Application of phenylpropionic acid as PPAR-gamma agonist in preparation of products for preventing, relieving and / or treating enteritis

Abstract

The invention discloses application of phenylpropionic acid as a PPAR-gamma agonist in preparation of a product for preventing, relieving and / or treating enteritis, relates to the technical field of medicines, and solves the problems that the existing medicines are poor in curative effect and do not have dual effects of preventing and relieving enteritis at the same time. Phenylpropionic acid is used as a PPAR-gamma agonist, can reduce infiltration of inflammatory cells into intestinal tissues by activating PPAR-gamma receptors and inhibiting expression of adhesion molecules, and can also regulate functions of immune cells, reduce release of inflammatory mediators, remarkably reduce generation of proinflammatory cytokines and effectively relieve intestinal inflammatory response, so that the intestinal inflammatory response is reduced, and the intestinal inflammatory response is reduced. Therefore, immune-mediated intestinal injury is relieved, immune response is adjusted, and the anti-inflammatory effect is remarkable; by inhibiting the expression of a fibrosis promoting factor, the process of intestinal fibrosis is slowed down or reversed, and complications such as intestinal stenosis are prevented.

Description

Technical Field

[0001] This invention relates to the field of pharmaceutical formulation technology, and in particular to the use of phenylpropionic acid as a PPAR-γ agonist in the preparation of products for the prevention, relief and / or treatment of enteritis. Background Technology

[0002] In recent years, the incidence of inflammatory bowel diseases such as functional gastrointestinal disorders, inflammatory bowel disease (IBD), ischemic bowel disease, necrotizing enterocolitis (NEC), and chemotherapy / radiotherapy-associated immune enteritis has increased significantly, severely impacting patients' quality of life and imposing a heavy socioeconomic burden. Currently used clinical treatments, such as 5-aminosalicylic acid (5-ASA), glucocorticoids, and anti-TNF-α biologics, while controlling symptoms to some extent, still have limitations including unstable efficacy, easy development of drug resistance, increased risk of infection, and high treatment costs, making it difficult to meet patients' needs for long-term maintenance therapy. Therefore, developing safer, long-term suitable novel treatment strategies with both preventative and remission effects has become an urgent research direction.

[0003] Plant-based diets are rich in natural polyphenols, and multiple studies have confirmed their protective effects against various chronic inflammatory diseases. Polyphenols exert beneficial effects through multiple mechanisms, including antioxidant, anti-inflammatory, and immunomodulatory mechanisms. However, their clinical application is severely limited by low bioavailability—approximately 90% of dietary polyphenols cannot be directly absorbed in the small intestine and must be metabolized by colonic microorganisms into secondary metabolites (such as cinnamic acid derivatives like phenylpropionic acid) before they can be absorbed by the body and exert systemic biological activity and effects. This metabolic characteristic suggests that directly increasing the levels of polyphenol colonic metabolites and targeting key secondary metabolites may be more effective than simply supplementing with polyphenols in translating their anti-inflammatory potential into clinical applications. However, systematic research and related clinical application protocols centered on this pathway are currently lacking.

[0004] Although some studies have attempted to intervene in intestinal inflammation by supplementing with foods rich in polyphenols (such as blueberries, grape skin extracts, or tea polyphenols), and the results have shown a certain anti-inflammatory trend, the overall efficacy is limited and there are significant individual differences. The key limiting factor is the low utilization rate of polyphenols.

[0005] Therefore, in response to the current predicament, future research urgently needs to focus on improving the metabolic level of polyphenols in vivo, especially promoting the generation of their colon flora-dependent metabolites, thereby promoting the effective transformation of the anti-inflammatory effects of polyphenols in the treatment of intestinal inflammatory diseases such as Crohn's disease (CD). Summary of the Invention

[0006] To address the above shortcomings, this invention provides an application of phenylpropionic acid as a PPAR-γ agonist in the preparation of products for the prevention, relief, and / or treatment of enteritis, where the application does not include disease diagnosis or treatment. This solves the problems of poor efficacy and lack of dual preventative and relief effects for enteritis in existing drugs. This invention uses phenylpropionic acid as a PPAR-γ agonist, which can activate PPAR-γ receptors, inhibit the expression of adhesion molecules, reduce the infiltration of inflammatory cells into intestinal tissues, regulate the function of immune cells, reduce the release of inflammatory mediators, significantly reduce the production of pro-inflammatory cytokines, effectively alleviate intestinal inflammation, thereby reducing immune-mediated intestinal damage and regulating the immune response, resulting in significant anti-inflammatory effects. Furthermore, by inhibiting the expression of pro-fibrotic factors, it slows down or reverses the progression of intestinal fibrosis and prevents complications such as intestinal stenosis. The specific technical solution is as follows: Application of phenylpropionic acid as a PPAR-γ agonist.

