CN108309967B - Traditional Chinese medicine monomer composition for antagonizing lung injury and application thereof - Google Patents

Traditional Chinese medicine monomer composition for antagonizing lung injury and application thereof Download PDF

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CN108309967B
CN108309967B CN201810240899.2A CN201810240899A CN108309967B CN 108309967 B CN108309967 B CN 108309967B CN 201810240899 A CN201810240899 A CN 201810240899A CN 108309967 B CN108309967 B CN 108309967B
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monomer composition
chinese medicine
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lung injury
medicine monomer
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CN108309967A (en
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曹珂
付志萍
郝建新
徐军
潘俊辉
王鹏
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Guangzhou Institute Of Respiratory Health
First Affiliated Hospital of Guangzhou Medical University
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First Affiliated Hospital of Guangzhou Medical University
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    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
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    • A61K31/335—Heterocyclic compounds having oxygen as the only ring hetero atom, e.g. fungichromin
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    • A61K31/352—Heterocyclic compounds having oxygen as the only ring hetero atom, e.g. fungichromin having six-membered rings with one oxygen as the only ring hetero atom condensed with carbocyclic rings, e.g. methantheline 
    • A—HUMAN NECESSITIES
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    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61K—PREPARATIONS FOR MEDICAL, DENTAL OR TOILETRY PURPOSES
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    • A61K31/7034—Compounds having saccharide radicals attached to non-saccharide compounds by glycosidic linkages attached to a carbocyclic compound, e.g. phloridzin
    • A61K31/704—Compounds having saccharide radicals attached to non-saccharide compounds by glycosidic linkages attached to a carbocyclic compound, e.g. phloridzin attached to a condensed carbocyclic ring system, e.g. sennosides, thiocolchicosides, escin, daunorubicin

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Abstract

The invention discloses a traditional Chinese medicine monomer composition for antagonizing lung injury, which mainly comprises active ingredients of quercetin, glycyrrhizic acid and ferulic acid. The invention also discloses application of the traditional Chinese medicine monomer composition. The traditional Chinese medicine monomer composition provided by the invention can regulate the respiratory tract immune system and avoid pathological damage caused by excessive immune response due to lack of or inhibition of an immune tolerance inhibiting mechanism by activating cAMP-dependent CFTR (circulating tumor necrosis factor), and can inhibit pulmonary fibrosis and promote the repair of damaged cells to normal cells.

Description

Traditional Chinese medicine monomer composition for antagonizing lung injury and application thereof
Technical Field
The invention relates to a medicament for resisting lung injury, in particular to a traditional Chinese medicine monomer composition for antagonizing lung injury. The invention also relates to application of the traditional Chinese medicine monomer composition.
Background
The innate immune system of the respiratory tract is the first line of defense of the body against pathogenic microorganisms. The research shows that: the body recognizes pathogen-associated molecular patterns (PAMPs) of pathogenic microorganisms through Pattern Recognition Receptors (PRRs), initiates an innate immune response against pathogens, recruits immune phagocytes into the lung by releasing inflammatory factors, chemokines and the like, and eliminates pathogens invading inside and outside cells, and the inflammatory process causes tissue cell damage. At the same time, the body can also initiate immune tolerance mechanisms to control the degree of inflammatory response and prevent tissue cell damage. The absence or suppression of immune tolerance mechanisms can lead to excessive immune responses that produce pathologic lesions of immunity. For example, the Hemagglutinin (HA) of highly pathogenic avian influenza virus H5N1 can inhibit the negative control NF-kB transcription function of immune inflammation regulator CFTR by inducing JAK3 abnormal activation, inhibit the immune tolerance mechanism of the organism, aggravate the immune response inflammatory reaction, and further promote the occurrence of immune pathological injury of the lung.
