CN116059230B - Application of cimicifuga rhizome glycoside in preparing medicine for inhibiting periodontitis and periodontal bone loss - Google Patents
Application of cimicifuga rhizome glycoside in preparing medicine for inhibiting periodontitis and periodontal bone loss Download PDFInfo
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Abstract
The invention relates to the technical field of biological medicines, in particular to application of cimicifuga rhizome glycoside in preparation of medicines for inhibiting periodontitis and periodontal bone loss. Wherein, the cimicifuga rhizome glycoside can inhibit the osteoclast differentiation of monocytes. The invention also prepares an in vitro macrophage culture medium which is RPMI 1640 culture medium containing cimicifuga rhizome glycoside. The invention successfully establishes a treatment scheme of the mouse ligature periodontitis model by utilizing the cimicifuga rhizome glycoside, and shows that the cimicifuga rhizome glycoside can be used for preparing medicines related to inhibiting periodontitis. In addition, the invention successfully establishes an in-vitro culture method of macrophages by utilizing the cimicifuga rhizome glycoside, can obtain a sufficient quantity of macrophages, inhibits the secretion of inflammatory factors of the macrophages stimulated by the cimicifuga rhizome glycoside, inhibits the osteoclast differentiation of monocytes, and shows that the cimicifuga rhizome glycoside can be used for preparing medicaments related to inhibiting periodontal bone loss.
Description
Technical Field
The invention relates to the technical field of biological medicines, in particular to application of cimicifuga rhizome glycoside in preparation of medicines for inhibiting periodontitis and periodontal bone loss.
Background
Periodontitis is a destructive inflammatory disease of periodontal tissue affecting the gums, periodontal ligaments, and alveolar bone. If not treated in time, the teeth can lose tissue support and even fall off. Periodontitis patients are at risk of missing teeth and masticatory dysfunction, affecting their nutrition, quality of life, and self-esteem, and creating tremendous socioeconomic impact and healthcare costs. The overall prevalence of periodontitis increases with age and will continue to rise with aging of the population.
Macrophages (Macrophage) are important constituent members of the human innate immune system and have powerful functions of identifying, phagocytizing, and eliminating bacteria and foreign anomalies. It not only promotes the aggregation of inflammatory cells and the clearance of pathogens at the initial stage of inflammatory reaction, but also plays an important role in the process of regulating bone destruction or bone regeneration during the subsequent stimulation of the immune reaction of the body and the resolution of inflammation; on the other hand, excessive aggregation and activation can also lead to tissue damage of the body, so that its dynamic balance plays a critical role in the homeostasis of the tissue.
The current research view suggests that tissue destruction of periodontitis is mainly caused by the host's immune response to infection. Macrophages are used as a first defense line for external bacterial infection in periodontitis tissues, and on one hand, germs can be killed through sterilization and phagocytosis; on the other hand, excessive activation of the tooth surface causes damage to periodontal tissue, and further aggravates periodontitis. Macrophages, as a pluripotent cell, induce polarization in different directions in different local microenvironments, cytokines, etc., and thus have different phenotypes. Functionally, macrophages can be classified into classical activated (M1) and alternating activated (M2) in the local microenvironment. Macrophages of different phenotypes play different roles in different stages of periodontitis development and progression.
Macrophages activated by bacteria can release a variety of inflammatory cytokines, causing gingival destruction and alveolar bone resorption. Macrophages are classified into pro-inflammatory macrophages and anti-inflammatory macrophages. Proinflammatory macrophages can produce a number of inflammatory cytokines, such as IL-1 beta and TNF-alpha, which can stimulate activation of T cells and polymorphonuclear neutrophils, resulting in alveolar bone loss. In addition, proinflammatory macrophages can increase local expression of RANKL, thereby promoting differentiation of osteoclasts in periodontal tissue. In contrast, anti-inflammatory macrophages are involved in the resolution of inflammation and tissue regeneration by secreting anti-inflammatory mediators. In the resolution of inflammation, anti-inflammatory macrophages contribute to the cytostatic effect of apoptotic osteoblasts, mediating bone formation.
Since the pro-inflammatory/anti-inflammatory macrophage imbalance is responsible for periodontal tissue destruction, converting the macrophage phenotype from pro-inflammatory to anti-inflammatory, or promoting monocyte polarization to M2-type macrophages, would be an effective method for treating periodontitis.
Radix Saposhnikoviae is a Chinese medicine, and is commonly used for treating fever rheumatism, cancer, etc. At present, the research on the cimicifuga rhizome glycoside mainly proves that the cimicifuga rhizome glycoside plays a certain role in resisting tumors, but the application of the cimicifuga rhizome glycoside in periodontitis and periodontal bone loss has not been shown in related researches.
