Application of CLIC5 gene in preparation of medicine for preventing and / or treating intestinal inflammation

Abstract

The invention belongs to the technical field of biological medicines, and particularly relates to application of a CLIC5 gene in preparation of a medicine for preventing and / or treating intestinal inflammation. The invention provides application of a CLIC5 gene in preparation of a medicine for preventing and / or treating intestinal inflammation. The nucleotide sequence of the CLIC5 gene is shown as SEQ ID NO: 1. Experiments find that the intestinal epithelial cell specific knockout CLIC5 can reduce the serum endotoxin level, improve the intestinal epithelial barrier function, increase the content of butyric acid, reduce the serum inflammatory factor level and reduce the gene expression level of inflammatory factors in ileum and colon. The invention reveals for the first time that intestinal epithelial cell specific knockout CLIC5 can effectively prevent or treat intestinal inflammation and reduce the level of body inflammatory factors, and provides a new target and a new method for treating human intestinal inflammation.

Description

Technical Field

[0001] The present invention belongs to the field of biomedicine technology, and specifically relates to the use of the CLIC5 gene in preparing a drug for preventing and / or treating intestinal inflammation. Background Art

[0002] Inflammatory bowel disease (IBD) is a chronic condition that causes intestinal inflammation, posing a serious threat to human health and placing a significant burden and cost on the healthcare system. Intestinal inflammation is linked to genetic susceptibility, environmental factors such as a Western diet, smoking, infection, and antibiotic use, as well as a complex interaction of multiple factors, including intestinal dysbiosis and immune system dysfunction. For example, in IBD, intestinal barrier function is disrupted, leading to microbial translocation, overactivation of the mucosal immune system, and the release of pro-inflammatory cytokines. Intestinal inflammation has profound consequences, with local effects manifesting as abdominal pain, diarrhea, and a significantly increased risk of colorectal cancer; and systemic effects manifesting as malnutrition, osteoporosis, fatigue, and a significantly increased risk of thrombosis, hepatobiliary disease, and joint disease. Furthermore, intestinal inflammation is strongly associated with a variety of diseases, including autoimmune diseases, metabolic disorders such as obesity and fatty liver disease, mental illness, and neurological disorders.

[0003] Despite advances in the treatment of intestinal inflammation with biologics, small molecule drugs, and combination therapies, most therapies remain ineffective in controlling intestinal inflammation, particularly in patients with chronic or refractory disease. Furthermore, intestinal inflammation involves multiple pathway interactions, and existing small molecule drugs lack targeted therapy for intestinal inflammation.

[0004] Chloride intracellular channels (CLICs) are found in the cytoplasm, cell membranes, and membranes of various organelles, and play a crucial role in the development of cardiovascular disease, cancer, and neurodegenerative diseases. The inventors previously discovered that overexpressing CLIC5 in skeletal muscle can accelerate muscle repair after injury, combat high-fat diet-induced obesity and metabolic syndrome, and effectively alleviate liver fat deposition. However, there have been no reports linking CLIC5 to intestinal inflammation. Summary of the Invention

[0005] To address the problem of the lack of drug targets for the prevention and / or treatment of intestinal diseases in the prior art, the present invention provides the use of the CLIC5 gene in the preparation of a drug for the prevention and / or treatment of intestinal inflammation, specifically including the following technical solutions:

[0006] Use of the CLIC5 gene in preparing a drug for preventing and / or treating intestinal inflammation, wherein the nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO: 1.

[0007] Preferably, the drug is used to specifically knock out or inhibit the expression of the CLIC5 gene in intestinal epithelial cells.

[0008] The present invention also provides use of an agent for inhibiting or silencing CLIC5 gene expression in the preparation of a medicament for preventing and / or treating intestinal inflammation. The nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO: 1.

[0009] Preferably, the prevention and / or treatment of intestinal inflammation includes: reducing serum endotoxin levels, reducing serum proinflammatory factor levels, reducing the level of inflammatory factors in the ileum, reducing the level of inflammatory factors in the colon, improving intestinal epithelial barrier function and increasing the content of butyric acid in the colon contents. One or more of the following.

[0010] The present invention also provides a drug for preventing and / or treating intestinal inflammation, comprising reagents and excipients for inhibiting or silencing CLIC5 gene expression, wherein the nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO: 1.

[0011] Preferably, the excipients include pharmaceutically acceptable excipients.

