CN115606802A - Application of lycopene in preparation of products for repairing intestinal barrier damage - Google Patents

Abstract

The invention belongs to the technical field of food nutrition, and particularly relates to application of lycopene in preparation of a product for repairing intestinal barrier damage, wherein the intestinal barrier damage comprises damage of intestinal epithelial mucosa and increase of intestinal permeability, and the damage of the intestinal epithelial mucosa comprises reduction of the number of intestinal epithelial cells, defect of a tight connection structure between the epithelial cells, reduction of intestinal mucus and imbalance of intestinal microenvironment. In the application, the lycopene is proved to improve the intestinal microenvironment by inhibiting colitis symptoms such as diarrhea, hematochezia and the like of a colitis mouse induced by dextran sodium sulfate and regulating the composition of intestinal flora, and meanwhile, the lycopene can promote the repair of intestinal epithelial cells and the increase of intestinal mucus, so that the intestinal barrier function is improved. The lycopene can be used as a safe and effective dietary nutrient for treating or preventing ulcerative colitis and related complications thereof, and indirectly drives the tomato processing industry to upgrade and transform to nutrition and health.

Description

Application of lycopene in preparation of products for repairing intestinal barrier damage

technical field

The invention belongs to the technical field of food nutrition, and particularly relates to the application of lycopene in the preparation of products for repairing intestinal barrier damage.

Background technique

Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is a chronic intestinal inflammatory disorder characterized by weight loss, severe diarrhea, and abdominal pain. In recent years, inflammatory bowel disease has gradually developed into a global disease, posing a serious threat to the lives and health of people all over the world. Patients with inflammatory bowel disease often show intestinal homeostasis imbalance and immune abnormalities, such as increased number of immune cells in the intestinal mucosa, enhanced local humoral or cellular immune activity in the intestine. The intestinal barrier composed of host intestinal epithelial cells plays an important role in maintaining intestinal homeostasis. It not only avoids the excessive response of the host immune system, but also prevents harmful intestinal components from transferring into the body and causing inflammatory reactions. The intestinal barrier is divided into mechanical barrier, chemical barrier, biological barrier and immune barrier, and its impaired function may be the primary event in some intestinal and extraintestinal inflammatory diseases.

At present, the traditional drug therapy based on aminosalicylate, glucocorticoid, mercaptopurine and other anti-inflammatory drugs and immunosuppressants is the main means of treating inflammatory bowel disease. However, from the perspective of long-term treatment, the therapeutic effect of these drugs is limited, the side effects are relatively large and the dependence is strong. Therefore, there is an urgent need for some emerging, safe and effective methods for preventing and treating inflammatory bowel disease and repairing the intestinal barrier that are suitable for long-term use.

Lycopene is widely found in tomatoes, tomato products, watermelon, grapefruit and other fruits, and is a natural pigment in the carotenoid family. Studies in recent years have shown that lycopene has good anti-inflammatory and antioxidant capabilities. Dietary supplements can play a variety of roles in suppressing obesity, treating cardiovascular diseases, and preventing cancer. Nutritional supplements with lycopene as the main active ingredient are very popular in Europe, America, Israel, Japan and other regions, and have broad prospects for industrialization. Patent CN112055543A discloses that carotenoids provide prebiotic effects and can be used to improve the health of the gut microbiome. In particular it was shown that oral administration of lycopene to moderately obese subjects resulted in changes in the gut microbiome with increased counts of Bifidobacterium adolescentis and decreased counts of Bacteroidetes. However, the mechanism of action of lycopene on improving inflammatory bowel disease has not been disclosed.

At present, there is no relevant report on whether lycopene has a definite effect on improving the intestinal barrier.

Contents of the invention

In view of the above technical problems, the purpose of the present invention is to propose a new application of lycopene, that is, the application of lycopene for repairing intestinal barrier damage, and the specific technical scheme is as follows:

Application of lycopene in the preparation of products for repairing intestinal barrier damage, the intestinal barrier damage includes intestinal epithelial mucosa damage and intestinal permeability increase.

Further, the product includes medicine, dietary supplement, food or beverage.

Further, the damage to the intestinal epithelial mucosa includes a decrease in the number of intestinal epithelial cells, a defect in the tight junction structure between epithelial cells, a decrease in intestinal mucus, and an imbalance in the intestinal microenvironment.