[0007] Preferably, phenylpropionic acid is used as a PPAR-γ agonist in the preparation of products for the prevention, relief and / or treatment of enteritis.

[0008] Preferably, the phenylpropionic acid is an active ingredient in the product, and its weight percentage in the product is 1-99%.

[0009] Preferably, the product further includes an adjuvant or carrier selected from one or more of physiological saline and dimethyl sulfoxide.

[0010] Preferably, the product is a solution.

[0011] Preferably, the phenylpropionic acid is used to activate the PPAR-γ receptor and reduce the expression levels of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β.

[0012] Preferably, the phenylpropionic acid is used to maintain the weight of patients with colitis caused by DSS.

[0013] Preferably, the phenylpropionic acid is used to maintain and / or shorten the colon length in patients with colitis.

[0014] Preferably, the phenylpropionic acid is used to reduce the activity and severity of colitis.

[0015] Preferably, the phenylpropionic acid is used to reduce mucosal erosion in patients with colitis caused by DSS, as well as to reduce crypt damage and infiltration of inflammatory cells in the colon.

[0016] Preferably, the cause of the enteritis is enteritis caused by functional gastrointestinal disorders, inflammatory bowel disease, ischemic bowel disease, necrotizing enterocolitis, and chemotherapy / radiotherapy-associated immune enteritis.

[0017] Preferably, the product is a pharmaceutical or health product.

[0018] Preferably, the chemical formula of the phenylpropionic acid is C9H. 10 O2; the structural formula is: .

[0019] Overactive immune responses are a crucial pathological basis for the persistence of enteritis. Previous research by the inventors of this invention has shown that overactivation of the PPAR-γ signaling pathway can effectively inhibit the release of inflammatory cytokines (TNF-α, IL-6, IL-1β) and improve the inflammatory environment of the intestinal mucosa. While existing synthetic PPAR-γ agonists (such as thiazolidinediones) have some therapeutic effects, their application in the field of enteritis is limited by adverse reactions such as edema and cardiovascular events. During the research process, the applicant discovered that the direct application of polyphenolic secondary metabolites (cinnamic acid derivatives such as phenylpropionic acid) may significantly increase polyphenol metabolism levels, thereby effectively alleviating intestinal inflammation and demonstrating good therapeutic potential. In further in-depth research, the inventors of this invention discovered a close correlation between phenylpropionic acid and PPAR-γ agonists, which is beneficial for the treatment of enteritis. Based on this, and given that phenylpropionic acid is readily available, has a simple synthetic route, and is highly safe, making it extremely valuable for industrialization and promotion, the applicant focuses on phenylpropionic acid as a starting point, concentrating on its anti-inflammatory, immunomodulatory, and anti-fibrotic potential in enteritis, aiming to break through the bottlenecks in the clinical application of polyphenols: by directly utilizing the active metabolite phenylpropionic acid, the effectiveness and reproducibility of the anti-inflammatory effects of polyphenols can be improved; alternatives or supplements for the synthesis of PPAR-γ agonists can be found: providing a safer, long-term usable natural molecule for clinical use, avoiding the systemic side effects of traditional TZDs.

[0020] Compared with the prior art, the beneficial effects of the present invention are: 1. Pro-inflammatory cytokines (such as TNF-α, IL-6, IL-1β, etc.) play a crucial role in the pathogenesis of enteritis, and their overexpression leads to inflammatory damage to the intestinal mucosa. This invention uses phenylpropionic acid as a PPAR-γ agonist, which can significantly reduce the production of pro-inflammatory cytokines by activating PPAR-γ receptors. By inhibiting the production of these pro-inflammatory factors, phenylpropionic acid can effectively alleviate intestinal inflammatory responses, exhibiting a significant anti-inflammatory effect.

