CN115252638A - Preparation method and application of quinoa dietary fiber for improving intestinal inflammation - Google Patents

Abstract

The invention provides a preparation method and application of quinoa dietary fiber for improving intestinal inflammation, and belongs to the field of biomedicine. As a food-derived bioactive ingredient, the quinoa dietary fiber is used for the first time in the preparation of products for preventing and improving ulcerative colitis, which can significantly improve weight loss, increased disease activity index, and colon shortening caused by intestinal inflammation. It can improve the structural integrity of the colon, inhibit the apoptosis of colon cells, and regulate the diversity and abundance of the intestinal flora in colitis, providing a new strategy for the prevention and treatment of colitis.

Description

Preparation method and application of quinoa dietary fiber for improving intestinal inflammation

technical field

The invention belongs to the field of biomedicine and relates to a preparation method and application of quinoa dietary fiber for improving intestinal inflammation.

Background technique

Inflammatory bowel disease, including ulcerative colitis and Crohn's disease, is a chronic, relapsing disease of the gut for which there is currently no effective treatment. In recent years, the prevalence of ulcerative colitis has increased worldwide and has risen sharply in many developing countries where the incidence was once considered low. Common causes of inflammatory bowel disease include genetics, dysregulated immune response, chronic inflammation, gut microbiota imbalance (dysnutrition), and defective mucosal barrier function, among others. Pathologically, ulcerative colitis is clinically manifested as abdominal pain, abdominal distension and mucus bloody stools, accompanied by weight loss and fever, epigastric filling discomfort, hernia, anorexia, nausea, vomiting, etc., and it is characterized by obvious infiltration of neutrophils Into the colon to cause lesions, epithelial cell necrosis, mucosal and submucosa ulceration, infiltrating neutrophils will release reactive oxygen species to cause local inflammation, and damage the barrier function. Normal intestinal epithelial barrier function depends on the integrity of the mucus layer, as well as the expression of tight junction proteins, which, if disrupted, can exacerbate colitis.

Gut microbes are the largest and most complex microecosystem in the human body, and they are closely related to the occurrence of ulcerative colitis. Intestinal microbes form a symbiotic relationship with the host. They and their metabolites not only regulate human health, but also serve as an important bridge between the diet and the host. They maintain the host’s physiology by promoting the growth of the intestinal epithelium and regulating the host’s immune defense. healthy. When gut microbiota is dysfunctional, it stimulates the body's immune-damaging processes and initiates inflammatory signaling pathways. Dietary interventions have been shown to treat or prevent inflammatory bowel disease by modulating effects on the mucosal immune system and enhancing gut microbiota diversity. Modern nutritional studies have shown that high molecular dietary fiber cannot be digested by the stomach and intestines, and most of it enters the intestines to regulate intestinal flora. Gut microbiota, as a novel functional target, plays an important role in modulating host gut health.

As a kind of "whole grain", quinoa is not only rich in protein, amino acid, unsaturated fatty acid, vitamin, mineral and dietary fiber, but also rich in a variety of biologically active substances, such as saponins, flavonoids, polyphenols, flower Penicillin, etc. have good preventive and adjuvant therapeutic effects on the prevention of obesity, cardiovascular disease, diabetes and cancer, and also have the effects of enhancing the body's immunity, anti-inflammation, and anti-oxidation. In addition to its high nutritional qualities, quinoa is also characterized as being gluten-free, a property that can provide celiac patients with more suitable foods and a wider variety of nutritional supplements. The dietary fiber content of quinoa seeds is about 13%, of which soluble fiber can be as high as 30% of the total dietary fiber, with a content of about 4%, which is higher than grain crops such as wheat and corn, and has many advantages compared with traditional grains. In addition, quinoa dietary fiber has high water holding capacity, glucose absorption capacity and chenodeoxycholic acid capacity. The extraction process of dietary fiber from quinoa bran is simple, low in cost, and can make full use of the by-products of grain processing and increase its added value; therefore, it is necessary to explore a quinoa bran that can significantly improve the intestinal flora imbalance caused by intestinal inflammation. Application of wheat dietary fiber.

Contents of the invention

Aiming at the problems in the prior art, the invention provides a preparation method and application of quinoa dietary fiber for improving intestinal inflammation. The present invention studies the regulating effect of quinoa dietary fiber on intestinal inflammation, intestinal barrier dysfunction, intestinal flora imbalance, etc. by extracting quinoa dietary fiber from quinoa bran, and further clarifies the use of quinoa dietary fiber. It has important clinical application significance to improve the mechanism of colitis, so as to further prevent inflammatory bowel disease, colon cancer and other diseases.

