Application of small molecule compound K3G in treatment of chlamydia infection

Abstract

The invention belongs to the technical field of biological medicine, and particularly relates to application of a small molecule compound K3G in treatment of chlamydia infection. According to the application, a small molecule compound capable of blocking combination of key pathogenic protein Pgp3 of chlamydia and TNF-alpha is screened out, and animal in-vivo experiments prove that injection of K3G can inhibit pathogenicity of chlamydia in an animal body by blocking combination of Pgp3 and TNF-alpha, so that the effect of treating chlamydia infection is achieved. The scheme is simple, effective, economical and practical, and drug resistance is not easy to generate.

Description

Technical Field

[0001] The present invention belongs to the technical field of biomedicine, and specifically relates to application of a small molecule compound K3G in treating chlamydia infection. Background Art

[0002] Chlamydia trachomatis (Ct) is a common bacterial pathogen of sexually transmitted diseases (STDs). Its urogenital tract infection is one of the important causes of female tubal infertility. After infection with Chlamydia, the clinical manifestations of different infection sites are different. Urogenital system infection usually manifests as nonspecific urogenital system inflammation. Mild cases include urethritis, epididymitis, salpingitis, prostatitis, endometritis, etc. Severe cases may cause ectopic pregnancy, tubal infertility, pelvic inflammatory disease, etc. Infection outside the urogenital tract may cause conjunctivitis, interstitial pneumonia, proctitis, pharyngitis, reactive arthritis, etc. At the same time, Chlamydia is also considered a risk factor for the development of cervical cancer and is associated with an increased risk of HIV transmission or acquisition. Therefore, infected individuals need early diagnosis and treatment to prevent the spread of the disease and serious sequelae.

[0003] The plasmid-encoded protein Pgp3 of Chlamydia trachomatis can be secreted into the inclusion body and the cytoplasm of host cells and is an important virulence factor for pathogenicity. TNF-α is an inflammatory cytokine produced by macrophages / monocytes during acute inflammation, which is responsible for various signal transduction events in cells, leading to cell necrosis or apoptosis.

[0004] In the previous studies, the applicant of the present application conducted structural analysis of Pgp3 and used in vitro affinity detection of protein peptides to clarify that Pgp3 can specifically bind to TNF-α. It was also clarified that the combination of Pgp3 and TNF-α can effectively inhibit TNF-α-induced cell apoptosis and enhance the inflammatory response.

[0005] There is currently no treatment for Chlamydia by specifically targeting protein binding. The existing traditional treatment for Chlamydia infection is antibiotic treatment, but Chlamydia infection is hidden, so if the treatment is not timely, it can cause a series of complications due to long-term persistent infection, and antibiotic treatment is prone to drug resistance. In addition, some patients do not recover after antibiotic treatment but enter a hidden persistent infection state, which will still cause a series of serious complications later. Summary of the invention

[0006] In order to solve the above problems, the present application screened out a small molecule compound that can block the binding of the key pathogenic protein Pgp3 of Chlamydia to TNF-α, and confirmed through in vivo animal experiments that injection of K3G can inhibit the pathogenicity of Chlamydia in animals by blocking the binding of Pgp3 to TNF-α, thereby achieving the effect of treating Chlamydia infection. This solution is simple and effective, economical and practical, and is not easy to produce drug resistance.

[0007] In order to achieve the above object, the technical solution adopted by the present invention is as follows: One of the technical solutions provided by the present invention is the use of the small molecule compound K3G in the preparation of drugs for inhibiting or treating chlamydia infection; The small molecule compound K3G is specifically kaempferol-3-O-β-D-glucuronide, and the molecular formula is: 21 H 18 O 12 ; The structure diagram of K3G is as follows Figure 1 As shown; Furthermore, the chlamydia includes but is not limited to Chlamydia trachomatis and Chlamydia trachomatis pneumoniae; Furthermore, the Chlamydia is Chlamydia trachomatis; Further, the chlamydia infection includes but is not limited to infection of the eyes, joints, respiratory system, nervous system, or urogenital system; Furthermore, the chlamydia infection is a reproductive tract infection; Furthermore, the small molecule compound K3G is used as a blocker for blocking the interaction between TNF-α and Pgp3, thereby achieving the effect of treating chlamydia infection by blocking the interaction between TNF-α and Pgp3; Preferably, the drug is an injection, which blocks the interaction between TNF-α and Pgp3 by intraperitoneal injection.