[0012] Preferably, in the above-mentioned use or medicine, the intestinal inflammation includes I) and / or II):

[0013] 1) Intestinal inflammation caused by a high-fat diet;

[0014] II) Colitis.

[0015] Preferably, the colitis comprises dextran sulfate sodium-induced colitis.

[0016] The present invention also provides a biological material for inhibiting or silencing CLIC5 gene expression. The nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO: 1.

[0017] Preferably, the biological material includes sgRNA for knocking out the CLIC5 gene, and the sgRNA is shown as SEQ ID NO: 2 and / or SEQ ID NO: 3.

[0018] The beneficial effects of the present invention are:

[0019] The present invention belongs to the field of biomedicine technology and specifically relates to the use of the CLIC5 gene in the preparation of a drug for preventing and / or treating intestinal inflammation. The present invention provides the use of the CLIC5 gene in the preparation of a drug for preventing and / or treating intestinal inflammation. The nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO: 1. Through a series of experiments, the present invention discovered that when mice with intestinal epithelial cell-specific knockout of CLIC5 were used as experimental animals and fed a normal diet, this knockout of CLIC5 reduced serum endotoxin levels, improved intestinal epithelial barrier function, and increased butyrate production. When the experimental mice were fed a high-fat diet, this knockout of CLIC5 reduced serum inflammatory factor levels and reduced gene expression of inflammatory factors in the ileum and colon. In a mouse colitis model established with sodium dextran sulfate, this knockout of CLIC5 reduced serum inflammatory factor levels. This present invention reveals for the first time that intestinal epithelial cell-specific knockout of CLIC5 can effectively prevent or treat intestinal inflammation and reduce the levels of inflammatory factors in the body, providing a new target and method for treating human intestinal inflammation. BRIEF DESCRIPTION OF THE DRAWINGS

[0020] In order to more clearly illustrate the embodiments of the present invention or the technical solutions in the prior art, the drawings required for use in the embodiments are briefly introduced below.

[0021] Figure 1 The agarose gel electrophoresis results of different groups of mice in Example 1;

[0022] Figure 2 This is the effect of CLIC5 knockout in intestinal epithelial cells on the expression level of colon tight junction proteins under normal diet conditions in Example 2; wherein, WT NCD is wild-type mice fed a normal diet; IKO NCD is intestinal epithelial cell CLIC5 knockout mice fed a normal diet. DETAILED DESCRIPTION

[0023] The present invention provides use of the CLIC5 gene in preparing a medicament for preventing and / or treating intestinal inflammation. The nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO: 1.

[0024] SEQ ID NO: 1: 5'-atgacggactcagcgacaactaatggggacgacagggaccccgagatcgagctct-3'.

[0025] In one embodiment, the drug is used to specifically knock out or inhibit the expression of the CLIC5 gene in intestinal epithelial cells. This specific knockout or inhibition of CLIC5 gene expression in intestinal epithelial cells can effectively prevent or treat intestinal inflammation and reduce the level of inflammatory factors in the body. In one embodiment, the intestinal inflammation includes I) and / or II): 1) intestinal inflammation caused by a high-fat diet; II) colitis. In one embodiment, the colitis includes colitis caused by dextran sulfate sodium.

[0026] The present invention also provides the use of an agent that inhibits or silences CLIC5 gene expression in the preparation of a drug for preventing and / or treating intestinal inflammation. The nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO: 1. In one embodiment, the prevention and / or treatment of intestinal inflammation comprises one or more of: reducing serum endotoxin levels, reducing serum proinflammatory cytokine levels, reducing inflammatory cytokine levels in the ileum, reducing inflammatory cytokine levels in the colon, improving intestinal epithelial barrier function, and increasing butyrate content in colonic contents. In one embodiment, the agent that inhibits or silences CLIC5 gene expression can be an agent that knocks out the CLIC5 gene. In one embodiment, the CLIC5 gene knockout agent can prevent intestinal inflammation in mice. In one embodiment, when the drug is administered to mice, intestinal epithelial cell-specific knockout of the CLIC5 gene can reduce serum endotoxin levels, improve intestinal epithelial barrier function, and increase butyrate content in colonic contents, while feeding a normal diet. In one embodiment, when the drug is administered to mice in a colitis model established with dextran sulfate sodium, intestinal epithelial cell-specific knockout of the CLIC5 gene can reduce serum inflammatory cytokine levels in mice. In one embodiment, the intestinal inflammation includes I) and / or II): 1) intestinal inflammation caused by a high-fat diet; II) colitis. In one embodiment, the colitis includes colitis caused by dextran sulfate sodium.