[0021] 2. The phenylpropionic acid and its derivatives of this invention are natural compounds, widely found in various plants, and can be synthesized in one step by hydrogenation of cinnamic acid. The raw materials are inexpensive and readily available, the synthetic route is a single step, the yield is >90%, and it is easily scaled up for industrial use. Furthermore, phenylpropionic acid is a GRAS-grade food additive with an acute toxicity LD50 >2000 mg / kg (rat), exhibiting no TZD-like side effects such as weight gain, edema, or cardiovascular side effects, demonstrating high safety. Compared to some synthetic drugs, phenylpropionic acid, as a natural product, may have lower toxicity, better safety, and better tolerability with long-term use, making it more suitable for the prevention and long-term remission of enteritis. It also shows significant potential in anti-inflammatory, immunomodulatory, and anti-fibrotic effects in enteritis.

[0022] 3. This invention uses phenylpropionic acid as a naturally sourced PPAR-γ agonist, which offers higher safety, accumulates in the gut, and can directly function as a polyphenol metabolite. It possesses the dual attributes of both a "polyphenol metabolite" and a "natural PPAR-γ agonist," and is expected to become an important bridge connecting the diet-microbiota-host interaction chain.

[0023] 4. This invention not only deepens the understanding of the mechanism of action of the "polyphenol-metabolite-PPAR-γ pathway" in the prevention and treatment of enteritis at the theoretical level, but also provides a feasible path for the development of novel, natural and safe anti-inflammatory drugs at the application level, which is of great significance to alleviating the global public health challenges of enteritis-related diseases such as IBD. Attached Figure Description

[0024] To more clearly illustrate the technical solutions of the embodiments of the present invention, the accompanying drawings used in the description of the embodiments will be briefly introduced below. Obviously, the drawings described below are some embodiments of the present invention. For those skilled in the art, other drawings can be obtained based on these drawings without creative effort.

[0025] Figure 1 The diagram below shows the mouse experiment design process for Example 1 of the present invention (A: Mouse experiment design process for Example 1; B: Mouse experiment design process for Example 2; C: Mouse experiment design process for Example 3). Figure 2 This is a graph showing the percentage change in body weight of mice in Example 1 of the present invention; Figure 3 This is a disease activity map of mice in Example 1 of the present invention; Figure 4 This is a schematic diagram of the colon morphology at the end of the experiment in Embodiment 1 of the present invention; Figure 5 This is a schematic diagram of the mouse colon length in Example 1 of the present invention; Figure 6 This is a graph showing the percentage change in mouse body weight in Example 2 of the present invention; Figure 7 This is a disease activity map of mice in Example 2 of the present invention; Figure 8 This is an image of the colon morphology and a representative H&E-stained mouse colon section at the end of the experiment in Example 2 of this invention. Figure 9 This is a schematic diagram of the mouse colon length in Example 2 of the present invention; Figure 10 This is a schematic diagram of the histopathological assessment of the severity of colitis in mice according to Example 2 of the present invention; Figure 11 This is a graph showing the percentage change in body weight of mice in Example 3 of the present invention; Figure 12 This is a disease activity map of mice in Example 3 of the present invention; Figure 13 This is an image of the colon morphology and a representative H&E-stained mouse colon section at the end of the experiment in Example 3 of this invention. Figure 14 This is a schematic diagram of the mouse colon length in Example 3 of the present invention; Figure 15 This is a schematic diagram of the histopathological assessment of the severity of colitis in mice in Example 3 of the present invention; Figure 16 This is a diagram from the dual-luciferase experiment report of phenylpropionic acid activating PPAR-γ in Example 3 of the present invention; Figure 17 This is an example diagram of the PPAR-γ dual reporter gene detection scheme in Embodiment 4 of the present invention; Figure 18 This is a graph showing the dependence of phenylpropionic acid activation of PPAR-γ on dose concentration in Example 4 of the present invention. Detailed Implementation

[0026] The specific embodiments of the present invention are described in detail below, but it should be understood that the scope of protection of the present invention is not limited to the specific embodiments. Unless otherwise defined, all technical terms used below have the same meaning as commonly understood by those skilled in the art. The technical terms used herein are for the purpose of describing specific embodiments only and are not intended to limit the scope of protection of the present invention. Unless otherwise specifically stated, all raw materials, reagents, instruments, and equipment used in the present invention are commercially available or can be prepared by existing methods.

[0027] 1. Experimental Materials The experimental mice used in this invention were all bred and raised by the Animal Center of the First Affiliated Hospital of Sun Yat-sen University. Each experiment used male SPF-grade mice aged 6-9 weeks that were on a low-protein diet (to maintain hippuric acid at a low level).