To achieve the above object, the technical scheme adopted in the present invention is as follows:

First of all, an application of quinoa dietary fiber in preparing products for improving intestinal inflammation is provided, and the extraction method of the quinoa dietary fiber includes the following steps:

(1) Mix quinoa bran and MES-tris buffer evenly, add α-amylase to react at 58-62°C, then add protease to react at 38-42°C, then add amyloglucosidase to react at 58°C React at -62°C;

(2) After the reaction in step (1) is completed, add trichloroacetic acid and centrifuge to get the supernatant, centrifuge the supernatant, alcohol precipitation, dialysis, and dry to obtain the quinoa dietary fiber.

Further, the weight ratio of quinoa bran, α-amylase, protease and amyloglucosidase in step (1) is 16-18:2.5-3.5:0.09-0.12:0.35-0.45.

In some specific embodiments, the extraction method of the quinoa dietary fiber comprises the following steps:

(1) After mixing 17.0g of quinoa bran powder with MES-tris buffer (0.05M, 25°C, pH 6.9) at a ratio of 1g:30mL, it was stirred at 50°C for 40min; then, at 60°C Add 3g of α-amylase ( ^3700U /g) in a water bath at ℃ and incubate for 30min to remove starch; Remove protein; finally, add 0.4 g amyloglucosidase (1×10 ⁵ U/g) in a water bath at 60° C. and incubate for 30 min to remove residual starch.

(2) After the enzyme reaction is over, add 10% trichloroacetic acid overnight at room temperature, settle the residual protein, and then remove the residue by centrifuging at a speed of 3600r/min for 20min; after the supernatant is precipitated with 4 times the volume of 95% ethanol for 2h, Centrifuge at a speed of 3600r/min for 15min to obtain crude quinoa dietary fiber; wash the crude quinoa dietary fiber with acetone, ether and 80% ethanol to remove residual oil, and use a 200Da dialysis bag for 36h to remove other impurities; °C in a vacuum oven to obtain purified quinoa dietary fiber.

Further, the monosaccharide composition of the purified quinoa dietary fiber is: mannose (0.44wt%), ribose (0.45wt%), glucose (78.16wt%), galactose (2.40wt%), xylose (0.13wt%), arabinose (1.52wt%), fucose (0.51wt%), glucuronic acid (1.49wt%), galacturonic acid (14.90wt%); the molecular weight is 5.57×10 ⁴ Da.

Further, the product is any one of medicine, food and health care products.

Further, the product is a medicine, and the medicine includes a pharmaceutically acceptable carrier or adjuvant, and the carrier or adjuvant includes one or more of a diluent, a binder, a disintegrant, and a lubricant.

Further, the diluent includes starch, microcrystalline cellulose, sucrose, dextrin, lactose, powdered sugar, and glucose.

Further, the binder includes ethanol, starch slurry, sugar syrup, hydroxypropylmethylcellulose, sodium hydroxymethylcellulose, and sodium alginate.

Further, the disintegrating agent includes tartaric acid and low-substituted hydroxypropyl cellulose.

Further, the lubricant includes magnesium stearate, stearic acid, sodium chloride, sodium oleate, poloxamer, and sodium lauryl sulfate.

Furthermore, when the product is a drug, it can be introduced into the body (such as muscle, intradermal, subcutaneous, vein, mucosal tissue) by oral administration, injection, injection, infiltration and other methods.

Further, the product is a product for improving body weight loss, disease activity index increase and colon shortening caused by colitis.

Further, the product is a product for improving the structural integrity of the colon and inhibiting colon cell apoptosis.

Further, the product is a product for resisting a defect in the mucosal barrier function.

Further, the product is a product for regulating intestinal flora imbalance.

Further, the product is a product for preventing and/or treating related diseases such as intestinal inflammation.

Further, the diseases include ulcerative colitis, Crohn's disease, immune response disorder, intestinal flora imbalance, abdominal distension and mucus and bloody stools, weight loss and fever, abdominal filling discomfort, hernia, anorexia, nausea, vomiting , Necrosis of intestinal epithelial cells, ulceration of mucosa and submucosa, chronic inflammation.