Cystic fibrosis transmembrane conductance regulator (CFTR) is a cyclic adenosine monophosphate (cAMP) activated ATP-gated chloride ion (Cl)-) A channel. Mainly provides a selective channel for trans-epithelial movement of chloride ions, and has important determining functions on trans-epithelial salt transportation, liquid flow, ion concentration regulation and the like. The cilia of the respiratory tract are infiltrated by the mucus layer, and in normal mucus, the cilia can swing back and forth to directionally convey the mucus and various pathogens and other harmful substances attached to the mucus, so that the respiratory tract is prevented from being stimulated. Mucus layer function is regulated by CFTR. Chloride channel of CFTR is identical to Ca2+Synergistic Cl secretion from activated chloride channels-And secrete intracellular water-soluble proteins and other macromolecules to the respiratory mucosa along with water. At the same time, CFTR chloride channels restrict the influx of Na into the airway epithelium+The activity of the channel further limits the reabsorption of water in the respiratory tract mucous membrane, thereby maintaining the normality of the respiratory tract mucous membrane and ensuring the function of clearing the respiratory tract. Na in the epithelium when the respiratory tract lacks CFTR+Excessive opening of the channels and excessive Na in the mucus+Into the cells, water is simultaneously transferred from the mucus to the blood. The mucus becomes thicker and the flagellum swingsMovement is blocked, the conveying function is weakened, secondary persistent bacterial infection can be caused, and large-area immune inflammation injury of the epithelium is caused. In addition, the damage of epithelial cells can also cause the accumulation of ceramide with proinflammatory effect, thereby not only enlarging the inflammatory response caused by viral infection or bacterial infection, but also further reducing the clearance of the organism to pseudomonas aeruginosa.
In addition, there is considerable evidence that CFTR is also a renaturation regulator of the NF-. kappa.B signaling pathway. The mutation of the lung tissue epithelial CFTR ion channel can cause the excessive activation of NF-kB to generate a large amount of proinflammatory factors, thereby accelerating the immune damage of the lung. This airway hyperinflammatory response can also be mimicked if in vitro intervention with the specific CFTR inhibitor CFTRinh-172 inhibits the CFTR channel of the airway epithelium. In addition, the highly proinflammatory environment in the airways can lead to infiltration of large numbers of macrophages. Although the recruited macrophages may to some extent phagocytose bacteria, dead epithelial cells, recruit neutrophils, and may also promote maturation of DCs, T cell activation, and priming of adaptive immunity. However, in the lung tissue of cystic fibrosis patients, NF-. kappa.B and MAPK signaling pathways are found to be over-activated within macrophages, releasing more proinflammatory factors and chemokines, such as IP-10, IL-6, IL-8, MCP-1, MIP-1. alpha., MIP-1. beta. and RENTES, and rather aggravating the damage to lung tissue, resulting in severe lung inflammation. Furthermore, it has been found that the phagocytic function of macrophages and neutrophils in lung tissue of cystic fibrosis patients is severely reduced, resulting in severe infection of lung tissue. In conclusion, CFTR has an immune tolerance function as an immunoinflammation regulator.
CFTR function is regulated by intracellular cAMP levels, which are regulated by Adenylate Cyclase (AC) and Phosphodiesterase (PDE) activity. The elevation of cAMP level activates CFTR, enhances the immune tolerance of the organism, and inhibits the immune inflammation damage. Meanwhile, the increased cAMP can inhibit Jagged1/Notch1 signal pathways through cAMP-PKA, and inhibit the occurrence of pulmonary fibrosis.
Disclosure of Invention
One of the purposes of the invention is to provide a traditional Chinese medicine monomer composition for antagonizing lung injury. The traditional Chinese medicine monomer composition regulates the respiratory tract immune system on one hand by activating cAMP-dependent CFTR, and avoids pathological damage caused by excessive immune response due to lack of immune tolerance mechanism or inhibition; on the other hand, the medicine inhibits pulmonary fibrosis and promotes the repair of damaged cells to normal cells.
One of the purposes of the invention is realized by the following technical scheme: a Chinese medicinal monomer composition for antagonizing lung injury comprises quercetin, glycyrrhizic acid and ferulic acid as main effective components.
The molar ratio of the quercetin to the ferulic acid to the glycyrrhizic acid is 1: 1-10: 1.
Further, the molar ratio of the quercetin to the ferulic acid to the glycyrrhizic acid is 1: 1-3: 1.