Further, the intestinal microenvironment imbalance includes a decrease in the number of beneficial bacteria, an increase in the number of harmful bacteria, and an increase in serum immunoglobulin.

Further, the beneficial bacteria are one or more of the genus Lactobacillus, Prevotella_UCG-001 (Prevotellaceae_UCG-001), Muribaculaceae or Faecalibaculum; The harmful bacteria are Escherichia coli-Shigella (Escherichia-Shigella).

Further, the molecular formula of the lycopene is C ₄₀ H ₅₆ , and the molecular structure of the lycopene includes one or more of trans-lycopene or cis-lycopene.

Further, the cis-lycopene includes 15-cis-lycopene, 13-cis-lycopene, 11-cis-lycopene, 9-cis-lycopene, 7-cis-lycopene or 5-cis-lycopene One or more of red pigments.

Further, the trans-lycopene is all-trans-lycopene.

The structural formulas of trans and cis lycopene isomers of the present invention are shown in the following formula (I):

Further, the intestinal barrier damage is the primary event of intestinal diseases, wherein the intestinal diseases are inflammatory bowel disease, diarrhea and blood in the stool.

Further, the product also includes pharmaceutically or food-acceptable carriers or excipients.

Further, the dosage form of the product is liquid, tablet, powder infusion, chewable tablet or soft gel.

Compared with prior art, the beneficial effect of the present invention is:

(1) The use of lycopene provided by the present invention in repairing intestinal barrier damage can be further applied to the prevention of inflammatory bowel diseases, such as ulcerative colitis and the like. Lycopene and liquid supplements containing said dose of lycopene have good effects on inflammatory bowel disease without adverse reactions, and can effectively inhibit dextran sodium sulfate (DSS)-induced weight loss, diarrhea and blood in the stool in mice Ulcerative colitis and other symptoms; it can also improve the intestinal barrier function by promoting the repair of intestinal epithelial cells and increasing intestinal mucus; by increasing the number of beneficial bacteria and/or reducing the number of harmful bacteria, it can improve the intestinal microenvironment.

(2) The application of lycopene provided by the present invention for improving intestinal flora and preventing inflammatory bowel disease shows that it can improve and treat intestinal diseases including inflammatory bowel disease, diarrhea and blood in the stool, and improve intestinal barrier function and intestinal microenvironment to open up a new way of dietary intervention, which has a significant role in promoting the application of lycopene in the market.

Description of drawings

The following is a brief description of the content expressed in the attached drawings of the manual:

Fig. 1 is the comparison chart of body weight change of the mouse inflammatory bowel disease model of four experimental groups in embodiment 1;

Fig. 2 is the comparison chart of the disease activity index (DAI) of the mouse inflammatory bowel disease model of four experimental groups in embodiment 1;

Fig. 3 is the comparative figure of the colon length of the mouse inflammatory bowel disease model of four experimental groups in embodiment 1;

Fig. 4 is the histopathological figure of the mouse inflammatory bowel disease model of four experimental groups in embodiment 1;

Fig. 5 is the comparative diagram of the intestinal permeability of the mouse inflammatory bowel disease model of the four experimental groups in Example 1;

Fig. 6 is the results comparison chart of the expression of tight junction protein in the colon of the mouse inflammatory bowel disease model of the four experimental groups in Example 1;

Fig. 7 is the comparison chart of the colonic mucus of the mouse inflammatory bowel disease model mice of the four experimental groups in Example 1;

Fig. 8 is the principal component analysis (PCA) of the colonies in the intestinal tract of the mouse inflammatory bowel disease model of the four experimental groups in Example 2;

Figure 9 is a comparison of the relative abundance of microbial colonies at the phylum level in the intestinal tract of the mouse inflammatory bowel disease model of the four experimental groups in Example 2;

Figure 10 is a comparison of the relative abundance of microbial colonies at the genus level in the intestinal tract of the mouse inflammatory bowel disease model of the four experimental groups in Example 2;

Fig. 11 is the comparative figure of the content of immunoglobulin (IgA) in serum and colon of the mouse inflammatory bowel disease model mice of four experimental groups in embodiment 2;