[0027] The present invention also provides a drug for preventing and / or treating intestinal inflammation, comprising an agent for inhibiting or silencing CLIC5 gene expression and excipients. The nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO: 1. In one embodiment, the drug comprises a biological product. In one embodiment, the biological product comprises a pharmaceutical for preventing and / or treating intestinal inflammation, prepared from biological materials such as microorganisms, cells, and various animal and human tissues and fluids obtained through biotechnologies such as genetic engineering, cell engineering, protein engineering, and fermentation engineering. In one embodiment, the excipients comprise pharmaceutically acceptable excipients. In one embodiment, the excipients comprise any one or more of excipients, solvents, coating agents, sustained-release agents, powder bases, and injection media. In one embodiment, the drug is in the form of tablets, injections, capsules, ointments, creams, granules, suppositories, or aerosols. In one embodiment, the intestinal inflammation includes I) and / or II): 1) intestinal inflammation caused by a high-fat diet; II) colitis. In one embodiment, the colitis includes colitis caused by sodium dextran sulfate.

[0028] The present invention also provides a biomaterial for inhibiting or silencing CLIC5 gene expression, the nucleotide sequence of the CLIC5 gene being shown in SEQ ID NO: 1. In one embodiment, the biomaterial comprises an sgRNA for knocking out the CLIC5 gene, the sgRNA being shown in SEQ ID NO: 2 and / or SEQ ID NO: 3.

[0029] SEQ ID NO: 2: 5'-CTTAGTATAGTAACAGCGGTTGG-3';

[0030] SEQ ID NO: 3: 5'-GTAGATGTTACGACGAGGTAAGG-3'.

[0031] The present invention has no particular limitation on the method for knocking out the CLIC5 gene, and a gene knockout method well known to those skilled in the art can be used, such as using the Cre / LoxP recombinase system to knock out the CLIC5 gene. loxp / loxp Transgenic mice, the construction method is consistent with the authorized patent ZL202311139530.X. The source of the Villin1-Cre transgenic mice of the present invention is preferably Jackson Laboratory (Cat. No. 021504). In the embodiment of the present invention, it is preferred to combine Villin1-Cre transgenic mice with CLIC5 loxp / loxp Transgenic mice were mated to obtain CLIC5 intestinal epithelial cell-specific knockout mice.

[0032] To further illustrate the present invention, the application of the CLIC5 gene provided by the present invention in the preparation of a medicament for preventing and / or treating intestinal inflammation is described in detail below with reference to the accompanying drawings and examples. However, these figures should not be construed as limiting the scope of protection of the present invention.

[0033] Example 1 Preparation of CLIC5 Intestinal Epithelial Cell-Specific Knockout Mice

[0034] This example refers to the method in patent: ZL202311139530.X to construct CLIC5 loxp / loxp Transgenic mice were constructed by Saiye (Guangzhou) Biotechnology Co., Ltd. The construction process is as follows:

[0035] The CLIC5 gene is located on mouse chromosome 17 (NCBI Reference Sequence: NM_172621; Ensembl: ENSMUSG00000023959). The CLIC5 gene consists of six exons, with exon 2 selected as the conditional knockout region. Two sgRNAs were designed based on the first and second introns. The sgRNA sequences are as follows:

[0036] sgRNA-1:5'-CTTAGTATAGTAACAGCGGTTGG-3' (SEQ ID NO: 2);

[0037] sgRNA-2:5'-GTAGATGTTACGACGAGGTAAGG-3' (SEQ ID NO: 3);

[0038] Villin1-Cre transgenic mice (i.e., Vil1-cre transgenic mice) and CLIC5 loxp / loxp The transgenic mice were mated, and the resulting offspring were genotyped using the mouse tail genome. The primer sequences are as follows:

[0039] loxp-F:5'-CGGAGTCATCCTTTAGTGCCTTAC-3' (SEQ ID NO:4);

[0040] loxp-R:5'-CTGCTCGGCTTCCTTGTCTAATA-3' (SEQ ID NO:5);

[0041] Cre-F:5'-CCATAGGAAGCCAGTTTCCCTTC-3' (SEQ ID NO:6);

[0042] Cre-R:5'-TTCCAGGTATGCTCAGAAAACGC-3' (SEQ ID NO:7);

[0043] After obtaining the transgenic mice, a 0.5 cm length of tail tip was cut to obtain the tail. The tail was added to a lysis buffer containing proteinase K (DirectPCR Lysis Reagent, Viagen, Cat#102-T) and lysed at 55°C for 5-6 hours to obtain a tail lysate containing the genome. PCR analysis was performed using the tail lysate.