Disclosure of Invention
The invention aims to provide application of cimicifuga rhizome glycoside in preparing medicines for inhibiting periodontitis and periodontal bone loss.
According to the invention, the main active ingredient cimicifuga rhizome glycoside (POG) in radix sileris can be used for inhibiting periodontitis and periodontal bone loss for the first time.
Specifically, the application provides the following technical scheme:
the invention provides application of cimicifuga rhizome glycoside in preparing medicines for inhibiting periodontitis and periodontal bone loss. Wherein the cimicifuga rhizome glycoside can inhibit the osteoclast differentiation of monocytes. In particular, the cimicifuga rhizome glycoside can inhibit the expression of an osteoclast core transcription factor Nfatc-1. In addition, mice can inhibit thread ligation-induced periodontitis by oral administration of cimicifuga rhizome glycoside.
Further, the method also comprises the step of preparing an in vitro macrophage culture medium, wherein the in vitro macrophage culture medium contains cimicifuga rhizome glycoside.
Specifically, the macrophage in-vitro culture medium is RPMI 1640 culture medium containing cimicifuga rhizome glycoside.
Further, the cimicifuga rhizome glycoside promotes polarization of macrophages to M2 in vitro.
Further, the cimicifuga rhizome glycoside inhibits secretion of macrophage inflammatory cytokines under LPS stimulation by inhibiting activation of NF- κB pathway in vitro.
The invention also provides an in vitro culture method of the macrophage, which comprises the following steps: adding cimicifuga rhizome glycoside into RPMI 1640 culture medium, and placing in 5% CO 2 Culturing in incubator at 37 deg.C at concentration every 2-3 daysFresh medium is replaced.
Compared with the prior art, the application of the cimicifuga rhizome glycoside in preparing the medicine for inhibiting periodontitis and periodontal bone loss has at least the following beneficial effects:
(1) The invention successfully establishes a treatment scheme of the mouse ligature periodontitis model by utilizing the cimicifuga rhizome glycoside, and shows that the cimicifuga rhizome glycoside can be used for treating periodontitis and can be used for preparing medicaments related to inhibiting periodontitis.
(2) The invention successfully establishes an in vitro culture method of macrophages by utilizing the cimicifuga rhizome glycoside, can obtain a sufficient quantity of macrophages, inhibits the secretion of inflammatory factors of the macrophages stimulated by the cimicifuga rhizome glycoside, and increases the M2 polarization under the stimulation of IL-4 (interleukin-4); the monocyte osteoclastic differentiation subjected to the stimulation of cimicifuga rhizome glycoside is inhibited, and the cimicifuga rhizome glycoside can be used for preparing medicaments related to inhibiting periodontal bone loss.
The application of the cimicifuga rhizome glycoside of the present invention in preparing the medicine for inhibiting periodontitis and periodontal bone loss will be further described with reference to the accompanying drawings.
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FIGS. 1-2 show the expression of macrophage inflammatory factor index IL-6, TNF- α, phosphorylated P65 and M2 macrophage marker Arg-1 after 1 day of THP-1 cell culture with or without LPS stimulation. FIG. 1 shows RT-qPCR and FIG. 2 shows protein expression level.
FIGS. 3-5 show the expression of the M2 macrophage associated markers Arg-1 and CD206 after 1 day of THP-1 cell culture with or without POG stimulation by IL-4. FIG. 3 shows RT-qPCR, FIG. 4 shows protein expression level, and FIG. 5 shows immunofluorescence staining.
FIGS. 6-8 show progression of periodontitis 7 days after C57BL/6N mice wire ligation induced periodontitis with or without POG lavage treatment. Fig. 6 is a Micro-CT scan of alveolar bone at the ligation of the maxillary threads of different mice in groups, fig. 7 is a HE staining pattern of the corresponding region, and fig. 8 is an immunofluorescence staining pattern.
FIG. 9 shows the in vitro culture of RAW264.7 cells using RANKL-supplemented osteoclast differentiation medium for 14 days with or without POG addition. Wherein, the left graph is TRAP staining graph, and the right graph is immunofluorescence staining graph of the osteoclast core transfer factor Nfatc-1.
Detailed Description
Example 1
Effect of POG on M1 macrophage inflammatory factor secretion
Verification was performed by RT-qPCR and Western Blot experiments.