Further, the dosage form of the product is any one of oral liquid, tablet, capsule, injection and granule.

Compared with the prior art, the present invention has the following beneficial effects:

(1) The quinoa dietary fiber prepared by this application is used as an active ingredient for the first time in the preparation of products that regulate inflammatory responses, inhibit cell apoptosis, and improve intestinal barrier dysfunction, in order to prevent and/or treat intestinal inflammation and other related diseases provide a new strategy;

(2) The quinoa dietary fiber prepared by the present application can significantly improve the imbalance of intestinal flora caused by intestinal inflammation, increase the content of short-chain fatty acids, and increase the diversity and abundance of intestinal flora.

Description of drawings

Figure 1: Transmission electron microscope image of quinoa dietary fiber;

Figure 2: (A) Body weight change graph (percentage of initial body weight), * indicates significant difference: P<0.05; (B) disease activity index (DAI), higher score indicates more severe symptoms, * indicates significant difference: P< 0.05; (C) the left picture is the colon image, (C) the right picture is the quantitative histogram of colon length;

Figure 3: (A) histopathological quantitative score; (B) quantitative histogram of the number of TUNEL positive cells/field of view cells;

Figure 4: (A) relative protein expression of TNF-α in colon tissue; (B) relative protein expression of IL-1β in colon tissue; (C) relative protein expression of pro-Caspase-1 in colon tissue;

Figure 5: (A) relative mRNA expression of TNF-α in colon tissue; (B) relative mRNA expression of MCP-1 in colon tissue; (C) relative mRNA expression of IL-10 in colon tissue;

Figure 6: (A) relative protein expression of TNF-α in serum; (B) relative protein expression of IL-1β in serum;

Figure 7: (A) relative protein expression of MUC2 in colon tissue; (B) relative protein expression of ZO-1 in colon tissue;

Figure 8: Relative mRNA expression of MUC2 (A), ZO-1 (B), Claudin-1 (C), Claudin-3 (D) and Occludin (E) in colon tissue;

Figure 9: Comparison of α-diversity of intestinal microbial communities in mouse fecal samples; (A) Chao 1 species richness index; (B) Ace species richness index; (C) Simpson diversity index; (D) Shannon diversity index;

Figure 10: Venn diagram, the overlap shows that the OTUs in the intestinal flora of mice in different treatment groups are the same;

Figure 11: (A) Histogram of comparison of intestinal flora structure at phylum level between different treatment groups; (B) Histogram of comparison of abundance at phylum level between different treatment groups;

Figure 12: Short-chain fatty acid levels in fecal samples from different treatment groups; (A) acetic acid; (B) propionic acid; (C) isobutyric acid; (D) butyric acid; (E) isovaleric acid; acid;

The letters above the error bars in Figures 2-9 and 11-12 indicate: if the same letters are included, the difference is not significant, P≥0.05; if the same letters are not included, the difference is significant, P<0.05; such as between a and a The difference is not significant, the difference between a and ab is not significant, and the difference between a and b is significant.

Detailed ways

It is worth noting that the raw materials used in the present invention are all common commercially available products, and their sources are not specifically limited.

The following sources of reagents and instruments are illustrative: quinoa bran powder (Qingbai No. 1, purchased from Qinghai Gaoyuan Jinhe Ecological Agriculture and Animal Husbandry Technology Co., Ltd.), fecal occult blood detection kit (purchased from Yisheng Biotechnology (Shanghai) ) Co., Ltd.), TUNEL cell apoptosis detection kit (purchased from Shanghai Biyuntian Biotechnology Co., Ltd.).

Example 1

Create a mouse model

1. Materials

Animals: 40 7-week-old BALB/c mice weighing 15-20 g were purchased from the Department of Veterinary Medicine of Peking University, all mice were male; feed (AIN-93G rodent diet), quinoa dietary fiber 1 (QBSDF) , quinoa dietary fiber 2 (QBSDF (L)), tap water (special water for animal rooms), tap water containing 2.5% (w/v) dextran sodium sulfate (DSS);

The extraction steps of quinoa dietary fiber 1 (QBSDF) are as follows:

(1) After mixing 17.0 g of quinoa bran powder with MES-tris buffer solution (0.05 M, 25 °C, pH value 6.9) at a ratio of 1 g: 30 mL, it was stirred at 50 °C for 40 min. Then, add 3g of α-amylase (3700U/g) in a water bath at 60°C and incubate for 30min to remove starch; add 0.09g of neutral protease (6×10 ⁴ U/g) in a water bath at 40°C Incubate for 30 min to remove protein; finally, add 0.4 g amyloglucosidase (1×10 ⁵ U/g) in a water bath at 60° C., and incubate for 30 min to remove residual starch.

