CN117695298A - Application of delphinidin-3-O-glucoside in preparation of anti-pulmonary fibrosis medicines or health care products - Google Patents
Application of delphinidin-3-O-glucoside in preparation of anti-pulmonary fibrosis medicines or health care products Download PDFInfo
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Abstract
The invention belongs to the technical field of health-care food and medicines, and particularly relates to application of delphinidin-3-O-glucoside in preparation of medicines or health-care products for resisting pulmonary fibrosis. The dosage of delphinidin-3-O-glucoside is 200-400mg/kg body weight for mice, and 0.8-8mg/d for adults. The delphinidin-3-O-glucoside effectively inhibits bleomycin-induced pulmonary fibrosis injury of mice by inhibiting the increase of pulmonary coefficients, inflammatory injury, in-vivo malondialdehyde, hydroxyproline content and alveolar structure damage of the pulmonary fibrosis mice, and plays a role in protecting the mice.
Description
Technical Field
The invention belongs to the technical field of health-care food and medicines, and particularly relates to application of delphinidin-3-O-glucoside in preparation of medicines or health-care products for resisting pulmonary fibrosis.
Background
Pulmonary fibrosis (Pulmonary fibrosis, PF) is a chronic, progressive and fatal pulmonary disease of unknown etiology with high incidence and poor therapeutic effect, with survival rates of only 30% to 50% over 5 years. The pathological characteristics of the lung tissue are mainly diffuse alveolitis, pulmonary interstitial disorder, massive fibroblast generation and activation, massive extracellular matrix release, compact scar tissue formation and normal lung tissue structure destruction. Because of the unclear etiology and pathogenesis, no reasonable and effective treatment means exists in clinic at present, and the lung fibrosis treatment drugs on the market only slow down the decline of the lung function and cannot be cured thoroughly.
The lung fibrosis medicine and the health care product can prevent the lung fibrosis to a certain extent, promote the health and reduce the lung injury. At present, main medicines for treating pulmonary fibrosis comprise pirfenidone, nidazole and acetylcysteine effervescent tablets, carbocisteine tablets and the like which are used together with anti-fibrosis medicines, but the chemically synthesized medicines have high cost and larger side effect and can influence endocrine function, digestive tract reaction and the like. Therefore, the search for substances with biological activity and the function of preventing pulmonary fibrosis from natural plants is of great significance in medicines, foods and health care products.
Delphinidin-3-O-glucoside (D3G), also known as Delphinidin-glucoside, is an anthocyanin monomer, widely distributed in various plants, for example: mulberry, tea, pomegranate, eggplant, roselle, and the like. The delphinidin-3-O-glucoside has extremely high oxidation resistance, has the characteristics of eliminating free radicals, resisting cancer, resisting inflammation, inhibiting bacteria, preventing cardiovascular and cerebrovascular diseases and the like and has high safety, so that the delphinidin-3-O-glucoside has very good medicinal value and has very considerable application prospect in clinic and medicines.
Disclosure of Invention
The invention aims to seek the development and utilization of novel efficient medicines or health-care products for preventing pulmonary fibrosis, screens out core targets of the interaction of delphinidin-3-O-glucoside and pulmonary fibrosis based on a biological information technology, provides the application of the delphinidin-3-O-glucoside in preparing medicines or health-care products for preventing pulmonary fibrosis, and verifies the effect of the delphinidin-3-O-glucoside on pulmonary fibrosis by using a pulmonary fibrosis mouse model. The effect effects of inflammatory accumulation, oxidative stress, tissue injury and the like of a pulmonary fibrosis model mouse are evaluated by using a bleomycin-induced pulmonary fibrosis mouse model, so that the delphinidin-3-O-glucoside has the effect of inhibiting pulmonary fibrosis.
The technical scheme adopted by the invention is as follows:
application of delphinidin-3-O-glucoside in preparing medicines or health products for resisting pulmonary fibrosis is provided.