Figure 12 is a comparison chart of the disease activity index (DAI) of the mouse inflammatory bowel disease model of the four experimental groups in Example 3;

Fig. 13 is the comparative figure of the colon length of the mouse inflammatory bowel disease model of four experimental groups in embodiment 3;

Figure 14 is a comparative diagram of the intestinal permeability of the mouse inflammatory bowel disease model of the four experimental groups in Example 3;

Fig. 15 is a comparison chart of colonic mucus in the mouse inflammatory bowel disease model of the four experimental groups in Example 3.

detailed description

The following will clearly and completely describe the technical solutions in the embodiments of the present invention with reference to the accompanying drawings in the embodiments of the present invention. Obviously, the described embodiments are only some of the embodiments of the present invention, not all of them. Based on the embodiments of the present invention, all other embodiments obtained by persons of ordinary skill in the art without creative efforts fall within the protection scope of the present invention.

Example 1

Dextran sodium sulfate (DSS) was used to induce the ulcerative model of inflammatory bowel disease in mice, and the improvement effect of lycopene on the ulcerative model of inflammatory bowel disease was verified by drug efficacy test.

1.1 Test method

(1) Animal grouping: 6-week-old C57BL/6J male mice (body weight 18-22g) were fed in a standard SPF barrier environment, maintained at a constant temperature (22°C), constant humidity (55%), 12 hours of day and night, and free feeding and drinking water. After one week of adaptive feeding, 24 mice were equally divided into blank control (Ctrl) group, lycopene (Lycopene) group, DSS group and Lycopene+DSS group. The mice in the 4 groups were fed with the same standard diet, free drinking water.

(2) Administration method: After one week of adaptive feeding, mice in Lycopene group and Lycopene+DSS group were given 0.25 mL of lycopene solution (dose: 1 mg/kg day) every day, and lycopene was fed with edible corn before use. The rats in the Ctrl group and the DSS group were given 0.25 mL of edible corn oil, administered orally once a day for 9 consecutive weeks.

(3) Model establishment: referring to the internationally recognized method of DSS-induced chronic ulcerative colitis, the drinking water of the mice in the DSS group and Lycopene+DSS group was replaced with 1.5% DSS aqueous solution with a molecular weight of 36000-50000, and the water was continuously available for 1 week. After that, change the drinking water back to normal drinking water for a week. Then repeat twice, changing the drinking water to DSS aqueous solution for 1 week, and then changing the drinking water back to normal drinking water for 1 week to induce chronic ulcerative colitis. During the experiment, the body weight and feces status of the mice were recorded daily; after the experiment, the mice were dissected, the length of the colon was measured, photographed, and the contents of the colon were collected, and the colon tissue samples were preserved with 4% formalin fixative.

The lycopene used in the experiment is a red powder with a content >95%.

(4) Measurement and evaluation methods of key indicators:

A. Histopathological analysis

The mouse colon tissue was collected to prepare tissue sections, and the hematoxylin-eosin (HE) stained sections were observed under an optical microscope. Calculate the total histopathological score.

B. Analysis of Colonic Mucus Barrier Function

The effect of lycopene on mucus barrier function in mouse colon was investigated using Alcian blue-periodic acid Schiff staining. Firstly, the paraffin sections of colon tissue were dewaxed in xylene, rehydrated with ethanol, placed in Alcian blue staining solution with pH=2.5 for 10 min, and washed twice with distilled water. Stain with periodate reagent and Schiff's reagent for 5 minutes respectively, and rinse with distilled water twice. After dehydration with ethanol, put it into xylene to make it transparent for mounting and microscopic examination.

C. Intestinal wall permeability test

Dissolve FITC-labeled dextran in PBS at a concentration of 100 mg/mL. After fasting for 4 hours, each mouse was orally administered 150 μl of FITC-dextran solution. After 4 hours, the blood was collected, and the serum was separated by centrifugation at 1000 rpm at 4°C for 20 minutes. The fluorescence intensity of FITC in serum was detected by a multifunctional fluorescent microplate reader, with an excitation wavelength of 495nm and an emission wavelength of 535nm.