The inventor finds that the single use of quercetin, glycyrrhizic acid and ferulic acid can activate cAMP-dependent CFTR to a certain extent through a comparative experiment. Furthermore, ferulic acid, glycyrrhizic acid and quercetin have respective side effects on the inhibition of inflammatory factors, and ferulic acid inhibits the expression of ICAM-1, IP-10, MCP-1 and MIP-1. Glycyrrhizic acid inhibits the expression of IP-10, IL-18, MCP-1, MIP-1 and MMP-7. Quercetin inhibits the expression of IP-10 and MMP-7. However, researches show that the composition of the three monomers has more remarkable effect of activating CFTR compared with each monomer, and can effectively inhibit the expression of each proinflammatory factor and chemokine ICAM-1, IP-10, IL-18, MCP-1, MIP-1 and MMP-7, so that the combined use of quercetin, glycyrrhizic acid and ferulic acid produces a synergistic effect, the respiratory tract immune system is regulated by activating cAMP-dependent CFTR, the release of each proinflammatory factor and chemokine is inhibited, and pathological damage caused by excessive immune response due to lack of or inhibition of an immune tolerance mechanism is avoided. On the other hand, the combination of quercetin, glycyrrhizic acid and ferulic acid can also inhibit pulmonary fibrosis and promote the repair of damaged cells to normal cells.
The second object of the present invention relates to the use of the above-mentioned Chinese medicinal monomer composition.
In particular to application of the traditional Chinese medicine monomer composition in preparing a lung injury resistant medicine. Relates to the application of the traditional Chinese medicine monomer composition in preparing the medicine for resisting acute lung injury.
The invention relates to an application of the traditional Chinese medicine monomer composition in preparing a medicine for resisting acute lung injury caused by virus. Relates to the application of the traditional Chinese medicine monomer composition in preparing the medicine for resisting acute lung injury caused by influenza virus. Relates to the application of the Chinese medicinal monomer composition in preparing a medicament for resisting acute lung injury caused by avian influenza virus. Relates to the application of the traditional Chinese medicine monomer composition in preparing the medicine for resisting acute lung injury caused by avian influenza virus H5N 1.
The invention also relates to application of the traditional Chinese medicine monomer composition in preparing a lung injury repair medicine.
The traditional Chinese medicine monomer composition can be administered by various routes, and the administration routes comprise oral administration, intravenous injection and the like. Correspondingly, the traditional Chinese medicine monomer composition can be prepared into oral preparations and injections with pharmaceutically acceptable carriers. Wherein the oral preparation comprises tablet, capsule, microcapsule, soft capsule, granule, dripping pill, oral liquid and powder. The injection includes intravenous injection and powder injection. Different medicinal carriers can be matched according to the requirement of the dosage form, and an antioxidant, an emulsifier, a stabilizer and a mildew preventive can be added at the same time.
Compared with the prior art, the invention has the following beneficial effects:
the traditional Chinese medicine monomer composition provided by the invention can activate a cAMP-dependent CFTR chloride channel under the synergistic action of quercetin, glycyrrhizic acid and ferulic acid, and inhibit the expression of ICAM-1, IP-10, IL-18, MCP-1, MIP-1 and MMP-7, so that the respiratory immune system is regulated, and the pathological damage to the lung caused by excessive immune response due to the lack of an immune tolerance mechanism or inhibition is avoided. Meanwhile, the traditional Chinese medicine monomer composition can remarkably up-regulate mRNA expression of E-cadherin (E-cadherin), remarkably down-regulate mRNA expression of Fibronectin (Fibronectin) and Vimentin (Vimentin), effectively inhibit the occurrence of EMT after airway epithelium injury, inhibit pulmonary fibrosis, and promote the repair of injured cells to normal cells.
Drawings
FIG. 1 shows the Isc response of quercetin, glycyrrhizic acid and ferulic acid monomers and the combination of traditional Chinese medicine monomers to stimulate airway epithelial tissue of mice;
qu is quercetin, GA is glycyrrhizic acid, FA is ferulic acid, Mix-1 is a Chinese medicinal monomer composition 1: FA 200. mu. M, GA 100. mu.M, Qu 100. mu.M. Mix-2 is a traditional Chinese medicine monomer composition 2: FA 100. mu. M, GA 100. mu.M, Qu 100. mu.M.