[0008] The second technical solution provided by the present invention is a drug for inhibiting or treating Chlamydia infection, wherein the drug contains a small molecule compound K3G; Furthermore, the chlamydia includes but is not limited to Chlamydia trachomatis and Chlamydia trachomatis pneumoniae; Furthermore, the Chlamydia is Chlamydia trachomatis; Furthermore, the drug has the small molecule compound K3G as an active ingredient; Furthermore, the drug further comprises one or more pharmaceutically acceptable excipients, such as phosphate buffer, etc.; Preferably, the drug is an injection.

[0009] Beneficial effects: Pgp3 can bind to TNF-α to inhibit its induced apoptosis to regulate the growth cycle of host cells, so that Chlamydia can grow and reproduce in a relatively favorable environment, eventually leading to long-term persistent infection. The present invention explores experimental studies and confirms that K3G can effectively inhibit the infection of Chlamydia trachomatis and Chlamydia trachomatis in the reproductive tract of mice by blocking the binding of Pgp3 to TNF-α, and can significantly reduce the occurrence of oviduct edema in mice. At the same time, K3G has unique advantages as a small molecule, such as good permeability and absorbability, stable properties and easy synthesis, etc., and is very suitable for application in the field of clinical treatment. Therefore, the present invention has clinical practicality, low cost and reliable effect. BRIEF DESCRIPTION OF THE DRAWINGS

[0010] Figure 1 This is the structural diagram of K3G.

[0011] Figure 2 This is the binding diagram of Pgp3 and TNF-α.

[0012] Figure 3 This is a schematic diagram of K3G blocking the binding of Pgp3 to TNF-α.

[0013] Figure 4 This is a kinetic analysis diagram of the binding of Pgp3 to TNF-α.

[0014] Figure 5 This is a kinetic analysis diagram showing that K3G can block the binding of Pgp3 to TNF-α.

[0015] Figure 6 K3G inhibits the Chlamydia load in the lower genital tract of mice infected with Chlamydia trachomatis pneumonia Among them, A is the immunofluorescence image of chlamydia load in the lower genital tract of mice, and B is the statistical graph of chlamydia data.

[0016] Figure 7 The effect of K3G on alleviating hydrosalpinx caused by Chlamydia trachomatis infection in mice.

[0017] Figure 8 The effect of K3G on alleviating the inflammatory response of the fallopian tube caused by Chlamydia trachomatis infection in mice.

[0018] Fig. 9 Chlamydia load in the lower genital tract of mice at different times after infection with Ct-D Note: The inclusion bodies were observed and counted under a fluorescence microscope, and the chlamydia load in each swab was calculated by the formula. The calculated IFUs were converted to Log10, and one-way ANOVA was used; X-axis: different experimental groups, Y-axis: Log10 IFUs represents the chlamydia load in the lower genital tract of mice; (*, p<0.05; **, p<0.01; ***, p<0.001; ****, P<0.0001). DETAILED DESCRIPTION

[0019] In order to make the purpose, technical solution and advantages of this patent more clear, this patent is further described in detail in combination with specific embodiments. It should be understood that the specific embodiments described here are only used to explain this patent and are not used to limit the present invention.

[0020] The plasmid-encoded protein Pgp3 of Chlamydia trachomatis can be secreted into the inclusion body and the cytoplasm of host cells and is an important virulence factor for pathogenicity. TNF-α is an inflammatory cytokine produced by macrophages / monocytes during acute inflammation, which is responsible for various signal transduction events in cells, leading to cell necrosis or apoptosis.

[0021] The preliminary research of the research group of this application has confirmed that Pgp3 can specifically bind to TNF-α through structural analysis of Pgp3 and in vitro affinity detection of protein peptides. It has also been confirmed that the combination of Pgp3 and TNF-α can effectively inhibit TNF-α-induced cell apoptosis and enhance the inflammatory response.

[0022] The present invention further clarifies the specific binding of TNF-α and Pgp3 through molecular docking technology, and its binding site is located at the C-terminus of the Pgp3 protein structure. The binding structure diagram is simulated and constructed, and small molecule compounds that can bind to the C-terminus of Pgp3 and TNF-α at the same time are screened. According to the docking score and the evaluation of biological activity, synthesizability, stability and other aspects, it is finally determined that kaempferol-3-O-β-D-glucuronide (K3G is used as a synonym in this application) is used as a blocker to block the interaction between TNF-α and Pgp3.