D. Detection of expression level of intestinal epithelial tight junction protein

The effect of related protein expression was detected by immunoblotting. Tissue or cells are lysed with RIPAbuffer Lysis Buffer containing 1% protein phosphatase inhibitors and protease inhibitors to harvest total protein. The extracted protein concentration was quantified using a biuret acid protein assay kit. Load an equal amount of protein samples into a sodium dodecyl sulfate-polyacrylamide gel electrophoresis gel and transfer to a polyvinylidene fluoride membrane. After blocking the membrane with skim milk, the primary antibody against the above protein was incubated at 4°C. After 24 h, incubation with horseradish peroxidase-linked secondary antibody was performed for 2-3 h.

1.2 Test results:

(1) Weight change

The body weight comparison data of the four groups of mice are shown in Figure 1. It can be seen from Figure 1 that after the induction of DSS in the 4th week, compared with the mice in the Ctrl group, the body weight of the mice in the DSS group decreased significantly. , the average body weight of the mice in the Ctrl group was 104.69±1.11% of the initial body weight, the average body weight of the mice in the Lycopene group was 101.25±1.48% of the initial body weight, and the average body weight of the mice in the DSS group was 94.58±2.51% of the initial body weight. The average body weight of the mice in the +DSS group was 101.28±1.13% of the initial body weight, and the difference was significant at p<0.01, indicating that lycopene can significantly inhibit the weight loss of mice induced by DSS.

(2) Disease activity index

Disease activity index (DAI) is an important indicator for evaluating the severity of the colitis model in combination with parameters such as weight loss of mice, feces sparseness, and blood in the stool. The comparison data of the ulcerative model mouse DAI is shown in Figure 2, where it can be seen from Figure 2 It was found that compared with the mice in the DSS group, the DAI of the mice in the Lycopene+DSS group was significantly reduced, that is, the symptoms of colitis in the mice were significantly improved, indicating that lycopene can significantly improve the DSS-induced disease activity index in mice.

(3) Colon length

Colon length is another important reference index for evaluating the severity of colonic inflammation. The comparison data of colon length in ulcerative model mice is shown in Figure 3. The colon lengths of the mice in the Ctrl group and the Lycopene group were normal, with an average length of 7.92±0.21cm and 7.84±0.32cm, respectively. Compared with the blank group, the colon length of the mice in the DSS group was significantly reduced (P<0.05). The colon length of the mice in the Lycopene+DSS group was significantly increased, that is, lycopene can significantly improve the shortening of the colon length of mice induced by DSS, as well as inflammatory symptoms such as congestion and edema.

(4) Histopathological analysis

As shown in Fig. 4, the observation under the optical microscope showed that the colon structure of the mice in the Ctrl group and the Lycopene group was clear, the crypt structure was complete, and the glands were not damaged. Local ulcers formed in the colon tissue of the mice in the DSS group, the epithelium of the colon mucosa was necrotic and exfoliated, and inflammatory cell infiltration was seen, and severe edema appeared in the mucosa and submucosa. Compared with the blank group, the histological injury index of the mice in the model group was significantly increased (P<0.05); after lycopene intervention, the infiltration of inflammatory cells in the mice was reduced, the structure of the intrinsic gland was improved, and the congestion and edema were relieved. Compared with the DSS group was significantly lower (P<0.05). The results showed that lycopene could effectively slow down DSS-induced chronic ulcerative colitis in mice.

(5) Intestinal permeability

As shown in Figure 5, the colonic permeability of the mice in the DSS group was significantly increased, and the intestinal permeability of the mice was weakened after lycopene intervention (P<0.05). This indicates that lycopene promotes the repair of the intestinal epithelial barrier, thereby preventing harmful substances from damaging the intestinal tract again, and alleviating the occurrence of colitis. The effect of lycopene on the expression of tight junction protein in mouse colon was further tested, and the results are shown in Figure 6. It can be seen that lycopene significantly increased the expression of tight junction proteins such as ZO-1, Occludin, Claudin-1 and Claudin-2 in the mouse colon (P<0.05), promoted the repair of the intestinal epithelial barrier, and then prevented The damage of harmful substances to the intestinal barrier can alleviate the occurrence of colitis.

