not deep enough, and the screening, mechanism and target of traditional Chinese medicine are not clear enough. Therefore, the research on traditional Chinese medicine is still worthy of further consideration, and the design of experiments needs to be more rigorous and perfect in the future, in order to make a breakthrough in the treatment of ARDS.