[0023] The molecular formula of K3G is: 21 H 18 O 12 , the structural formula is Figure 1 In vitro, the binding of Pgp3 and TNF-α and the inhibition of K3G on the binding between the two were detected and analyzed by using the Biacore S200 biomacromolecule interaction analyzer. In vivo, animal experiments confirmed that the injection of K3G can inhibit the pathogenicity of Chlamydia in animals. We speculate that this is because K3G blocks the binding of Pgp3 and TNF-α.

[0024] The animal laboratory of the present invention is constructed in mice by Chlamydia muridarum (Cm) and Chlamydia trachomatis (Ct). The effect of K3G on the chlamydia load in the lower reproductive tract of mice before and after administration was examined by Ct. At the same time, Chlamydia muridarum Cm and Chlamydia trachomatis Ct have a high degree of similarity in gene sequence (≥97%), and are also very similar in biological characteristics and pathogenicity. The infection and pathological changes caused by Cm in the reproductive tract of mice are very similar to those caused by Ct in humans, especially the hydrosalpinx and inflammatory lesions caused by Cm in mice are very similar to the human urogenital tract infection caused by Ct. Therefore, the mouse reproductive tract infection model constructed with Cm to study the pathogenic effect of Ct on the human reproductive tract has become a conventional means of studying Ct in the field. Therefore, the Cm mouse reproductive tract infection model is currently often used to explore the immune protection effect of Chlamydia trachomatis and its pathological damage mechanism.

[0025] The present invention is further explained by the following specific examples. Unless otherwise specified, the reagents and materials used in the following examples are commercially available.

[0026] Example 1 Screening experiment of small molecule compounds that block the binding of TNF-α and Pgp3 The protein structures of TNF-α and Pgp3 (PDBID: 4JDM) were retrieved from the Protein Data Bank (PDB) database and saved as PDB format files.

[0027] The screened TNF-α protein molecular structure was docked with the C-terminus and N-terminus of Pgp3 using Hex8.0.0 software. Based on the protein binding structure, small molecule compounds that can structurally bind to TNF-α and Pgp3 and block the binding between the two were screened. Biacore was used to measure the protein binding ability and the blocking effect of small molecule compounds was clarified. BiacoreS200 Control Software was used to analyze and process the data.

[0028] The results are as follows: (1) If Figure 2 As shown in the figure, the binding affinity of TNF-α to the C-terminus of Pgp3 (745.06) is significantly higher than that to the N-terminus (453.83), which indicates that the binding site of TNF-α to Pgp3 is mainly located at the C-terminus of Pgp3.

[0029] (2) If Figure 1 As shown, the structure diagram of the screened small molecule compound K3G that can structurally bind to TNF-α and Pgp3 and can block the binding between the two. Figure 3Surface binding map and interaction map of K3G and two proteins. The map shows that the protein residues of the dominant binding sites after docking are GLU-27, ASN-64, ASN-92, and VAL-123.

[0030] (3) Using Biacore S200 Control Software, we first performed a kinetic analysis of the binding of TNF-α to His-Pgp3. The results are as follows: Figure 4 As shown, the response is expressed in resonance units (‌RU)‌ and is proportional to the surface mass. The affinity is expressed as ‌KD. The figure shows that as the concentration of TNF-α increases, the signal value increases, with a certain saturation trend. The fitted KD (M) value is 8.288e-8, indicating that TNF-α can specifically bind to His-Pgp3.

[0031] Then, 1 mg / mL TNF-α and 10 mg / mL K3G were mixed evenly at a mass ratio of 10:1, and incubated in a 37°C constant temperature incubator for 30 min in advance. The resulting mixture was subjected to kinetic analysis with His-Pgp3. Figure 5 As shown, after TNF-α was co-incubated with K3G in advance, there was no obvious trend in the signal value as the concentration increased, which indicated that kaempferol-3-O-β-D-glucuronide (K3G) could block the specific binding of TNF-α to His-Pgp3.

[0032] The above kinetic experiments are as follows: 5% DMSO running buffer was prepared, 4.5% DMSO stock solution and 5.8% DMSO stock solution were prepared for concentration correction, His-Pgp3 was diluted to 500 μM with 1.05×PBS-P solution, TNF-α was diluted in half to 50 μM, 25 μM, 12.5 μM, 6.25 μM, 3.125 μM, and 0 μM, and injected into the channel coupled with His-Pgp3 protein and the blank channel. In the kinetic experiment of K3G blocking, the mixture of TNF-α and small molecule blockers co-incubated 30 minutes in advance was diluted to 50 μM, 25 μM, 12.5 μM, 6.25 μM, 3.125 μM, 1.56 μM, and 0 μM, and injected into the channel coupled with His-Pgp3 protein and the blank channel, and the blank channel was used for correction, and multiple cycles were used for detection.

