Long-chain non-coding RNA and application thereof

Abstract

The invention discloses a long-chain non-coding RNA (Ribonucleic Acid) and application thereof, and belongs to the field of biomedicine. The long-chain non-coding RNA is an LncRNANORAD gene, an adeno-associated virus overexpressing the LncRNANORAD gene is injected into a mouse suffering from atherosclerosis through caudal vein injection, it is found through detection of related indexes that the LncRNANORAD gene can effectively treat the atherosclerosis and relieve the atherosclerosis, and therefore the LncRNANORAD gene can be used for preparing the medicine for treating or relieving the atherosclerosis.

Description

Technical Field

[0001] The invention relates to a long-chain non-coding RNA and an application thereof, and belongs to the field of biomedicine. Background Art

[0002] Cardiovascular disease (CVD) is the leading cause of death among Chinese residents. The current number of CVD patients in my country is estimated to be 290 million, including 13 million strokes and 11 million coronary heart disease. Atherosclerosis (AS) is the main cause of CVD, and its main complications, myocardial infarction (MI) and ischemic stroke, are the diseases with the highest mortality rates in the world. AS usually occurs in the aorta and muscular arteries, such as the coronary arteries, cerebral arteries, renal arteries, and carotid arteries, leading to stenosis of the large arteries and the formation of systemic lesions of atherosclerotic plaques. The occurrence and development of AS are related to multiple factors, including hyperlipidemia, hypertension, diabetes, smoking, and many other exogenous and genetic factors, such as genetics, aging, and gender. With the aging of the population and the increase in obesity, the prevalence of AS will increase day by day, and with changes in diet and living standards, AS is gradually developing towards younger people. Controlling the occurrence and development of AS is a problem that needs to be solved urgently around the world.

[0003] At present, the pathogenesis of AS is not fully understood, so the drugs used to treat AS are mainly lipid-lowering, anticoagulant and thrombolytic drugs, but the treatment effects are not ideal. Therefore, continuing to explore the pathogenesis of atherosclerosis and finding new therapeutic breakthroughs is the focus of current medical research. Summary of the invention

[0004] The present invention provides a long non-coding RNA, wherein the non-coding RNA is LncRNA NORAD, and the nucleotide sequence is shown in SEQ ID NO:1.

[0005] The gene was injected into mice with atherosclerosis via adeno-associated virus, and it was found that it could effectively alleviate atherosclerosis, providing a basis for the preparation of atherosclerosis drugs.

[0006] The present invention is achieved through the following technical solutions:

[0007] 1. Animal breeding and establishment of atherosclerosis model

[0008] Twenty-four 7-week-old male APOE- / - mice were purchased and kept at room temperature of 20-24℃, with 12h day and night alternation, free diet, and randomly divided into 4 groups after 1 week of adaptive feeding, including control group (A), model group (B), empty vector control group (C), and LncRNANORAD overexpression group (D). The mice in the control group (A) were fed normally every day for 8 weeks; the mice in the model group (B), empty vector control group (C) and LncRNANORAD overexpression group (D) were fed high-fat diet every day for 8 weeks. After 8 weeks (week 9), the mice in the empty vector control group (C) were fed high-fat diet every day, and each mouse was given a tail vein injection of 100 μL of overexpressed AAV-NC virus control (with fluorescence), with a virus titer of 7.6x10 7 IFUs, once a week for 4 weeks. Mice in the LncRNA NORAD overexpression group (D) were fed a high-fat diet every day. At the same time, each mouse was injected with 100 μL of LncRNA NORAD-AAV virus (with fluorescence) through the tail vein. The virus titer was 7.6x10 7 IFUs, once a week for 4 weeks; the control group (A) was fed normally for 4 weeks; the model group (B) mice were fed high-fat diet daily for 4 weeks, and then fed according to the feeding requirements of each group for another week after virus injection. During these 14 weeks, the body weight of the mice was measured once a week.

[0009] 2. Experimental materials and testing

[0010] After 14 weeks, the mice were intraperitoneally injected with 50 mg / kg of 1% sodium pentobarbital. After the mice were anesthetized, the chest and abdominal cavities were opened, and the origin of the mouse aorta to the branch of the abdominal aorta and renal arteries were dissected and cut off. The mouse aortic arch was stored in liquid nitrogen for subsequent testing.