Further, in the above application, the delphinidin-3-O-glucoside inhibits an increase in lung coefficient caused by pulmonary fibrosis.
Further, in the above application, the delphinidin-3-O-glucoside inhibits the expression level of inflammatory factor TNF-alpha mRNA caused by pulmonary fibrosis.
Further, in the above application, the delphinidin-3-O-glucoside inhibits the rise of malondialdehyde content caused by pulmonary fibrosis.
Further, in the above application, the delphinidin-3-O-glucoside inhibits the increase of hydroxyproline caused by pulmonary fibrosis.
Furthermore, in the application, the dosage of delphinidin-3-O-glucoside in the anti-pulmonary fibrosis medicine or the health care product is as follows: the dosage of the mice is 200-400mg/kg body weight.
Furthermore, in the application, the dosage of delphinidin-3-O-glucoside in the anti-pulmonary fibrosis medicine or the health care product is as follows: the dosage for adults is 0.8-8mg/d.
The beneficial effects of the invention are as follows:
1. according to the invention, a target gene prediction database of three small molecular compounds SwisstargetPrediction, SEAPrediction and Superhed and an on-line GeneCard database are utilized to screen the acting targets of delphinidin-3-O-glucoside and pulmonary fibrosis, and a core target is screened out through Wen analysis, so that the result proves that the delphinidin-3-O-glucoside can resist pulmonary fibrosis.
2. The invention adopts the delphinidin-3-O-glucoside, induces the pulmonary fibrosis of the mice by the way of dripping bleomycin into the trachea, and is obtained by experiments in the pulmonary fibrosis model mice, the delphinidin-3-O-glucoside can reduce the pulmonary coefficient and the inflammation level of the pulmonary fibrosis mice, can also reduce the content of malondialdehyde in the body and the content of hydroxyproline in the lung tissues, achieves the effect of relieving oxidative damage, maintains the pulmonary alveolus structure of the mice to be fine and uniform, has less fibrin deposition, no inflammatory cellulose deposition and the like. Therefore, delphinidin-3-O-glucoside has the effect of resisting pulmonary fibrosis, and is a good choice for developing novel and efficient natural anti-pulmonary fibrosis medicines or health care products.
Drawings
FIG. 1 is a diagram of the Wen's graph of the target site of action of the active ingredient of delphinidin-3-O-glucoside associated with pulmonary fibrosis.
Fig. 2 is a graph of comparison of lung coefficients of mice in each group, compared with Control group, p <0.05, < p <0.01, < p <0.001; comparing with Model #p <0.05, #p <0.01, #p <0.001.
Fig. 3 is a graph showing comparison of expression levels of inflammatory factor TNF- α mRNA in lung tissues of mice in each group, with p <0.05, p <0.01, p <0.001 compared to Control group; comparing with Model #p <0.05, #p <0.01, #p <0.001.
Fig. 4 is a graph showing the comparison of Malondialdehyde (MDA) content in lung tissue of mice in each group, wherein p <0.05, < p <0.01, < p <0.001; comparing with Model #p <0.05, #p <0.01, #p <0.001.
Fig. 5 is a graph of comparison of Hydroxyproline (HYP) content in lung tissue of mice in each group, where p <0.05, < p <0.01, < p <0.001, compared to Control group; comparing with Model #p <0.05, #p <0.01, #p <0.001.
FIG. 6 is a graph showing comparison of the staining of lung tissue HE and Masson of each group of mice.
Detailed Description
Example 1
Acquisition of delphinidin-3-O-glucoside and pulmonary fibrosis target
Inquiring the molecular structural formula of delphinidin-3-O-glucoside by using Pubchem, and introducing the molecular structural formula into a database for predicting target genes of three small molecular compounds, namely SwisstargetPrediction, SEAPrediction and Superhed; searching the pulmonary fibrosis name in the GeneCard online database according to the English name of the pulmonary fibrosis; the target genes for delphinidin-3-O-glucoside and pulmonary fibrosis were screened. The results showed that 227 delphinidin-3-O-glucoside target genes and 7722 pulmonary fibrosis-related target genes were co-screened after deleting the duplicate data.