(6) Analysis of colonic mucus barrier function

The physiological structure composed of the mucus layer secreted by intestinal epithelial cells plays an important role in maintaining the intestinal barrier function and preventing intestinal bacteria and other pathogenic antigens from entering the body's blood circulation and other tissues and organs. As shown in Figure 7, the number of intestinal goblet cells and mucin significantly decreased after DSS treatment (P<0.05); lycopene could significantly increase intestinal mucin and restore the mucosal barrier.

Example 2

Dextran sodium sulfate (DSS) was used to induce the ulcerative model of inflammatory bowel disease in mice, and lycopene was used to intervene to detect the intestinal microenvironment of mice.

The intestinal microbial community and its metabolites play an important role in maintaining the homeostasis of the host intestinal mucosal epithelial cells and immune system. In particular, beneficial bacteria including Lactobacillus, Akkermansia muciniphila, Faecailbacterium and other metabolites such as short-chain fatty acids help maintain the intestinal epithelial mucosal barrier and help prevent foreign Bacterial invasion stimulates the establishment, improvement and maintenance of intestinal immune function, and promotes the body's resistance to inflammation.

2.1 Test method

Taking the DSS-induced colitis in mice in Example 1 as a research model, the 16S rRNA sequencing technology was used to analyze the effect of lycopene on the structure of the intestinal microbial flora in mice.

The test adopts the same (1) animal grouping, (2) administration method and (3) model establishment as in 1.1 test method.

(4) Measurement and evaluation methods of key indicators:

A 16s RNA sequencing

After extracting mouse colon tissue RNA, 400ng of total RNA was used to construct the RNA sequencing library Library, the library was sequenced using a sequencing platform, the original sequencing data was saved in fastq format, and the original data was evaluated for sequencing-related quality using fastx_toolkit_0.0.14 software ; Use SeqPrep software to perform quality control on the original data to obtain high-quality quality control data, compare it with the mouse reference genome GRCm38.p5, and obtain Reads for subsequent transcript assembly, expression calculation, etc.; assemble the Reads The reference gene was obtained by splicing, and the expression level of the reference gene was quantitatively analyzed using the expression calculation software, and the DESeq2 software based on the negative binomial distribution was used to select the gene expression multiples greater than 1 in the two groups of samples and the p value was still less than 0.05 after multiple test correction Differentially expressed genes in the gene set were established, compared with the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, and KEGG functional enrichment analysis was performed on the genes in the gene set.

2.2 Test results

(1) Difference analysis of colony composition

In order to further study the changes in the overall structure and composition of intestinal flora, the differences among microbial communities were further analyzed and evaluated by principal co-ordinates analysis (PCoA) based on the NMDS algorithm. As shown in Figure 8, there were significant differences in the composition of intestinal microbes among the four groups. Compared with the DSS group, the β-diversity of the microbiota in the Lycopene+DSS group was closer to that of the Ctrl and Lycopene groups, which indicated that lycopene significantly alleviated the decrease in diversity induced by DSS and returned to a flora structure similar to that of the normal group.

(2) Analysis of colony composition and structure

As shown in Figure 9, at the phylum level, the main flora in the mouse intestine are Firmicutes, Bacteroidetes, Actinobacteria, Proteobacteria, etc. . Among them, Firmicutes and Bacteroidetes were the most important two types of flora. Lycopene intervention significantly reduced the increase of Firmicutes and Proteobacteria induced by DSS, and increased the content of Bacteroidetes and Actinomycetes. content.

As shown in Figure 10, at the genus level, DSS treatment significantly reduced Lactobacillus (Lactobacillus), Prevotella _UCG-001 (Prevotellaceae_UCG-001), Muribaculaceae and Faecalibaculum (Faecalibaculum) The abundance level of the above-mentioned flora significantly increased after lycopene intervention; DSS treatment significantly increased the levels of Turicibacter, Romboutsia, and Escherichia-Shigella (Escherichia-Shigella) and other flora, After the intervention of lycopene, the levels of the above-mentioned flora were significantly reduced (P<0.05).