[0011] The results showed that when mice with atherosclerosis were injected with the overexpressed LncRNA NORAD-AAV virus, the expression of TG, CHO, and LDL in the mice was significantly reduced, and the expression of HDL was increased. The lipid accumulation in the AS aorta was observed by Oil Red O staining, and the results showed that LncRNA NORAD could alleviate the lipid accumulation in the AS aorta. Tunel detection of apoptosis in the aortic endothelial tissue of mice showed that LncRNA NORAD played a certain role in regulating the aortic endothelial tissue. Immunohistochemistry was used to detect the changes in inflammatory factors MCP-1 and IL-10, and it was found that LncRNA NORAD could reduce the expression of inflammatory factors MCP-1 and IL-10.

[0012] Beneficial Effects of the Invention

[0013] The present invention injects an adeno-associated virus that overexpresses the LncRNANORAD gene into mice with atherosclerosis, and finds that the LncRNANORAD gene can improve atherosclerosis. Therefore, the LncRNANORAD gene can be used to prepare drugs for treating and alleviating atherosclerosis, providing a new approach and new ideas for the treatment and alleviation of atherosclerosis. BRIEF DESCRIPTION OF THE DRAWINGS

[0014] Figure 1 Count the body weight of mice.

[0015] Figure 2 Results of TG, TC, HDL and LDL test in blood lipids of different groups of mice

[0016] Figure 3 The Oil Red O staining results of aortic tissues of mice in different groups.

[0017] Figure 4 The results of HE staining of aortic tissues of mice in different groups.

[0018] Figure 5 The results of TUNEL detection of aortic endothelial tissue apoptosis in different groups of mice.

[0019] Figure 6 Immunohistochemistry was used to detect the changes of inflammatory factor MCP-1 in different groups of mice.

[0020] Figure 7 Immunohistochemistry was used to detect the changes in the inflammatory factor IL-10 in different groups of mice. DETAILED DESCRIPTION

[0021] The technical solution of the present invention is further described below in conjunction with the accompanying drawings and through specific implementation methods. However, the following embodiments are only simple examples of the present invention and do not represent or limit the scope of protection of the present invention. The scope of protection of the present invention shall be subject to the claims.

[0022] The experimental methods for establishing animal atherosclerosis models, sampling of experimental materials, blood lipid detection, Oil Red O staining, HE staining, Tunel detection, and immunohistochemistry detection mentioned in the examples are all conventional methods well known to those skilled in the art.

[0023] LncRNA NORAD-AAV virus and AAV-NC virus were purchased from Anzhen Biotechnology (Shanghai).

[0024] LncRNANORAD-AAV indicates adeno-associated virus overexpressing the LncRNANORAD gene;

[0025] AAV-NC stands for adeno-associated virus that contains only the vector but no genes.

[0026] All reagents used in the experiment can be obtained from conventional commercial sources.

[0027] Example 1

[0028] 1. Animal husbandry and establishment of atherosclerosis model

[0029] Twenty-four 7-week-old male APOE- / - mice were purchased and kept at room temperature of 20-24℃, with 12h day and night alternation, free diet, and randomly divided into 4 groups after 1 week of adaptive feeding, including control group (A), model group (B), empty vector control group (C), and LncRNANORAD overexpression group (D). The mice in the control group (A) were fed normally every day for 8 weeks; the mice in the model group (B), empty vector control group (C) and LncRNANORAD overexpression group (D) were fed high-fat diet every day for 8 weeks. After 8 weeks (week 9), the mice in the empty vector control group (C) were fed high-fat diet every day, and each mouse was given a tail vein injection of 100 μL of overexpressed AAV-NC virus control (with fluorescence), with a virus titer of 7.6x10 7 IFUs, once a week for 4 weeks. Mice in the LncRNA NORAD overexpression group (D) were fed a high-fat diet every day. At the same time, each mouse was injected with 100 μL of LncRNA NORAD-AAV virus (with fluorescence) through the tail vein. The virus titer was 7.6x10 7 IFUs, once a week for 4 weeks; the control group (A) was fed normally for 4 weeks; the model group (B) mice were fed high-fat diet daily for 4 weeks, and then fed according to the feeding requirements of each group for another week after virus injection. During these 14 weeks, the body weight of the mice was measured once a week.