(II) screening core targets
Intersection of the active ingredient regulatory gene in D3G and the target gene for pulmonary fibrosis is carried out to obtain a core target, and the result is shown in a Wen diagram of FIG. 1.
As shown in fig. 1, 227 action targets were left for the active ingredient in D3G, 7722 action targets were right for pulmonary fibrosis, and 142 core targets were intersected. The result shows that the D3G can have stronger relevant action effect on PF.
Example 2
Medicine preparation
delphinidin-3-O-glucoside: the monomer is purchased, the Hebei wangyou organism is purchased, and the purity is 95-98%.
Pirfenidone: 1g, ancient cooking vessel and China prosperous biotechnology Limited liability company.
10% chloral hydrate: 10.0g of chloral hydrate powder is weighed, 100mL of double distilled water is added, dissolved and filtered, and the mixture is stored in a dark place.
Bleomycin BLM solution formulation: 25mg of BLM is dissolved in 750 mu L of physiological saline to prepare 50U/mL of storage solution, 150 mu L of storage solution is split charging, 7.35mL of physiological saline is added to 150 mu L of storage solution when in use, and the storage solution is diluted into 1U/mL of working solution.
(II) test of efficacy
Animal feeding and treatment: laboratory animals were kept for 1 week to suit the laboratory conditions, kept in separate cages, sterilized in house, and the litter was replaced every two days. The illumination of a laboratory is controlled, the illumination is carried out for 12 hours, the darkness is carried out for 12 hours, the indoor temperature is 20+/-1 ℃, and the humidity is 55+/-10%.
Grouping of experimental animals: 50C 57BL/6 male mice, weighing 20+ -2 g, were randomly divided into 5 groups of 10 mice each.
(1) Normal Control group (Control);
(2) A pulmonary fibrosis model group (BLM);
(3) Positive control group (PFD): pirfenidone group 50mg/kg (PFD);
(4) Drug administration group: delphinidin-3-O-glucoside 400mg/kg (D3G-H);
(5) Drug administration group: delphinidin-3-O-glucoside 200mg/kg (D3G-L)
Healthy male mice of 6-8 weeks old are selected, and after adapting to the raising environment for one week, modeling is started. Except for the normal control group, the other mice were subjected to molding by tracheal instillation of 0.1mLBLM (1U/mL). The administration was carried out while molding, and in addition to normal control group and pulmonary fibrosis model group mice were administered with physiological saline water, the administration group mice were administered with delphinidin-3-O-glucoside 400mg/kg and 200mg/kg, respectively, the state of the mice was observed daily, the death was recorded, and the body weight was weighed every other day and recorded. At 5 weeks of the experiment, the test was performed.
(III) detection results
1. Mice were sacrificed after blood collection, lung tissue was collected and weighed, and lung coefficients were calculated. The result of comparison of the lung coefficients is shown in fig. 2.
As shown in fig. 2, the lung coefficient of mice in the pulmonary fibrosis model group was significantly higher than that in the normal group (p < 0.001), and the delphinidin-3-O-glucoside administration was able to interfere with the increase in lung coefficient caused by pulmonary fibrosis, and the administration group was able to significantly suppress the increase in lung coefficient of mice (p < 0.05) compared to the pulmonary fibrosis model group. Experimental results show that delphinidin-3-O-glucoside has a remarkable intervention effect on the increase of lung coefficients in the pulmonary fibrosis process of mice and is dose-dependent.