(3) Immunoglobulin (IgA) level

Serum IgA levels can reflect whether the humoral immune function is normal, and the main function of intestinal mucosal IgA is to shape the microbiome and regulate intestinal homeostasis. As shown in Figure 11, DSS treatment significantly increased the serum IgA level, which proved that the immune function of the body was activated. However, after the intervention of lycopene, the serum IgA of the mice was significantly decreased (P<0.05), and the colon IgA was significantly increased (P<0.05). This is because lycopene stimulates the immune barrier and produces a large amount of intestinal IgA to wrap and cover harmful bacteria such as Escherichia coli and excreted with feces, thereby weakening the attack of harmful bacteria on the host under pathological conditions and reducing the occurrence of inflammatory reactions . In addition, the level of IgA in the blood after supplementing lycopene was lower than that of DSS, which further confirmed the decrease of the body's inflammatory response. The immunoglobulin results also demonstrated that lycopene supplementation can regulate the intestinal microenvironment.

Example 3

On the basis of ensuring lycopene as the main active ingredient, the preventive and protective effects of lycopene on symptomatic enteropathy were verified by supplementing dietary supplements.

3.1 Test method

Using DSS-induced colitis in mice as a research model, the prevention and treatment effect of lycopene liquid supplement on inflammatory bowel disease was explored:

(1) Animal grouping: 6-week-old C57BL/6J male mice (body weight 18-22g) were fed in a standard SPF barrier environment, maintained at a constant temperature (22°C), constant humidity (55%), 12 hours of day and night, and free feeding and drinking water. After 1 week of adaptive feeding, 24 mice were equally divided into blank control (CON) group, lycopene liquid supplement (LJ) group, disease model (DSS) group and lycopene liquid supplement intervention group (LJ +DSS) group, 4 groups of mice were fed with the same standard diet and had free access to drinking water.

(2) Administration method: After one week of adaptive feeding, the mice in the LJ group and the LJ+DSS group were given 0.35 mL of lycopene liquid supplement (dose: 1 mg/kg body weight/day); the mice in the Ctrl group and the DSS group Give 0.35mL 0.9% sodium chloride solution, orally once a day, for 9 consecutive weeks.

(3) Model establishment: DSS was used to induce chronic ulcerative colitis as described in 1.1.

3.2 Test results

(1) Disease activity index

As shown in Figure 12, compared with the model group mice, the colitis symptom-related disease activity index was significantly improved in mice supplemented with lycopene liquid supplements.

(2) Colon length

Lycopene liquid supplements can also significantly improve DSS-induced shortening of colon length and inflammatory symptoms such as congestion and edema, the results are shown in Figure 13. This shows that lycopene liquid supplement can significantly resist DSS-induced colitis symptoms in mice.

(3) Intestinal permeability

As shown in Figure 14, the colonic permeability of the mice in the DSS group was significantly increased, and the intestinal permeability of the mice was weakened after the intervention of the lycopene liquid supplement (P<0.05). This indicates that lycopene liquid supplements can promote the repair of the intestinal epithelial barrier, thereby preventing harmful substances from damaging the intestinal tract again.

(4) Analysis of colonic mucus barrier function

Goblet cells in the gut produce mucin to form the mucosal barrier. As shown in Figure 15, the number of intestinal goblet cells and mucins were significantly reduced after DSS treatment (P<0.05); lycopene liquid supplements could significantly restore the mucosal barrier.

Example 4

Using Lycopene Tablets to Improve the Symptoms of Inflammatory Bowel Disease in Mice Induced by Dextran Sulfate (DSS): On the basis of ensuring lycopene as the main active ingredient, the sensory quality was developed by adding food additives to meet the general market consumption Lycopene tablets needed by patients, and verify its preventive and protective effect on inflammatory bowel disease.

4.1 Test method

Production of lycopene tablets: Weigh 10% lycopene powder, 55% starch, and 35% β-cyclodextrin, mix the above materials, spray with 80% ethanol solution, then granulate, and dry at 55°C for 3 hours After that, sieve. Take the granules between 20 and 40 meshes as the tableting material, put them in the tableting machine, and press the tablet under 15kN～20kN to make 0.5g tablet;

Taking DSS-induced colitis in mice as a research model, the effect of lycopene tablets on DSS-induced mice was explored. The model was established as follows:

(1) Animal grouping: 6-week-old C57BL/6J male mice (body weight 18-22g) were fed in a standard SPF barrier environment, maintained at a constant temperature (22°C), constant humidity (55%), 12 hours of day and night, and free feeding and drinking water. After adaptive feeding for 1 week, 12 mice were evenly divided into a disease model (DSS) group and a lycopene tablet group (LJ+DSS) group, with free access to water.