[0028] 2. The preparation method for the experimental reagents is as follows: Preparation of phenylpropionic acid solutions: Dissolve phenylpropionic acid powder in physiological saline to prepare phenylpropionic acid solutions with mass concentrations of 100 mg / kg, 50 mg / kg, and 10 mg / kg, respectively.

[0029] Preparation of rosiglitazone: In animal experiments, rosiglitazone is prepared by dissolving rosiglitazone powder in physiological saline to prepare phenylpropionic acid solutions with a mass concentration of 100 mg / kg. In cell experiments, rosiglitazone is prepared by dissolving rosiglitazone powder in DMSO to prepare a rosiglitazone stock solution with a mass concentration of 100 mM, and then further diluting the stock solution with serum-free DMEM medium to a rosiglitazone solution of 100 μM.

[0030] Preparation of 2-chloro-5-nitroanilinebenzene (GW9662): 2-chloro-5-nitroanilinebenzene (GW9662) powder was dissolved in physiological saline to prepare a solution with a mass concentration of 100 mg / kg.

[0031] Preparation of DSS: Dissolve solid DSS in physiological saline to prepare DSS solutions with concentrations of 2% and 2.5%, respectively.

[0032] After conducting numerous innovative experiments, the inventors of this invention discovered that phenylpropionic acid and its derivatives differ in their modes of action, speculating that it may be a mild PPAR-γ agonist. The inventors innovatively hypothesized that phenylpropionic acid itself may possess the function of a PPAR-γ agonist. To investigate whether phenylpropionic acid supplementation could modify colitis induced by DSS, the inventors conducted the following experiments: Example 1: Animal in vivo experiments with rosiglitazone and phenylpropionic acid 1. Test methods: such as Figure 1 As shown, 18 mice maintained on a low-protein diet were selected and randomly divided into 3 groups of 6 mice each. Each group of mice was pretreated with saline for three days, followed by daily intraperitoneal injections of saline, 2-chloro-5-nitroanilinebenzene, and phenylpropionic acid, after which they were given drinking water containing 2% DSS. The specific injection details for each group are as follows: Control group: Intraperitoneal injection of 200 μL of physiological saline per mouse; Experimental group 1: After the mice were given drinking water containing 2% DSS on the fourth day, each mouse was injected intraperitoneally with 200ul of phenylpropionic acid with a mass concentration of 100mg / kg every day. Experimental Group 2: On the fourth day, mice were given drinking water containing 2% DSS, and then each mouse was injected intraperitoneally with 200 μL of rosiglitazone at a mass concentration of 1 mg / kg daily.

[0033] Mice in each group were injected intraperitoneally at the same time each day, and all other mice were managed in the same manner. Three days after injection, mice were allowed free access to drinking water containing 2% DSS for six days to establish an enteritis model. During the experiment, daily changes in mouse body weight (calculating the percentage change in body weight, with initial body weight calculated as 100%), fecal characteristics, and occult blood were recorded. On the sixth day of DSS treatment, mice were sacrificed by cervical dislocation, and colon tissue was collected for histological, Western blot, and qRT-PCR analysis.

[0034] 2. Data Analysis: Experimental results are as follows Figure 2 , Figure 3 , Figure 4 , Figure 5 As shown. By Figure 2 , Figure 3 , Figure 4 , Figure 5 The experimental results showed that, in terms of the severity of weight loss and disease activity index, the therapeutic effect of phenylpropionic acid was significantly higher than that of rosiglitazone treatment group.

[0035] Example 2: The effect of phenylpropionic acid on improving colitis in vivo via PPAR-γ like Figure 1 As shown, in order to determine whether phenylpropionic acid alleviates DSS-induced colitis through the PPAR-γ signaling pathway, the inventors used 2-chloro-5-nitroanilinebenzene (GW9662), a potent, irreversible and specific antagonist of PPAR-γ.