THP-1 cells were cultured in RPMI 1640 medium and placed in 5% CO 2 Culturing in incubator at 37 deg.C, and changing fresh culture medium every 2-3 days. After PMA is added to THP-1 cells of a blank group, a control group and an experimental group for stimulating adherence for one day, a POG solution with the concentration of 40 mu M is added to THP-1 of the experimental group, an equal volume of a drug solvent DMSO is added to THP-1 of the control group and the blank group, LPS with the concentration of 0.01 mu g/mL is added to the control group and the experimental group after culturing for one day, RT-qPCR is carried out to detect the expression level of M1 type macrophage-related inflammatory factors TNF-alpha and IL-6 and M2 type macrophage markers Arg-1 in THP-1 cells after culturing for one day, and Western Blot experiments are carried out to detect the phosphorylation level of NF-kappa B channel-related protein P65 in THP-1 cells.
Results:
RT-qPCR results show that the expression levels of the inflammatory factors IL-6 and TNF-alpha in the LPS control group are obviously up-regulated compared with that in the blank group, and the expression levels of the inflammatory factors IL-6 and TNF-alpha in the experimental group are obviously reduced after POG dry treatment; in addition, the M2 macrophage marker Arg-1 of the LPS control group is obviously reduced, and the same level as that of the blank group is maintained in the POG experimental group, so that the experimental group and the control group have statistical significance, and the experimental group and the control group are shown in figure 1;
western Blot results show that the P65 phosphorylation level of the LPS control group is obviously up-regulated compared with that of the blank group, and the P65 phosphorylation level of the experimental group is obviously down-regulated after POG dry treatment, as shown in figure 2.
Conclusion:
the results of RT-qPCR and Western Blot experiments of THP-1 treated by POG prove that in vitro POG intervention can inhibit secretion of THP-1 inflammatory factors induced by LPS and inhibit phosphorylation of P65 protein.
Example 2 Effect of POG on macrophage polarization towards M2 type
Verification was performed by RT-qPCR, western Blot and immunofluorescent staining experiments.
After PMA is added to THP-1 cells of a blank group, a POG group, an IL-4 group and an IL-4+POG group to stimulate adherence for one day, IL-4 cytokines of 20ug/mL are added to the IL-4 and IL-4+POG groups to culture for one day, then a POG solution with the concentration of 40 mu M is added to THP-1 in the POG group and the IL-4 group, an equal volume of a drug solvent DMSO is added to THP-1 in the blank group and the IL-4 group, and after culturing for one day under the same condition, RT-qPCR and Western Blot experiments are carried out to detect the expression level of M2 type macrophage markers Arg-1 and CD206 in the THP-1 cells.
Results:
RT-qPCR, western Blot and immunofluorescence staining results show that the expression levels of M2 type macrophage markers Arg-1 and CD206 in the POG group and the IL-4 group are not obviously increased compared with that in the blank group, and the expression levels of Arg-1 and CD206 are obviously up-regulated after the POG and IL-4 are dried together in the experimental group, as shown in figures 3-5.
Conclusion:
the RT-qPCR and Western Blot experiment results of the THP-1 treated by POG prove that the in vitro POG intervention can promote the polarization of THP-1 cells to M2 type macrophages under the condition of IL-4 induction.
EXAMPLE 3 inhibition of periodontitis by POG in vivo
The model of periodontitis induced by ligation of the mouse silk thread is verified by Micro-CT, HE staining and immunofluorescence staining experiments.
C57BL/6N female mice of 6-8 weeks of age were selected and divided into a blank group, a ligation control group and a ligation POG experimental group. After the mice were fully anesthetized, the blank group was left untreated, and a sterilized 5-0 wire was placed between the first molar and the second molar of the right upper jaw of the control group and the experimental group of mice and ligated to induce periodontitis. Mice were then given to the experimental group by gavage for 7 days at 20mg/kg/d POG, and the blank group and the control group were given an equivalent amount of physiological saline by gavage, and the mice were euthanized by injection of excess gunpowder and the maxilla was removed and fixed to 4% paraformaldehyde for 7 days after the operation. The maxilla of the mice after the fixation was evaluated for alveolar bone resorption during wire ligation by micro-CT scanning. Tissue decalcification is carried out on the sample after scanning, HE staining and immunofluorescence staining are carried out after the section is embedded after subsequent dehydration.