(2) After the enzyme reaction, add 10% trichloroacetic acid overnight at room temperature to settle the residual protein, and then centrifuge at 3600r/min for 20min to remove the residue. After the supernatant was precipitated with 4 times the volume of 95% ethanol for 2 hours, it was centrifuged at a speed of 3600 r/min for 15 minutes to obtain the crude quinoa dietary fiber. The crude quinoa dietary fiber was washed with acetone, ether and 80% ethanol to remove residual oil, and was dialyzed for 36 hours using a 200Da dialysis bag to remove other impurities. Finally, it was dried in a vacuum oven at 65° C. to obtain purified quinoa dietary fiber 1 (QBSDF). A transmission electron microscope experiment was performed on the QBSDF obtained above. The experimental results are shown in FIG. 1 .

The extraction steps of quinoa dietary fiber 2 (QBSDF(L)) are as follows:

(1) After mixing 15.0 g of quinoa bran powder with MES-tris buffer solution (0.05 M, 25 °C, pH value 6.9) at a ratio of 1 g: 30 mL, it was stirred at 50 °C for 40 min. Then, add 2g of α-amylase (3700U/g) in a water bath at 60°C and incubate for 30min to remove starch; add 0.15g of neutral protease (6×10 ⁴ U/g) in a water bath at 40°C Incubate for 30 min to remove protein; finally, add 0.3 g amyloglucosidase (1×10 ⁵ U/g) in a water bath at 60° C., and incubate for 30 min to remove residual starch.

(2) After the enzyme reaction, add 10% trichloroacetic acid overnight at room temperature to settle the residual protein, and then centrifuge at 3600r/min for 20min to remove the residue. After the supernatant was precipitated with 4 times the volume of 95% ethanol for 2 hours, it was centrifuged at a speed of 3600 r/min for 15 minutes to obtain the crude quinoa dietary fiber. The crude quinoa dietary fiber was washed with acetone, ether and 80% ethanol to remove residual oil, and was dialyzed for 36 hours using a 200Da dialysis bag to remove other impurities. Finally, it was dried in a vacuum oven at 65° C. to obtain purified quinoa dietary fiber 2 (QBSDF (L)).

Breeding conditions: standard SPF grade environment, temperature 20-25°C, humidity 55%, 12h light and dark cycle, free access to food and water.

2. Method

BALB/c mice were divided into 5 groups with 8 mice in each group:

Control group (CON): intake of common feed;

Quinoa dietary fiber group (QBSDF): intake of common feed and intake of quinoa dietary fiber 1;

DSS group (DSS): intake of common feed and tap water with 2.5% (w/v) DSS;

QBSDF and DSS group (DSS+QBSDF): intake of common feed and tap water of QBSDF and 2.5% (w/v) DSS;

QBSDF(L) and DSS group (DSS+QBSDF(L)): Ingest common feed and tap water with QBSDF(L) and 2.5% (w/v) DSS;

The mice were divided into three groups after one week of acclimatization, one group (n=16) was treated with QBSDF by gavage, the second group (n=8) was treated with QBSDF (L) by gavage, and the third group (n=16) was treated with tap water (Special water for animal room) treatment. The amount of QBSDF or QBSDF (L) administered to mice was 1.5g/kg/d. Two weeks later, one group and three groups of mice were randomly divided into two subgroups, and they were allowed to drink ordinary tap water and tap water containing 2.5% (w/v) DSS respectively, and the second group was allowed to drink water containing 2.5% (w/v) v) Tap water for DSS. These five groups can be divided into: blank group (CON, n=8), DSS group (DSS, n=8) drinking only 2.5% (w/v) DSS, DSS+QBSDF group (DSS+QBSDF, n=8 ), the QBSDF group (QBSDF, n=8), the DSS+QBSDF(L) group (DSS+QBSDF(L), n=8). CON group and QBSDF group drank normal tap water, DSS group, DSS+QBSDF group, DSS+QBSDF(L) group drank tap water containing 2.5% (w/v) DSS, and after 7 days, mice in all groups drank normal tap water. Euthanasia was performed with tap water on day 7, and mice were fasted for 12 hours before euthanasia.