[0033] Example 2 Animal Experimental Verification of K3G Blocking Effect (Cm Infection Model) Drug preparation: K3G was purchased from Chengdu Pusi Biotechnology Co., Ltd., CAS No. 22688-78-4. The small molecule powder was dissolved in a small amount of DMSO, and then prepared into different concentrations with PBS phosphate buffer. The specific drug concentrations are as follows: (1) 0.02 mg / mL K3G; (2) 0.2 mg / mL K3G; (3) 2 mg / mL K3G; (4) PBS: concentration is 10 mM, pH range is between 6.0-8.0.

[0034] Female BALB / c mice aged 4-6 weeks were randomly divided into four groups (8 mice in each group): Cm group (Cm refers to Chlamydia trachomatis pneumoniae), low concentration K3G group (0.1 mg / kg), medium concentration K3G group (1.0 mg / kg), and high concentration K3G group (10 mg / kg).

[0035] All mice were vaginally inoculated with wild-type Cm to construct a Cm infection model in the reproductive tract. 2 × 10 5 IFU / mL purified wild-type Cm EBs were slowly injected into the vagina of mice, with a volume of about 10 μL, so that the mice were fully inoculated and infected with Chlamydia. D3 was used to detect the Chlamydia load in the lower reproductive tract of mice in each group. IFA detection revealed inclusion bodies, proving that all mouse reproductive tract Cm infection models had been successfully infected.

[0036] The day of inoculation was set as D0. 30 minutes before inoculation, each group was given an intraperitoneal injection of the corresponding drug solution according to the different groups. After that, the drug was given at a fixed time every day for 14 consecutive days. After 14 days, no intraperitoneal injection was performed and the group was fed with water normally. The specific groups are as follows: Cm group: about 100 μL of PBS was injected intraperitoneally, and the drug was administered once a day at a fixed time after infection for 14 consecutive days; Low-concentration K3G group (0.1 mg / kg): The injection volume for each mouse was calculated based on the mouse weight at 0.1 mg (K3G) / kg (mouse weight), and 0.02 mg / mL K3G was injected intraperitoneally. The drug was administered once a day at a fixed time after infection for 14 consecutive days. Medium concentration K3G group (1.0 mg / kg): The injection dose for each mouse was calculated based on the weight of the mouse according to 1.0 mg / kg, and 0.2 mg / mL of K3G was injected intraperitoneally. The drug was administered once a day at a fixed time after infection for 14 consecutive days; High-concentration K3G group (10 mg / kg): The injection dose for each mouse was calculated based on the weight of the mouse at 10.0 mg / kg, and 2 mg / mL of K3G was intraperitoneally injected. The K3G was intraperitoneally injected at 0.02 mg / mL. The drug was administered once a day at a fixed time after infection for 14 consecutive days. On the 3rd, 7th, 14th, 21st, 28th and 35th days after inoculation, the exfoliated cells of the lower genital tract of mice were taken for in vitro cell culture and IFA detection to determine the chlamydia load in the lower genital tract of mice. The complete genital tract of mice was isolated 60 days after infection, and the degree of hydrops in the fallopian tubes of mice was scored by naked eye. The pathological sections were stained with H&E to evaluate the degree of dilation and inflammatory infiltration of the fallopian tubes. This evaluation clarified the inhibitory effect of the blocker on the pathogenicity of Pgp3. The experimental results are as follows: (1) Detect the chlamydia load in the lower reproductive tract of mice on days 3, 7, 14, 21, 28, and 35 after infection. Figure 6 As shown ( Figure 6 A in the middle is the immunofluorescence image of chlamydia load in the lower genital tract of mice. Figure 6 (B in the figure is a statistical graph of chlamydia data). On days 3, 7, 14, and 21 after infection with chlamydia, the number of IFU in the lower genital tract of mice in the 0.1 mg / kg, 1.0 mg / kg, and 10.0 mg / kg groups after K3G intervention was significantly lower than that in the Cm group (P < 0.05), but there was no significant difference in the number of IFU between the groups with different concentrations of K3G intervention. On day 28 after infection, no chlamydia was detected in the exfoliated cells in the lower genital tract of mice in the groups that were intraperitoneally injected with K3G, and no chlamydia was detected in the lower genital tract of mice in the Cm group on day 35 after infection.