FIG. 2 is a peak pattern of Isc response induced by stimulation of mouse airway epithelial tissue by quercetin, glycyrrhizic acid and ferulic acid monomers and the traditional Chinese medicine monomer composition;
FIG. 3 shows the transient and sustained phases of Isc response induced by different ratios of pharmaceutical compositions to stimulate airway epithelial tissue in mice;
the Mix-1 is the instant phase of the traditional Chinese medicine monomer composition 1, the Mix-2 is the instant phase of the traditional Chinese medicine monomer composition 2, the Mix-1-C is the continuous phase of the traditional Chinese medicine monomer composition 1, and the Mix-2-C is the continuous phase of the traditional Chinese medicine monomer composition 2.
FIG. 4 shows that the Chinese medicinal monomer composition can activate CFTR.
FIG. 5 is the ability of ferulic acid monomer to activate CFTR.
FIG. 6 is a graph of the reduction of HA-induced acute lung injury by quercetin, glycyrrhizic acid and ferulic acid monomers and the inventive herbal monomer composition;
a is lung tissue section of normal mouse, B is lung tissue section of HA mouse, C is lung tissue section of HA mouse treated by ferulic acid, D is lung tissue section of HA mouse treated by glycyrrhizic acid, E is lung tissue section of HA mouse treated by quercetin, and F is lung tissue section of HA mouse treated by the monomer composition of the invention.
FIG. 7 shows that quercetin, glycyrrhizic acid and ferulic acid monomers and the traditional Chinese medicine monomer composition of the invention inhibit the expression of inflammatory factors.
FIG. 8 shows that the quercetin, glycyrrhizic acid and ferulic acid monomers and the traditional Chinese medicine monomer composition inhibit the occurrence of EMT after airway epithelial injury.
Detailed Description
The invention is illustrated below by experiments and examples.
The traditional Chinese medicine monomer composition (composition for short) can activate cAMP-dependent CFTR
1.1 determination of short-circuit Current
Active transport of electrolytes on both sides of epithelial tissue creates differences in ion concentration and composition on both sides, resulting in the formation of a potential difference across the epithelium. The directional movement of electrolytes on both sides of the cell results in the generation of an electric current, which in turn results in a series of electrophysiological parameters including current, voltage and even resistance. The short-circuit current technology is to research the ion channel, transporter and the like of the epithelial cell by measuring the electrical parameters, and qualitatively and quantitatively judge the relationship between the activators and the blockers by using the activators and the blockers. The short-circuit current technology can be used for researching the physiological function of different drugs acting on the epithelial tissue ion channel and judging the possible action target points of the drugs, and the pharmacological and physiopathological mechanisms of the drugs are analyzed from the ion transport angle.
1.2 Experimental methods
1.2.1 the combination of Quercetin, glycyrrhizic acid, Ferulic acid and Chinese medicinal monomer causes the reaction of mouse airway Isc
In the following experiments, the amounts of Ferulic Acid (FA), Glycyrrhizic Acid (GA) and quercetin (Qu) were 100. mu.M each. Traditional Chinese medicine monomer composition 1 (Mix-1): FA 200. mu. M, GA 100. mu.M, Qu 100. mu.M. Traditional Chinese medicine monomer composition 2 (Mix-2): FA 100. mu. M, GA 100. mu.M, Qu 100. mu.M.