Example 2

Weight loss rate, disease activity index (DAI) value and colon length detection experiment of colitis mice:

The DAI value is evaluated and analyzed through three aspects: the weightlessness rate of the mice (0-4 points), the thick and thin stool (0-4 points) and the bloody stool (0-4 points). DAI scores were scored during DSS induction and recovery. The blood in feces of mice was detected by fecal occult blood detection kit. As shown in Figure 2, the intake of quinoa dietary fiber 1 (QBSDF) significantly improved the mice's weight loss, DAI score increase and colon shortening, while quinoa dietary fiber 2 (QBSDF(L)) had no effect on the above three conditions. The improvement effect was relatively poor, indicating that the prepared QBSDF had a significant improvement effect on the colitis symptoms of BALB/c mice. Therefore, the detection experiments of Examples 3-7 no longer study DSS+QBSDF(L).

Experimental example 3

Colon injury and colon cell apoptosis detection experiment:

Colonic injury was analyzed by histopathological score and colonic cell apoptosis was analyzed by TUNEL cell apoptosis detection kit.

As shown in Fig. 3, QBSDF ingestion significantly ameliorated the increase of histopathological score of DSS-induced colitis in mice, and in addition, QBSDF intervention significantly reduced the number of colonic epithelial TUNEL-positive cells. This shows that quinoa dietary fiber can significantly reduce the apoptosis of colonic epithelial cells and significantly improve colonic inflammation.

Example 4

Detection of colonic inflammatory proteins and gene expression:

Detection method: Western blotting was used to detect the expression of inflammation-related (TNF-α, 1L-1β, pro-Caspase-1) proteins in colon tissue, and qRT-PCR was used to detect colitis-related genes (TNF-α, MCP-1, 1L- 10), using enzyme-linked immunosorbent assay (ELISA) to measure the expression of TNF-α and IL-1β in serum. Eight parallel experiments were performed in each group and the mean value was taken.

As shown in Figures 4 and 6, QBSDF intake significantly improved the expression levels of inflammatory proteins IL-1β, TNF-α, and pro-Caspase-1 in mice with colitis, and reduced the levels of IL-1β and TNF-α in serum. Protein expression; as shown in Figure 5, in the DSS group, the gene expression levels of TNF-α and MCP-1 were significantly increased, and under the intervention of QBSDF, the expression levels of TNF-α and MCP-1 were significantly reduced. This shows that QBSDF can directly inhibit the expression of inflammatory factors, and by promoting the expression of the anti-inflammatory factor IL-10, it can inhibit the secretion of intestinal inflammatory factors such as IL-1β and TNF-α (as shown in Figure 6) to improve colitis role.

Example 5

Colonic mucosa tight junction protein and gene expression detection:

Detection method: Western blotting was used to detect the expression of tight junction protein in colonic mucosa. The colon tissue was lysed to extract the protein, the protein was denatured, and the target protein was separated by SDS-PAGE electrophoresis, the antibody was used to bind the target protein, and the target protein was developed with a gel imager and quantified by image lab. Eight replicates were used for each group and the mean value was taken. The expression of colonic tight junction protein-related genes (Claudin-1, Claudin-3, MUC2, ZO-1, Occludin) was detected by qRT-PCR.

As shown in Figure 7, QBSDF intake significantly improved the reduction of MUC2 and ZO-1 protein expression in the colon tissue of DSS-induced colitis mice; The expressions of Claudin-3, MUC2, ZO-1, Occludin were significantly decreased. Under the intervention of QBSDF, the expression levels of Claudin-1, Claudin-3, MUC2, ZO-1 and Occludin were significantly increased. This indicated that QBSDF significantly improved the mucin and gene expression reduction in the relevant protective epithelial tissues of the mouse colon after DSS treatment, thereby playing a role in protecting the gut.

Example 6

Detection of the structure and composition of intestinal flora:

Detection method: 16S rRNA gene sequencing was used to analyze the intestinal flora of mice, the original sequencing sequence of Trimmomatic software was used for quality control, and FLASH software was used for splicing. The UPARSE software (version 7.1 http://drive5.com/uparse/) used was used to perform OTU clustering on sequences based on a 97% similarity and remove chimeras. RDPclassifier (http://rdp.cme.msu.edu/) was used to annotate the species classification of each sequence, compared to the Silva database (SSU128), and the comparison threshold was set to 70%.