[0037] The above results show that intraperitoneal injection of K3G can inhibit Chlamydia infection and significantly shorten the clearance period of Chlamydia. Figure 4-Figure 5 Kinetic experiments further confirmed that K3G inhibited infection by blocking the binding of Pgp3 to TNF-α.

[0038] (2) After mice were inoculated and infected with Cm via vaginal route, hydrosalpinx could be caused by ascending infection. Mice in each group were killed 60 days after infection, and the reproductive tracts of the mice were completely removed. The severity of hydrosalpinx was evaluated by naked eye observation and scoring criteria. Figure 7 As shown in the figure, obvious hydrosalpinx was observed in the Cm group, and the scores of hydrosalpinx in the groups injected with K3G were significantly lower than those in the Cm group. There was no significant difference in the scores of hydrosalpinx between the groups injected with different concentrations of K3G. The results show that intraperitoneal injection of K3G can reduce hydrosalpinx caused by chlamydia infection.

[0039] Scoring criteria for the severity of hydrosalpinx: 0 points if no hydrosalpinx is observed with the naked eye; 1 point if the hydrosalpinx cannot be clearly observed with the naked eye and requires the use of a magnifying glass; 2 points if the hydrosalpinx is clearly observed with the naked eye, but the size of the water at the lesion is smaller than that of the ipsilateral ovary; 3 points if the hydrosalpinx is clearly observed with the naked eye, but the size of the water at the lesion is equal to that of the ipsilateral ovary; 4 points if the hydrosalpinx is clearly observed with the naked eye, but the size of the water at the lesion is larger than that of the ipsilateral ovary.

[0040] (3) After mice were infected with Chlamydia, in addition to hydrosalpinx, they could also induce tubal dilatation and inflammatory cell infiltration in the fallopian tubes. The fallopian tube sections of mice in each group were stained with H&E, and the pathological changes of the fallopian tube tissues of mice in each group were observed under a microscope.

[0041] like Figure 8 As shown, when mice were intraperitoneally injected with different concentrations of K3G, no obvious inflammatory cell infiltration and lumen dilation were observed in their oviducts, while obvious inflammatory cell infiltration was observed in the oviducts of mice in the Cm group, and the lumen dilation and thinning occurred to varying degrees, the mucosal folds were reduced, and the cilia on the top disappeared.

[0042] According to the fallopian tube dilatation score and inflammatory cell infiltration score, the fallopian tube dilatation score and inflammatory infiltration score of each group injected with K3G were significantly lower than those of the Cm group, and there was no significant difference in the degree of fallopian tube dilatation and inflammatory infiltration between the groups injected with different concentrations of K3G. The results show that intraperitoneal injection of K3G can reduce the fallopian tube inflammation induced by Chlamydia infection.

[0043] Scoring criteria for fallopian tube dilatation: no obvious dilatation of the fallopian tube under microscopic observation was scored as 0 points; a single dilated cross-section was scored as 1 point; 1 to 3 dilated cross-sections were scored as 2 points; 3 or more dilated cross-sections were scored as 3 points; and obvious fusion dilatation was scored as 4 points.

[0044] Scoring criteria for the degree of inflammatory cell infiltration in the fallopian tube: no obvious inflammatory cell infiltration in the fallopian tube under microscopic observation was scored as 0 points; a single lesion with inflammatory infiltration was scored as 1 point; 2 to 4 lesions with inflammatory infiltration were scored as 2 points; 4 or more lesions with inflammatory infiltration were scored as 3 points; and 4 points were scored when inflammatory infiltration foci were observed in the entire fallopian tube wall.

[0045] Example 3 Animal Experiment Verification of K3G Blocking Effect (Ct Infection Model) 1. Mouse grouping and model construction Drug preparation: K3G was purchased from Chengdu Pusi Biotechnology Co., Ltd., CAS No. 22688-78-4. The small molecule powder was dissolved in a small amount of DMSO, and then prepared into different concentrations with PBS phosphate buffer. The specific drug concentrations are as follows: (1) 0.02 mg / mL K3G; (2) 2 mg / mL K3G; (3) PBS: concentration is 10 mM, pH range is between 6.0-8.0.

[0046] After 1 week of adaptive feeding, 4-6 week old female SPF BALB / c mice were randomly divided into 3 groups, 6 mice in each group, marked as Ct-D (Ct-D refers to Chlamydia trachomatis serotype D) group, low concentration K3G group (0.1 mg / kg), and high concentration K3G group (10 mg / kg).