[0044] Amplification was performed using PCR. The PCR amplification system (10 μL) consisted of: 2× PCR reagent (5 μL); upstream primer (0.25 μL); downstream primer (0.25 μL); ddH₂O (4.1 μL); and mouse tail lysis buffer (0.4 μL). PCR reaction conditions were: 95°C for 5 min, followed by 35 cycles of (95°C for 30 s, 60°C for 30 s, and 72°C for 45 s); 72°C for 5 min, and a 4°C hold.

[0045] The PCR products were detected by agarose gel electrophoresis. Figure 1 As shown. Figure 1It can be seen that 1, 2, 5, 8, 11, 12, 13, 15, 17, 20, and 23 are intestinal epithelial cell-specific CLIC5 knockout mice (IKO), and their genotype is Villin1-Cre: CLIC5 loxp / loxp ; 3, 4, 6, 7, 9, 10, 14, 18, 19, 21, 22 are wild-type mice (WT), genotype is CLIC5 loxp / loxp .

[0046] Example 2 Effect of CLIC5 knockout in intestinal epithelial cells on intestinal inflammation under normal diet

[0047] This example used 8-week-old intestinal epithelial cell-specific CLIC5 knockout mice (hereinafter referred to as IKO mice) and wild-type mice (hereinafter referred to as WT mice) fed a standard diet prepared in Example 1. In this example, the IKO and WT mice were fed a standard diet according to conventional feeding methods, with free access to the diet. The standard diet is a feed commonly used for feeding C57BL / 6 mice and was purchased from Spefox (Beijing) Biotechnology Co., Ltd.

[0048] The experimental method was as follows: IKO and WT mice were fasted for 12 hours before slaughter. Blood was collected from the IKO and WT mice by enucleation. The blood was centrifuged at 4500 × g for 15 minutes, and the supernatant was aliquoted and stored at -80°C. Serum proinflammatory cytokines, including tumor necrosis factor α (TNF-α), interferon γ (IFN-γ), interleukin 6 (IL6), and interleukin 1β (IL1β), were measured. Serum endotoxin LPS was also measured using kits purchased from Nanjing Jiancheng Bioengineering Institute (China). The procedures were performed according to the kit instructions. The results are shown in Table 1.

[0049] Table 1 Effects of CLIC5 knockout in intestinal epithelial cells on serum inflammatory factors and endotoxin levels under normal diet (n=8)

[0050] project WT group IKO group P-value Tumor necrosis factor α (TNF-α), pg / mL 58.93±4.86 56.26±4.38 0.311 Interferon gamma (IFN-γ), pg / mL 29.19±2.93 28.22±1.90 0.498 Interleukin 6 (IL6), pg / mL 135.24±7.04 132.64±9.76 0.572 Interleukin-1β (IL1β), pg / mL 23.83±1.42 22.28±2.99 0.220 Lipopolysaccharide (LPS), EU / mL 0.32±0.04 0.27±0.03 0.025

[0051] Note: n represents the sample size.

[0052] As shown in Table 1, intestinal epithelial cell-specific knockout of CLIC5 had no effect on the levels of serum proinflammatory factors in mice, but significantly reduced the level of serum LPS (Table 1, P = 0.025). Serum LPS is one of the commonly used inflammatory markers in clinical practice, reflecting intestinal permeability.

[0053] Furthermore, after slaughtering IKO and WT mice, four representative samples were randomly selected from each treatment for testing. The colon tissues and colon contents of the mice were collected, quickly frozen in liquid nitrogen, and stored at −80°C for Western blot analysis or short-chain fatty acid analysis. The results are shown in Table 1. Figure 2As shown in Tables 2 and 3.