As shown in Figure 9, QBSDF significantly ameliorated the decrease in the diversity and abundance of gut microbiota in DSS-induced colitis mice. Compared with the DSS group, Chao 1, Ace and Shannon indexes in QBSDF intervention group increased significantly, while Simpson index decreased significantly. As shown in Figure 10, the QBSDF group, DSS group, and DSS+QBSDF group shared 792, 629, and 687 OTUs with the control group, respectively, indicating that quinoa dietary fiber has a significant effect on reducing the diversity of intestinal flora in colitis mice improvement effect. As shown in Figure 11, QBSDF significantly increased the abundance of Firmicutes and Patescibacteria, and significantly decreased the abundance of Bacteroidetes and Epsilonbacteraeota. Quinoa dietary fiber can regulate the change of key flora in inflammatory mice to the normal ratio, which indicates that quinoa dietary fiber can improve the intestinal flora structure and intestinal microenvironment, and has a certain protective effect on the intestinal barrier.

Example 7

Analysis and detection of intestinal short-chain fatty acid content:

Detection method: Gas chromatography-mass spectrometry (GC-MS) was used to measure the level of short-chain fatty acids (SCFAs) in feces. Take a mouse feces sample (0.1 g) and dissolve it in 1 ml of distilled water, add 0.5 mL of sulfuric acid (volume fraction 50%) to treat it for 10 min. The mixture was mixed with 2 mL of ether, extracted on ice for 30 min, and the supernatant was collected by centrifugation for GC-MS analysis.

As shown in Figure 12, DSS significantly decreased the content of acetic acid, butyric acid, isovaleric acid and valeric acid in colitis mice, while QBSDF significantly increased the content of acetic acid and butyric acid, which indicated that quinoa dietary fiber could increase short-chain Fatty acid production improves intestinal inflammation.

Finally, it should be noted that the above content is only used to illustrate the technical solution of the present invention, rather than to limit the scope of protection of the present invention. Simple modifications or equivalent replacements to the technical solution of the present invention by those skilled in the art will not depart from the present invention. The essence and scope of the technical solution of the invention.

Claims (10)

1. The application of the quinoa dietary fiber in preparing a product for improving intestinal inflammation is characterized in that the extraction method of the quinoa dietary fiber comprises the following steps:

(1) Mixing quinoa bran and MES-tris buffer solution uniformly, adding alpha-amylase to react at 58-62 ℃, then adding protease to react at 38-42 ℃, and then adding amyloglucosidase to react at 58-62 ℃;

(2) And (2) after the reaction in the step (1) is finished, adding trichloroacetic acid, centrifuging, taking supernatant, centrifuging the supernatant, precipitating with ethanol, dialyzing, and drying to obtain the quinoa dietary fiber.

2. The use according to claim 1, wherein the weight ratio of the quinoa bran, the alpha-amylase, the protease and the amyloglucosidase in step (1) is 16-18:2.5-3.5:0.09-0.12:0.35-0.45.

3. The use according to any one of claims 1-2, wherein the product is any one of a pharmaceutical, a food, a nutraceutical.

4. The use of claim 3, wherein the product is a medicament comprising a pharmaceutically acceptable carrier or excipient, wherein the carrier or excipient comprises one or more of a diluent, a binder, a disintegrant, and a lubricant.

5. Use according to claim 1, wherein the product is a product for ameliorating weight loss, increased disease activity index, and colon shortening due to colitis.

6. The use according to claim 1, wherein the product is a product for improving the structural integrity of the colon and inhibiting apoptosis of colon cells.

7. Use according to claim 1, wherein the product is a product intended to be resistant to defects in the barrier function of the adhesive membrane.

8. Use according to claim 1, wherein the product is a product for modulating an imbalance in intestinal flora.

9. The use according to claim 1, wherein the product is a product for the prevention and/or treatment of diseases associated with intestinal inflammation and the like.

10. The use according to claim 9, wherein said diseases include ulcerative colitis, crohn's disease, immune response disorders, intestinal dysbacteriosis, abdominal distension and mucous bloody stools, weight loss and fever, epigastric fullness discomfort, colic, anorexia, nausea, vomiting, enterocyte necrosis, mucosal and submucosal ulcerations, chronic inflammation.

Images