[0036] 1. Experimental Methods: Twenty-four mice maintained on a low-protein diet were selected and randomly divided into four groups of six mice each. Each group was pretreated with saline for three days, followed by daily intraperitoneal injections of saline, 2-chloro-5-nitroanilinebenzene, and phenylpropionic acid, administered with drinking water containing 2.5% DSS. Specific injection details for each group are as follows: Control group: After the mice were given drinking water containing 2.5% DSS on the fourth day, each mouse was injected intraperitoneally with 200 μL of physiological saline every day. Experimental group 1: On the fourth day, mice were given drinking water containing 2.5% DSS, and then each mouse was injected intraperitoneally with 200 μL of phenylpropionic acid with a mass concentration of 100 mg / kg every day. Experimental group 2: On the fourth day, mice were given drinking water containing 2.5% DSS, and then each mouse was injected intraperitoneally with 200 μL of 2-chloro-5-nitroanilinebenzene (GW9662) at a mass concentration of 100 mg / kg daily. Experimental Group 3: On the fourth day, after the mice were given drinking water containing 2.5% DSS, each mouse was injected intraperitoneally daily with 100 μL of 2-chloro-5-nitroanilinebenzene (GW9662) + 100 μL of phenylpropionic acid with a mass concentration of 100 mg / kg.

[0037] Mice in all experimental groups were administered intraperitoneal injections at the same time each day, with all other management procedures remaining the same. Three days after injection, mice were given free access to drinking water containing 2% DSS for six days to induce enteritis. On the sixth day of DSS treatment, mice were euthanized by cervical dislocation, and colon tissue was collected for histological, Western blot, and qRT-PCR analysis. Throughout the experiment, mouse weight, fecal characteristics, and occult blood levels were recorded daily.

[0038] 2. Analyze the data: Seven consecutive days of injection of 2.5% DSS resulted in significant weight loss in mice. Compared to the control group (without the drug and treated with GW9662), phenylpropionic acid significantly reduced weight loss, disease severity, and colonic shortening. Combining GW9662 with phenylpropionic acid weakened these protective effects compared to phenylpropionic acid alone, leading to more pronounced weight loss, shorter colonic length, and increased disease activity. This indicates that PPAR-γ activation contributes to the protective effect of phenylpropionic acid, and that phenylpropionic acid still possesses some protective effect under the action of the antagonist GW9662. In contrast, daily administration of rosiglitazone did not alleviate colitis symptoms in mice.

[0039] Experimental results are as follows Figure 6 , Figure 7 , Figure 8 , Figure 9 , Figure 10 As shown, by Figure 6-10 It can be seen that, in terms of the severity of weight loss (calculated as the percentage change in mouse body weight, with initial body weight calculated as 100%), disease activity index, colon length, and histopathological score, the protective effect of phenylpropionic acid against enteritis in this invention is significantly better than that in the control group and the PPAR-γ inhibitor group, indicating that prophylactic administration of phenylpropionic acid can alleviate colitis induced by DSS.

[0040] Example 3: Effects of different phenylpropionic acid concentrations on the in vivo improvement of colitis by PPAR-γ 1. Experimental Methods: 120 mice were selected and randomly divided into 20 groups of 6 mice each. The experiment lasted for 9 days. Before administration of DSS, the mice received intraperitoneal injections of either a control agent or different concentrations of phenylpropionic acid daily. The specific injection details for each group are shown in Table 1 below.

[0041] Table 1 2. Analyze the data: In this system, the ligand-binding domain of PPAR-γ fuses with the DNA-binding domain of GAL4, and upon ligand binding, activates the GAL4-UAS ecdysonephric luciferase reporter gene. An example of a PPAR-γ dual reporter gene detection scheme is shown below. Figure 16 As shown, phenylpropionic acid reaches its maximum activation state at a concentration of 1 mmol, equivalent to 10–25% of the activity induced by 100 μmol and 50 μmol of rosiglitazone, with the optimal activation concentration in the range of 354.54–397.06 μM.

[0042] Experimental results are as follows Figure 11 , Figure 12 , Figure 13 , Figure 14 , Figure 15 , Figure 16 As shown, by Figure 11-16 It was found that DSS treatment led to a gradual decrease in body weight, with the control group mice experiencing a weight loss of approximately 15% of their initial body weight (initial body weight calculated as 100%). Compared to the control group, treatment with 100 mg / kg phenylpropionic acid improved colitis and had the greatest protective effect against weight loss.

[0043] Example 4: In vitro experiment The inventors conducted a conversion activation experiment using a fusion-type GAL4-PPAR-γ in HEK293 cells.

[0044] 1.1 Cell plating: Human embryonic kidney cell line HEK239T cells were used at a rate of 5 × 10⁻⁶ 4 The cells were seeded at a density of 200 μl of DMEM complete medium (89% DMEM medium + 10% fetal bovine serum + 1% penicillin / chloramphenicol) per well in a 48-well plate and incubated at 37°C for 24 hours.