Results:
the Micro-CT result shows that the height of the alveolar bone between the first molar and the second molar of the mouse of the ligation control group is obviously reduced, and the reduction degree of the alveolar bone at the corresponding part of the mouse of the POG experiment group is weaker than that of the ligation control group; the statistical results of bone density and bone/tissue volume fraction show that the experimental group has higher histological density than the ligation group, the high-density image volume ratio is larger, the ligation control group has lower high-density image volume ratio, and the high-density image volume ratio of the experimental group and the control group has statistical significance, as shown in fig. 6;
HE staining results show that the first molar and the second molar of the ligature control group mice have higher alveolar bone loss degree, and inflammatory cell infiltration is obvious; the alveolar bone loss degree of the corresponding part of the mice in the POG experimental group is weaker than that of the ligation control group, and inflammatory cell infiltration is less obvious, as shown in fig. 7;
in order to observe the infiltration condition of periodontitis, macrophage markers CD68 and M2 type macrophage markers CD206 immunofluorescence staining is carried out on the ligature corresponding gingival area of each group of mice, and the result shows that the CD206 positive fluorescence intensity of the gingival area of the POG experimental group is higher than that of the ligature control group corresponding gingival area; immunofluorescence staining results for inflammatory factor iNOS showed that the iNOS positive fluorescence intensity in gingival area of POG experimental group was lower than that in the corresponding area of ligation control group, see fig. 8.
Conclusion:
Micro-CT and HE staining experiments of a periodontitis model induced by ligation of a mouse silk thread prove that POG has a certain rescue effect on the progress of periodontitis and bone loss caused by periodontitis, and the rescue effect is possibly related to the promotion of macrophage polarization to M2 phenotype in periodontal tissues by the POG.
Example 4 action of POG on osteoclast differentiation of mononuclear macrophages in vitro
The demonstration was performed by TRAP staining and immunofluorescence staining of RAW264.7 cells.
Both control and experimental groups were cultured in vitro with RANKL-added osteoclast differentiation medium for 14 days, during which time 40 μm POG was added simultaneously to the experimental group cells for co-culture. Cells were harvested after 14 days for TRAP staining and immunofluorescence staining.
Results:
TRAP staining results show that cells of the RANKL control group have aggregation cavitation osteoclast nodules, and the osteoclast differentiation is obvious; only a certain cell aggregation occurs in the RANKL+POG experimental group, and the osteoclast differentiation is inhibited, and the left graph of the graph is shown in fig. 9;
immunofluorescent staining of the osteoclast core transcription factor Nfatc-1 was performed on both groups of cells, and the results showed that the number of osteoclast core transcription factor Nfatc-1 positive cells in the RANKL+POG experimental group was smaller than that in the RANKL experimental group, indicating that the osteoclast differentiation was inhibited, as shown in the right graph of FIG. 9.
Conclusion:
the cell immunofluorescence staining and TRAP staining experiments prove that the POG can inhibit the osteoclastic differentiation of the mononuclear macrophages to a certain extent in vitro.
The above examples are only illustrative of the preferred embodiments of the present invention and are not intended to limit the scope of the present invention, and various modifications and improvements made by those skilled in the art to the technical solution of the present invention should fall within the scope of protection defined by the claims of the present invention without departing from the spirit of the present invention.
Claims (7)
1. The use of cimicifuga rhizome glycoside as the sole active ingredient in the preparation of a medicament for inhibiting periodontal bone loss.
2. Use of cimicifuga rhizome glycoside according to claim 1 as sole active ingredient for the preparation of a medicament for inhibiting periodontal bone loss, characterized in that: the cimicifuga rhizome glycoside can inhibit monocyte osteoclast differentiation.
3. Use of cimicifuga rhizome glycoside according to claim 2 as sole active ingredient for the preparation of a medicament for inhibiting periodontal bone loss, characterized in that: the cimicifuga rhizome glycoside can inhibit the expression of the core transcription factor Nfatc-1 of the bone breaking.
4. Use of cimicifuga rhizome glycoside according to claim 1 as sole active ingredient for the preparation of a medicament for inhibiting periodontal bone loss, characterized in that: comprises the preparation of an in vitro macrophage culture medium, wherein the in vitro macrophage culture medium contains cimicifuga rhizome glycoside.
5. Use of cimicifuga rhizome glycoside according to claim 4 as sole active ingredient for the preparation of a medicament for inhibiting periodontal bone loss, characterized in that: the macrophage in-vitro culture medium is RPMI 1640 culture medium containing cimicifuga rhizome glycoside.
6. Use of cimicifuga rhizome glycoside according to claim 5 as sole active ingredient for the preparation of a medicament for inhibiting periodontal bone loss, characterized in that: the cimicifuga rhizome glycoside promotes polarization of macrophages to M2 in vitro.
7. Use of cimicifuga rhizome glycoside according to claim 5 as sole active ingredient for the preparation of a medicament for inhibiting periodontal bone loss, characterized in that: the cimicifuga rhizome glycoside inhibits secretion of macrophage inflammatory cytokines under LPS stimulation by inhibiting activation of NF- κB pathway in vitro.
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