(1) Quercetin, glycyrrhizic acid, ferulic acid and traditional Chinese medicine monomer composition can cause Isc reaction of mouse airway
Adding Ferulic Acid (FA), Glycyrrhizic Acid (GA), quercetin (Qu), Chinese medicinal monomer composition 1(Mix-1) and Chinese medicinal monomer composition 2(Mix-2) into normal K-H solution, respectively, to induce different Isc reactions, wherein short-circuit current reaction caused by Glycyrrhizic Acid (GA), Ferulic Acid (FA) and mixture thereof is most obvious, and the Isc values are 36.9 + -1.7 muA/cm2And 33.2. + -. 7.1. mu.A/cm2While quercetin (Qu) of the same concentration can only cause a slight short-circuit current reaction, and the Isc value is 7.1 +/-1.5 mu A/cm2See fig. 1. Indicating that Ferulic Acid (FA) and Glycyrrhizic Acid (GA) act on epithelial cells of mouse airwayThe top film surface can induce short circuit current reaction, and quercetin (Qu) can cause reaction, but the reaction intensity is too small. Both Mix-1 and Mix-2 were able to elicit a higher Isc response with values of 44.2. + -. 4.5. mu.A/cm, respectively2And 41.9. + -. 3.3. mu.A/cm2。
(2) The peak types of the mouse airway Isc reaction caused by the quercetin, the glycyrrhizic acid, the ferulic acid and the traditional Chinese medicine monomer composition are different
The peak pattern of fig. 2 shows that quercetin (Qu) causes a lower instantaneous phase peak value and a lower sustained phase value, which is substantially equivalent to the basal value. The transient phase caused by Ferulic Acid (FA) is high, the sustained level is high, and the sustained time is long. The peak of the transient phase reaction caused by Glycyrrhizic Acid (GA) was higher than that caused by Ferulic Acid (FA), but the action time was short, and the transient phase was over and quickly returned to baseline level. Both Mix-1 and Mix-2 can cause a transient phase and a long duration phase. Wherein, the sustained phase value of Mix-2 is lower, and the sustained phase value of Mix-1 is higher, and the effect is better than that of Mix-2.
(3) Different mouse airway Isc reactions caused by traditional Chinese medicine monomer compositions with different proportions
The values of the transient phase of the Isc response caused by the stimulation of the airway epithelial cells of the mice by Mix-1 and Mix-2 are not significantly different, and are respectively 44.2 +/-4.5 muA/cm2And 41.9. + -. 3.3. mu.A/cm2However, their sustained phase value was 6.5. + -. 1.2. mu.A/cm2Only 39% of Mix-1. Since Mix-1 and Mix-2 only differed in the dose of ferulic acid, while FIG. 2 shows that the Isc response caused by ferulic acid had a longer duration, the results indicate that the difference in the magnitude of the Isc response duration phase between Mix-1 and Mix-2 was due to the difference in the amount of ferulic acid (see FIG. 3).
1.2.2 Ferulic acid monomer and Chinese medicinal monomer composition can activate cAMP-dependent CFTR
In normal K-H solution, Na is administered+Pretreating a channel blocker Amiloride for 10min, adding a traditional Chinese medicine monomer composition 1(Mix-1), acting on delta Isc induced by airway epithelial tissues of mice, having no significant difference compared with a normal control group, and respectively administering an extracellular calcium ion chelating agent EGTA and a cellThe inner calcium chelating agent BAPTA and the L-type calcium channel chelating agent nifedipine (nif) are pretreated for 10min, and then the traditional Chinese medicine monomer composition 1 is added, and the induced delta Isc is reduced to different degrees compared with the control group (Ctrl group) (figure 4E).
Respectively adopt Cl-free-K-H solution, HCO2 -free-K-H solution and Cl-&HCO2 -free-K-H solution, and then the traditional Chinese medicine monomer composition 1 is acted on the airway epithelial tissue of the mouse, and the induced delta Isc is reduced to a different degree compared with the normal K-H solution (figure 4C). Respectively adding calcium ions to activate Cl in a normal K-H solution-Channel blockers (DIDS), CFTR Cl-Channel blockers (Gli), non-selective Cl-Pretreating channel blocker (DPC) for 10min, and adding Chinese medicinal monomer composition 1. The results show that traditional Chinese medicine monomer composition 1 can significantly reduce the Δ Isc induced previously relative to the control group (fig. 4D). The above results demonstrate that the Chinese medicinal monomer composition 1 can activate Cl-Channels, are CFTR and calcium ion activated Cl-The channels act together as a result. The function of CFTR is regulated by intracellular cAMP levels. In normal K-H solution, cAMP-dependent protein kinase PKA inhibitor H89 and adenylate cyclase AC inhibitor MDL were administered for 20min, respectively, and then traditional Chinese medicine monomer composition 1 was added to induce a first peak of Isc that was 61.1% and 52.7% lower than the normal control, respectively (fig. 4F left panel). The second peak was reduced by 86.2% and 81.8%, respectively, compared to the normal control group (fig. 4F right panel). The above results show that the composition induces Cl-Being the dominant Isc, the CFTR ion channel predominates.