[0045] 1.2 Plasmid transfection: Using a polyethyleneimine (PEI)-based transfection reagent, add 2 ng of plasmid SV40, 30 ng of PPAR-γ, and 150 ng of BP1 per well to the PEI transfection reagent. Transporter™ 5 (Polysciences; DNA:PEI ratio 1:3) was used. Following the manufacturer's instructions, the Renilla luciferase control plasmid driven by the SV40 promoter (2 ng per well, internal control) and the firefly luciferase reporter plasmid containing the GAL4 reaction element (upstream activation sequence, UAS; 180 ng per well) were transfected into cells along with pcDNA3.1-GAL4-PPARγ (30 ng per well) or pcDNA3.1-GAL4 (30 ng per well). Cells were incubated at 37°C for 24 hours.

[0046] 1.3 Phenylacetic acid irritation: Prepare a stock solution by dissolving phenylpropionic acid in DMSO. Dilute the stock solution 1:1000 with serum-free DMEM medium, with DMSO comprising 0.1% of each well. Discard the original medium and add 200 μl to each well of a 48-well plate. Incubate at 37°C for 24 hours.

[0047] 1.4 For dual-fluorescein kit detection, follow the instructions: Experimental results are as follows Figure 17 , Figure 18 As shown, Figure 17 As shown, without co-transfection with GAL4-PPAR-γ, the PPAR-γ agonist rosiglitazone did not increase the activity of the GAL4-UAS reporter gene as expected, because reporter gene activation is strictly dependent on the GAL4-PPAR-γ fusion protein, and phenylpropionic acid activation of PPAR-γ showed a dose-dependent response. In contrast, co-expression of GAL4-PPAR-γ enabled rosiglitazone to achieve significant activation (as a positive control), revealing that phenylpropionic acid significantly enhanced reporter gene activity, while trans-cinnamic acid showed only a slight activation effect, and benzoic acid had no effect. Figure 18 Experimental results show that phenylpropionic acid at a concentration of 100 μM has a higher PPAR-γ agonist effect than rosiglitazone at a concentration of 50 μM, with an EC50 of 375.8 ± 21.26 μM.

[0048] The foregoing description of specific exemplary embodiments of the invention is for illustrative and explanatory purposes. These descriptions are not intended to limit the invention to the precise forms disclosed, and it will be apparent that many changes and variations can be made in accordance with the foregoing teachings. The exemplary embodiments were chosen and described in order to explain the specific principles of the invention and its practical application, thereby enabling those skilled in the art to implement and utilize various different exemplary embodiments of the invention, as well as various different choices and variations. The scope of the invention is intended to be defined by the claims and their equivalents.

Claims

1. Application of phenylpropionic acid as a PPAR-γ agonist.

2. The use of phenylpropionic acid as a PPAR-γ agonist in the preparation of products for the prevention, relief and / or treatment of enteritis.

3. The application according to claim 2, characterized in that, The phenylpropionic acid is an active ingredient in the product, and its weight percentage in the product is 1-99%.

4. The application according to claim 2, characterized in that, The product also includes an adjuvant or carrier, which is selected from one or more of physiological saline and dimethyl sulfoxide.

5. The application according to claim 2, characterized in that, The product is a solution.

6. The application according to claim 2, characterized in that, The phenylpropionic acid is used to activate the PPAR-γ receptor and reduce the expression levels of pro-inflammatory cytokines TNF-α, IL-6, and IL-1β.

7. The application according to claim 2, characterized in that, The phenylpropionic acid is used to maintain the weight of patients with colitis caused by DSS; the phenylpropionic acid is used to maintain and / or shorten the colon length of patients with colitis.

8. The application according to claim 2, characterized in that, The phenylpropionic acid is used to reduce the activity and severity of colitis; the phenylpropionic acid is used to reduce mucosal erosion in patients with colitis caused by DSS, as well as to reduce crypt destruction and colonic inflammatory cell infiltration.

9. The application according to claim 2, characterized in that, The causes of the enteritis are functional gastrointestinal disorders, inflammatory bowel disease, ischemic bowel disease, necrotizing enterocolitis, and chemotherapy / radiotherapy-associated immune enteritis.

10. The application according to any one of claims 2 to 5, characterized in that, The product in question is a pharmaceutical or health supplement.

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