(2) Administration method: crush lycopene tablet into powder, weigh 25g, add casein 178g, L-cysteine 2g, corn starch 280g, maltodextrin 33g, sucrose 327g, cellulose 47g, 23g of soybean oil, and 19g of lard were made into mouse feed, and each mouse was fed with 0.3g of feed every day, and the mice drank normal drinking water;

(3) Model establishment: DSS was used to induce chronic ulcerative colitis as described in 1.1. During the induction process, the body weight and feces status of the mice were recorded daily; after the experiment, the mice were dissected, the length of the colon was measured, photographed, and the contents of the colon were collected, and the colon tissue samples were preserved with 4% formalin fixative.

4.2 Experimental results

Compared with the mice in the disease model group, the disease activity index related to the symptoms of colitis in the mice fed lycopene tablets was significantly improved; the lycopene tablets could significantly improve the shortening of the colon length induced by DSS and congestion, Inflammatory symptoms such as edema, indicating that lycopene tablets can significantly resist DSS-induced colitis symptoms in mice. In addition, feeding lycopene tablets can also significantly promote the proliferation of intestinal epithelial cells and mucus production in mice, improve the colonic barrier function of healthy mice, and enhance their resistance to intestinal disease infection or disease resistance.

The above is only a preferred embodiment of the present invention, it should be pointed out that, for those of ordinary skill in the art, without departing from the principle of the present invention, some improvements and modifications can also be made, these improvements and Retouching should also be regarded as the protection scope of the present invention.

Claims (10)

1. The application of lycopene in the preparation of products for repairing intestinal barrier damage, characterized in that the intestinal barrier damage includes intestinal epithelial mucosa damage and intestinal permeability increase. 2. The application of lycopene according to claim 1 in the preparation of products for repairing intestinal barrier damage, characterized in that the products include medicines, dietary supplements, food or beverages. 3. The application of lycopene according to claim 1 in the preparation of products for repairing intestinal barrier damage, wherein the damage to the intestinal epithelial mucosa includes a reduction in the number of intestinal epithelial cells, structural defects in tight junctions between epithelial cells, Decreased intestinal mucus and imbalanced intestinal microenvironment. 4. The application of lycopene according to claim 1 in the preparation of products for repairing intestinal barrier damage, characterized in that, the imbalance of the intestinal microenvironment includes a decrease in the number of beneficial bacteria, an increase in the number of harmful bacteria, and a decrease in the number of serum immunoglobulins. Increase. 5. the application of lycopene according to claim 4 in the preparation of products for repairing intestinal barrier damage, wherein said beneficial bacteria are Lactobacillus, Prevotella_UCG-001, Muribaculaceae bacteria One or more of the family or Faecalibacterium; the harmful bacteria are Escherichia coli-Shigella. 6. The application of lycopene according to claim 1 in the preparation of products for repairing intestinal barrier damage, characterized in that the molecular formula of said _lycopene is _C40H56 , and the molecular structure of said lycopene comprises One or more of trans-lycopene or cis-lycopene. 7. The application of lycopene according to claim 6 in the preparation of products for repairing intestinal barrier damage, wherein the cis-lycopene comprises 15 cis-lycopene, 13 cis-lycopene, One or more of 11-cis-lycopene, 9-cis-lycopene, 7-cis-lycopene or 5-cis-lycopene; the trans-lycopene is all-trans-lycopene. 8. The application of lycopene according to claim 1 in the preparation of products for repairing intestinal barrier damage, characterized in that the intestinal barrier damage is the primary event of intestinal diseases, wherein the intestinal diseases are Inflammatory bowel disease, diarrhea, and blood in stool. 9. The application of lycopene according to claim 1 in the preparation of a product for repairing intestinal barrier damage, characterized in that the product further comprises pharmaceutically or food-acceptable carriers or adjuvants. 10. The application of lycopene according to claim 9 in the preparation of a product for repairing intestinal barrier damage, characterized in that the dosage form of the product is liquid, tablet, powder granule, chewable tablet or soft gel.

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