[0054] Table 2 Effects of CLIC5 knockout in intestinal epithelial cells on the expression levels of colonic tight junction proteins under normal diet (n=4)

[0055] project WT group IKO group P-value ZO-1 0.40±0.03 0.55±0.10 0.033 Occludin 0.70±0.14 1.14±0.33 0.053 Claudin-1 1.09±0.29 1.09±0.21 0.988

[0056] Note: n represents the sample size.

[0057] Table 3 Effects of CLIC5 knockout in intestinal epithelial cells on the content of short-chain fatty acids in the colon under normal diet (μg / mg, n=8)

[0058] project WT group IKO group P-value Acetic acid 4.06±0.30 4.05±0.83 0.992 Propionic acid 0.88±0.14 0.87±0.14 0.883 Butyric acid 0.70±0.22 1.12±0.38 0.039 Isobutyric acid 0.07±0.01 0.06±0.02 0.245 Valeric acid 0.06±0.02 0.06±0.01 0.755 Isovalerate 0.06±0.02 0.04±0.03 0.249

[0059] Note: n represents the sample size.

[0060] Depend on Figure 2 As shown in Tables 2 and 3, Western blot analysis or short-chain fatty acid analysis is consistent with Table 1. Intestinal epithelial cell-specific knockout of CLIC5 significantly increased the protein expression level of ZO-1 in mouse colon tissue (Table 2, P = 0.033), and the protein expression level of Occludin showed an increasing trend (Table 2, P = 0.053), indicating that the intestinal epithelial barrier function has been significantly improved. Short-chain fatty acids can promote the expression of tight junction proteins, improve intestinal barrier integrity, and inhibit intestinal inflammatory response. Further analysis in this example found that intestinal epithelial cell knockout of CLIC5 significantly increased the content of butyrate in colonic contents (Table 3, P = 0.039).

[0061] In summary, under normal dietary conditions, knocking out CLIC5 in intestinal epithelial cells improved intestinal epithelial barrier function and reduced intestinal inflammation.

[0062] Example 3: Effect of CLIC5 knockout in intestinal epithelial cells on the alleviation of intestinal inflammation under high-fat diet

[0063] The experiment was conducted using 8-week-old intestinal epithelial cell-specific knockout CLIC5 mice (hereinafter referred to as IKO mice) and wild-type mice (hereinafter referred to as WT mice) fed a normal diet prepared in Example 1. Each group consisted of 8 mice. The 8-week-old IKO mice and WT mice were fed a high-fat diet (60% fat calories, purchased from Beijing Huafukang Biotechnology Co., Ltd., product number H10060) according to conventional feeding methods. The mice were fed ad libitum and distilled water was used as drinking water for 12 weeks. After the experiment, the mice were fasted for 12 hours and anesthetized and sacrificed as described in Example 2. Serum samples were collected for the detection of serum proinflammatory factors TNF-α, IFN-γ, and IL-6.

[0064] Ileal and colon tissues were collected, and qRT-PCR was used to measure mRNA expression levels of TNF-α, IL-6, IL-1β, and IL-10. Primer sequences are shown in Table 4. The qRT-PCR amplification system (10 μL) consisted of 5 μL of 2× TaqPCR mastermix, 0.3 μL of upstream primer, 0.3 μL of downstream primer, 4 μL of cDNA, and 0.4 μL of ddH₂O. The qRT-PCR reaction conditions were: 95°C for 5 min, followed by 15 s at 95°C, 15 s at the annealing temperature (as shown in Table 4), and 15 s at 72°C, with 2 to 4 cycles, and a 4°C hold.

[0065] Table 4 qRT-PCR primer sequences (5'-3')

[0066]

[0067] Table 5 Effects of CLIC5 knockout in intestinal epithelial cells on serum inflammatory factor levels under high-fat diet (n=8)

[0068] project WT group IKO group P-value Tumor necrosis factor α (TNF-α), pg / mL 49.86±4.27 38.97±2.71 <0.001 Interferon gamma (IFN-γ), pg / mL 37.25±2.07 30.70±3.36 <0.001 Interleukin 6 (IL6), pg / mL 149.12±3.89 133.03±17.84 0.037

[0069] Note: n represents the sample size.

[0070] As shown in Table 5, under high-fat diet conditions, CLIC5 knockout in intestinal epithelial cells significantly reduced the levels of serum TNF-α (P<0.001), IFN-γ (P<0.001), and IL6 (P=0.037) compared with wild-type mice.