2. Detecting the expression level of inflammatory factor TNF-alpha mRNA in lung tissue. The results are shown in FIG. 3.
As shown in FIG. 3, induction of BLM resulted in a significant increase in the expression level of inflammatory factor TNF-. Alpha.mRNA in the lung tissue of mice (p < 0.001). In the administration group, D3G inhibits the expression of inflammatory factors at mRNA level, has remarkable effect (p < 0.01) and has dose dependency. The D3G has obvious inhibition effect on the increase of the expression level of inflammatory factor mRNA in lung tissues of mice with pulmonary fibrosis caused by BLM induction.
3. The content of malondialdehyde in lung tissue was examined. The results are shown in FIG. 4.
As shown in fig. 4, the lung fibrosis model group had significantly increased Malondialdehyde (MDA) content (p < 0.001) compared to the blank group, and the delphinidin-3-O-glucoside administration group was able to interfere with the malondialdehyde content increase caused by lung fibrosis. The result shows that the delphinidin-3-O-glucoside has good capability of relieving oxidative damage of lung tissues, has obvious intervention effect on pulmonary fibrosis and is dose-dependent.
4. Detecting the content of the fibrosis marker hydroxyproline in lung tissues. The results are shown in FIG. 5.
As shown in fig. 5, the Hydroxyproline (HYP) content of mice in the pulmonary fibrosis model is significantly higher than that of the normal group (p < 0.001), and the delphinidin-3-O-glucoside administration can interfere with the increase of hydroxyproline caused by pulmonary fibrosis, and compared with the pulmonary fibrosis model group, the administration group can significantly inhibit the increase of hydroxyproline in the mice (p < 0.05). The results show that delphinidin-3-O-glucoside can reduce the rise of hydroxyproline in lung tissues, reduce excessive deposition of extracellular matrix, and further relieve pulmonary fibrosis caused by bleomycin.
5. The structure and morphology of lung tissue of mice with pulmonary fibrosis were observed by HE and Masson staining, and the results are shown in fig. 6.
As shown in fig. 6, HE and Masson section results showed that the lung tissue structure of the mice in the blank group was normal, and no proliferation fibrous tissue was seen. Compared with the mice in the model group, the lung tissue injury of the mice in the delphinidin-3-O-glucoside administration group is obviously improved, so that the lung tissue can maintain the integrity, and the fresh lung tissue has inflammatory infiltration, wherein the high-dose administration group has more remarkable influence. Experimental results show that delphinidin-3-O-glucoside can relieve pulmonary fibrosis caused by bleomycin.
Claims (7)
1. Application of delphinidin-3-O-glucoside in preparing medicines or health products for resisting pulmonary fibrosis is provided.
2. The use according to claim 1, wherein the delphinidin-3-O-glucoside inhibits an increase in pulmonary coefficient caused by pulmonary fibrosis.
3. The use according to claim 1, wherein the delphinidin-3-O-glucoside inhibits the expression level of TNF- α mRNA, an inflammatory factor caused by pulmonary fibrosis.
4. The use according to claim 1, wherein the delphinidin-3-O-glucoside inhibits an increase in malondialdehyde content caused by pulmonary fibrosis.
5. The use according to claim 1, wherein the delphinidin-3-O-glucoside inhibits the increase of hydroxyproline caused by pulmonary fibrosis.
6. The use according to claim 1, wherein the delphinidin-3-O-glucoside is administered in an amount such that: the dosage of the mice is 200-400mg/kg body weight.
7. The use according to claim 1, wherein the delphinidin-3-O-glucoside is administered in an amount such that: the dosage for adults is 0.8-8mg/d.
Priority Applications (1)
| Application Number | Priority Date | Filing Date | Title |
|---|---|---|---|
| CN202311697581.4A CN117695298A (en) | 2023-12-12 | 2023-12-12 | Application of delphinidin-3-O-glucoside in preparation of anti-pulmonary fibrosis medicines or health care products |
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| CN202311697581.4A CN117695298A (en) | 2023-12-12 | 2023-12-12 | Application of delphinidin-3-O-glucoside in preparation of anti-pulmonary fibrosis medicines or health care products |
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