[0047] Five days before infection, each mouse was subcutaneously injected with progesterone according to body weight, with an injection volume of about 2.5 mg, to synchronize the physiological cycle of the mice to increase their susceptibility to EB. The day before the mice were inoculated with Chlamydia EB, the vaginal secretions of the mice were cleaned with a male cotton swab, and the detached vaginal epithelial cells were gently scraped to avoid excessive secretions from affecting the Ct-D infection process. Five days after the progesterone injection, the reproductive tracts of all mice were inoculated with Chlamydia trachomatis (Ct-D). The day of inoculation was set as D0. The purified Ct-D: EBs were diluted with ice SPG, and 20 µL 2×10 was inoculated into the vagina of each mouse. 6 IFU / mL of EBs were used to detect the chlamydia load in the lower reproductive tract of each group of mice, and IFA test found inclusion bodies, proving that all mouse reproductive tract Ct-D infection models had been successfully infected.

[0048] 30 minutes before inoculation, each group was given an intraperitoneal injection of the corresponding drug solution according to the different groups. After that, the drug was given at a fixed time every day for 14 consecutive days. After 14 days, no intraperitoneal injection was performed and the group was fed with water normally. The specific groups are as follows: Ct-D group: about 100 μL of PBS was injected intraperitoneally, and the drug was administered once a day at a fixed time after infection for 14 consecutive days; Low-concentration K3G group (0.1 mg / kg): The injection dose for each mouse was calculated according to 0.1 mg (K3G) / kg (mouse weight) based on the mouse body weight, and 0.02 mg / mL K3G was injected intraperitoneally. The drug was administered once a day at a fixed time after infection for 14 consecutive days.

[0049] High-concentration K3G group (10 mg / kg): The injection volume for each mouse was calculated based on 10 mg (K3G) / kg (mouse weight) according to the mouse weight, and 2.0 mg / mL K3G was injected intraperitoneally. The drug was administered once a day at a fixed time after infection for 14 consecutive days; 2. Chlamydia load detection Vaginal exfoliated cells were collected from mice on days 3, 7, 14, and 21 after Chlamydia infection, and in vitro cell culture and IFA tests were performed to determine the Chlamydia load in the mouse vagina. The results are as follows: (1) In this experiment, mice were infected with Chlamydia trachomatis serotype D. The genital chlamydia load in mice was tested 3, 7, 14, and 21 days after infection. The results are as follows: Fig. 9 As shown: 3, 7, 14, and 21 days after infection, the 0.1 mg / kg group and the 10 mg / kg group were significantly lower than the Ct-D group (p<0.001), but there was no significant difference between the groups intervened with different concentrations of K3G.

[0050] (2) 21 days after infection, no chlamydia was detected in the reproductive tracts of the two groups of mice treated with K3G; 28 days after infection, no chlamydia was detected in the reproductive tracts of the mice in the Ct-D group, indicating that intraperitoneal injection of K3G can inhibit chlamydial infection and shorten the chlamydial clearance cycle by blocking the binding of Pgp3 to TNF-α.

[0051] The above-mentioned embodiments only express several implementation methods of the present invention, and the descriptions thereof are relatively specific and detailed, but they cannot be understood as limiting the scope of the patent. It should be pointed out that, for ordinary technicians in this field, the above-mentioned implementation methods can also be modified, combined and improved without departing from the concept of this patent, which all belong to the protection scope of this patent. Therefore, the protection scope of this patent shall be based on the claims.

Claims

1. Use of compound K3G in the preparation of a drug for inhibiting or treating chlamydia infection, characterized in that: The compound K3G is kaempferol-3-O-β-D-glucuronide, and its molecular formula is: 21 H 18 O 12 .

2. The use according to claim 1, characterized in that The chlamydia include but are not limited to Chlamydia trachomatis and Chlamydia trachomatis pneumoniae.

3. The use according to claim 1, characterized in that The chlamydial infections include, but are not limited to, infections of the eyes, joints, respiratory system, nervous system, or genitourinary system.

4. Use of compound K3G as a blocker for blocking the interaction between TNF-α and Pgp3.

5. A drug for inhibiting or treating chlamydia infection, characterized in that: The medicament contains compound K3G.

6. The drug according to claim 5, characterized in that The drug uses compound K3G as an active ingredient.

7. The drug according to claim 6, characterized in that The medicament further comprises one or more pharmaceutically acceptable excipients.

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