[0071] Table 6 Effects of CLIC5 knockout in intestinal epithelial cells on intestinal inflammatory gene expression levels under high-fat diet (n=8)

[0072]

[0073] Note: n represents the sample size.

[0074] As shown in Table 6, the qRT-PCR results showed that knockout of CLIC5 in intestinal epithelial cells significantly reduced the mRNA expression level of IL6 in the ileum and colon of mice (P=0.001 and 0.007).

[0075] Example 4: Alleviating Effect of CLIC5 Knockout in Intestinal Epithelial Cells on Inflammatory Response in Colitis Model

[0076] 8-week-old IKO mice and WT mice prepared as described in Example 1 were used, with 8 mice in each group. The drinking water of the mice was replaced with a prepared 2.5% sodium dextran sulfate (DSS) solution, and the mice were fed with the conventional feed as described in Example 2 according to the conventional feeding method, and the mice were allowed to eat freely. A colitis model was constructed. The sterile water with DSS added was replaced once every 2 days for 8 days. On the 9th day, the blood of the mice was collected by enucleation, and the serum was collected for the detection of serum pro-inflammatory factors TNF-α, IFN-γ, IL6 and IL1β. The results are shown in Table 7.

[0077] Table 7 Effects of CLIC5 knockout in intestinal epithelial cells on serum inflammatory factor levels in colitis models (n=8)

[0078] project WT group IKO group P-value Tumor necrosis factor α (TNF-α), pg / mL 71.49±7.84 49.33±5.09 <0.001 Interferon gamma (IFN-γ), pg / mL 40.74±3.30 28.67±3.48 <0.001 Interleukin 6 (IL6), pg / mL 154.40±10.30 126.73±8.84 <0.001 Interleukin-1β (IL1β), pg / mL 31.78±2.68 24.33±2.47 <0.001

[0079] Note: n represents the sample size.

[0080] As shown in Table 7, knockout of CLIC5 in intestinal epithelial cells significantly reduced the levels of serum proinflammatory factors in the mouse colitis model (P<0.001).

[0081] In summary, intestinal epithelial cell-specific knockout of CLIC5 can enhance intestinal epithelial barrier function, reduce intestinal inflammation, and improve the body's overall inflammatory response. CLIC5 has a potential target role in the prevention or treatment of intestinal inflammation.

[0082] Although the above embodiment describes the present invention in detail, it is only a part of the embodiments of the present invention, not all of the embodiments. People can also obtain other embodiments like this embodiment without creativity, and these embodiments all fall within the scope of protection of the present invention.

Claims

1. Use of the CLIC5 gene in preparing a medicament for preventing and / or treating intestinal inflammation, wherein the nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO:

1.

2. The use according to claim 1, characterized in that The drug is used for specifically knocking out or inhibiting the expression of the CLIC5 gene in intestinal epithelial cells.

3. Use of an agent for inhibiting or silencing CLIC5 gene expression in the preparation of a medicament for preventing and / or treating intestinal inflammation, wherein the nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO:

1.

4. The use according to claim 3, characterized in that The prevention and / or treatment of intestinal inflammation includes: reducing serum endotoxin levels, reducing serum pro-inflammatory factor levels, reducing the level of inflammatory factors in the ileum, reducing the level of inflammatory factors in the colon, improving intestinal epithelial barrier function and increasing the content of butyric acid in colon contents. One or more of the following.

5. A drug for preventing and / or treating intestinal inflammation, characterized in that: The invention comprises reagents and auxiliary materials for inhibiting or silencing CLIC5 gene expression, wherein the nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO:

1.

6. The drug according to claim 5, wherein The excipients include pharmaceutically acceptable excipients.

7. The use according to any one of claims 1 to 4 or the medicine according to claim 5 or 6, characterized in that The intestinal inflammation includes I) and / or II): 1) Intestinal inflammation caused by a high-fat diet; II) Colitis.

8. The use according to any one of claims 1 to 4 or the medicine according to claim 5 or 6, characterized in that: The colitis includes colitis caused by dextran sulfate sodium.

9. A biomaterial for inhibiting or silencing CLIC5 gene expression, characterized in that: The nucleotide sequence of the CLIC5 gene is shown in SEQ ID NO:

1.

10. The biomaterial according to claim 9, wherein The biological material includes an sgRNA for knocking out the CLIC5 gene, and the sgRNA is shown in SEQ ID NO: 2 and / or SEQ ID NO: 3.

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