FIG. 2 shows that Ferulic Acid (FA) causes a higher transient phase, a higher sustained level and a longer duration. Indicating that Ferulic Acid (FA) has better effect than Glycyrrhizic Acid (GA) and quercetin (Qu). Therefore, the inventors simultaneously performed the above experiments on ferulic acid monomers, and fig. 5G, 5H, 5I and 5J show that ferulic acid monomers can activate cAMP-dependent CFTR ion channels and play a major role in the traditional Chinese medicine monomer composition activating cAMP-dependent CFTR function.
Secondly, the traditional Chinese medicine monomer composition reduces acute lung injury induced by hemagglutinin protein (HA) by regulating inflammatory factors
HA mediates severe acute lung injury by inhibiting the airway epithelial inflammatory regulator CFTR. Then whether a composition that can activate cAMP-dependent CFTR can alleviate HA-induced acute lung injury.
In the traditional Chinese medicine monomer composition, FA is 200 mu M, GA100 mu M and Qu is 100 mu M.
2.1 in vivo experiments
Model group: mice were given HA for 12 h. Establishing a medicine group, namely a traditional Chinese medicine monomer composition group: the traditional Chinese medicine monomer composition is injected into the abdominal cavity of the mouse 1h before HA administration, and the lung tissue of the mouse is observed after 12 h. Ferulic acid group: the mouse was injected with ferulic acid intraperitoneally 1h before HA administration, and the lung tissue of the mouse was observed 12h later. Glycyrrhizic acid group: 1h before HA administration, glycyrrhizic acid is injected into the abdominal cavity of the mouse, and lung tissues of the mouse are observed after 12 h. Quercetin group: before HA administration for 1h, the mice were injected with quercetin intraperitoneally, and the lung tissues of the mice were observed after 12 h.
Pathological results of mouse lungs showed that compared with lung tissues of HA-only mice (fig. 6B), the degree of alveolar structure damage, pulmonary interstitial edema, inflammatory cell infiltration, and the like of each drug group were significantly reduced (fig. 6C, 6D, and 6E), and the effect of the traditional Chinese medicine monomer composition group was the best and the degree of lung damage was the least (fig. 6F).
2.2 in vitro experiments
The model group stimulated 16HBE cells with HA 40. mu.g/ml for 12 h. Establishing a medicine group, namely a traditional Chinese medicine monomer composition group: the combined traditional Chinese medicine monomer composition with HA 40 mug/ml stimulates 16HBE cells for 12 h. Ferulic acid group: 16HBE cells were stimulated with HA 40. mu.g/ml in combination with ferulic acid for 12 h. Glycyrrhizic acid group: 16HBE cells were stimulated with HA 40. mu.g/ml in combination with glycyrrhizic acid for 12 h. Quercetin group: 16HBE cells were stimulated with HA 40. mu.g/ml in combination with quercetin for 12 h. The inhibition effect of each drug group on the inflammatory factors is observed. The results show that each drug group was able to significantly reduce the expression of inflammatory factors in the cell supernatant by HA compared to the model group (fig. 7G-7L). The inhibitory effects of ferulic acid, glycyrrhizic acid and quercetin on inflammatory factors are each emphasized, as shown in FIGS. 7G-7L, ferulic acid inhibits the expression of ICAM-1, IP-10, MCP-1 and MIP-1. Glycyrrhizic acid inhibits the expression of IP-10, IL-18, MCP-1, MIP-1 and MMP-7. Quercetin inhibits the expression of IP-10 and MMP-7. The traditional Chinese medicine monomer composition can inhibit the expression of ICAM-1, IP-10, IL-18, MCP-1, MIP-1 and MMP-7, and has optimal synergistic effect.
Thirdly, the traditional Chinese medicine monomer composition (Mix) inhibits the generation of airway epithelial cell-mesenchymal transition (EMT).
The A549 cell cytomix (C-mix) is stimulated for 72 hours, so that the mRNA expression of E-cadherin (E-cadherin) can be remarkably reduced, the mRNA expression of Fibronectin (Fibronectin) and Vimentin (Vimentin) can be up-regulated, and the occurrence of EMT is promoted. However, when Mix was administered before cytomix stimulation or quercetin, glycyrrhizic acid and ferulic acid were administered separately for 30min, the expression of mRNA of E-cadherin was significantly up-regulated in the Mix group and the expression of mRNA of fibrinectin and Vimentin was significantly down-regulated, inhibiting the occurrence of EMT, compared to cytomix alone (fig. 8A-8C). Wherein, the glycyrrhizic acid and the ferulic acid respectively play a regulating role, but the synergistic effect of the glycyrrhizic acid and the ferulic acid is the best. The results show that Mix can effectively inhibit the occurrence of EMT after the airway epithelium is damaged, and effectively repair the damaged tissues. The traditional Chinese medicine monomer composition (Mix) adopts the traditional Chinese medicine monomer composition 1.
Example one
The molar ratio of quercetin to glycyrrhizic acid to ferulic acid is 1:1:1, namely the molar concentration of ferulic acid is 100 μ M, the molar concentration of glycyrrhizic acid is 100 μ M, and the molar concentration of quercetin is 100 μ M. Mixing with pharmaceutically acceptable carrier, and making into tablet by conventional method.
Example two
The molar ratio of quercetin to glycyrrhizic acid to ferulic acid is 1:2: 1. The molar concentration of ferulic acid is 200 μ M, the molar concentration of glycyrrhizic acid is 100 μ M, and the molar concentration of quercetin is 100 μ M. Mixing with pharmaceutically acceptable carrier, and making into capsule by conventional method.
EXAMPLE III
The molar ratio between quercetin, glycyrrhizic acid and ferulic acid is 1:3: 1. The molar concentration of ferulic acid is 300 μ M, the molar concentration of glycyrrhizic acid is 100 μ M, and the molar concentration of quercetin is 100 μ M. Mixing with pharmaceutically acceptable carrier, and making into microcapsule by conventional method.
The present invention may be embodied in other specific forms without departing from its spirit or essential characteristics. The above-described embodiments of the present invention are to be considered as illustrative and not restrictive, and therefore all slight modifications, equivalent changes and modifications made to the above examples in accordance with the spirit of the present invention are within the scope of the present invention.

Claims (8)

1. A traditional Chinese medicine monomer composition for antagonizing lung injury is characterized in that main active ingredients of the composition comprise quercetin, glycyrrhizic acid and ferulic acid, wherein the molar ratio of the quercetin to the ferulic acid to the glycyrrhizic acid is 1: 1-3: 1.
2. The use of the monomeric composition of a traditional Chinese medicine of claim 1 in the preparation of a medicament for treating lung injury.
3. The use of the monomeric composition of a traditional Chinese medicine of claim 1 in the preparation of a medicament for treating acute lung injury.
4. The use of the monomeric composition of a Chinese medicinal material as claimed in claim 1 in the preparation of a medicament for the treatment of acute lung injury caused by viruses.
5. The use of the Chinese medicinal monomer composition of claim 1 in the preparation of a medicament for treating acute lung injury caused by influenza virus.
6. The use of the Chinese medicinal monomer composition of claim 1 in the preparation of a medicament for treating acute lung injury caused by avian influenza virus.
7. The use of the Chinese medicinal monomer composition of claim 1 in the preparation of a medicament for treating acute lung injury caused by avian influenza virus H5N 1.
8. The use of the traditional Chinese medicine monomer composition of claim 1 in the preparation of a medicament for the repair of lung injury.
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