[0030] The breeding of mice and the injection of viruses are routine operations well known to those skilled in the art, and thus will not be described in detail.

[0031] After 14 weeks, the mice were intraperitoneally injected with 50 mg / kg of 1% sodium pentobarbital. After the mice were anesthetized, the chest and abdominal cavities were opened, and the origin of the mouse aorta to the branch of the abdominal aorta and renal arteries were dissected and cut off. The mouse aortic arch was stored in liquid nitrogen for subsequent testing.

[0032] 2. Animal Weight Changes

[0033] In order to clarify whether the overexpression of LncRNA NORAD-AAV virus affects the weight of mice, the weight of mice was tested once a week for a total of 14 weeks. The weight changes of mice were counted and analyzed. The weight changes of mice in the control group (A), model group (B), empty vector control group (C), and LncRNA NORAD overexpression group (D) were observed. The results are shown in the figure. Figure 1As shown, the body weight data showed that the body weight gradually increased among the four groups, showing an upward trend, indicating that overexpression of LncRNA NORAD-AAV virus would not affect the body weight of mice.

[0034] 3. Mouse blood lipid detection

[0035] The four indicators of blood lipids (TG, TC, HDL, LDL) are the detection of mouse serum total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. The results are as follows Figure 2 The results showed that compared with the control group, the model group had increased TG, CHO, and LDL expressions, and decreased HDL expression; compared with the empty vector control group, the LncRNA NORAD overexpression group had decreased TG, CHO, and LDL expressions, and increased HDL expression; compared with the model group, the LncRNA NORAD overexpression group had decreased TG, CHO, and LDL expressions, and increased HDL expression.

[0036] , LDL expression is reduced, and HDL expression is increased, so LncRNA NORAD can effectively regulate blood lipid levels.

[0037] 4. Oil Red O staining to observe lipid accumulation in AS aorta

[0038] Oil Red O is a fat-soluble dye that is highly soluble in fat and specifically colors neutral fats such as triglycerides in tissues. During the staining process, the solubility of Oil Red O dye in intracellular lipids is greater than that in organic solvents. Therefore, when the dye is added to tissue sections, the dye will transfer from the dye solution to the stained lipids, making the lipids appear red. This staining method is suitable for analyzing the lipid status in cell samples, and the staining results can be used to determine the presence and quantity of fat droplets in tissues or cells.

[0039] In order to observe the lipid accumulation in the AS aorta of the four components A, B, C, and D of mice, Oil Red O was used to stain the above four components. The specific steps are as follows:

[0040] 1. Preparation of frozen sections

[0041] (1) Take the aorta tissue stored at -80°C, place it in a mold, immerse it in OCT, and place it in a freezing microtome for quick freezing.

[0042] (2) Adjust the temperature of the chassis and blade, cut into slices with a thickness of about 6 μm, attach the slices, dry them in the shade at room temperature, and store them in a refrigerator at 20°C.

[0043] 2. Preparation of paraffin sections

[0044] (1) Sampling: The remaining tissues of the mouse aorta stored at -80°C were trimmed and cleaned with physiological saline.

[0045] (2) Fixation: Place the cleaned aorta tissue in 4% paraformaldehyde and fix it for 24 hours.

[0046] (3) Flushing: After fixation with 4% paraformaldehyde, flush the aorta tissue with water.

[0047] (4) Dehydration: The aorta tissue was dehydrated in alcohols from low to high concentrations in order: 70% ethanol for 2 hours, 80% ethanol for 1 hour, 90% ethanol for 30 minutes, 95% ethanol for 30 minutes, and 100% ethanol for 30 minutes. Place in a clearing agent for 30 minutes.

[0048] (5) Wax embedding: The aortic tissue is infiltrated with liquefied paraffin and placed in a selected mold for fixation. The paraffin is then cooled and fixed.

[0049] (6) Sectioning: After fixing the wax block, adjust the slicer, trim the wax block to the desired part, and cut it into 6 μm thick sections. Expand the slices in 37°C water, fix them on a glass slide, and dry them on a baking table at 65°C.

[0050] 3. Oil Red O staining of frozen sections

[0051] (1) Preparation of Oil Red O working solution: Add 1.5 times the amount of saturated Oil Red O staining solution to distilled water, mix thoroughly, warm in a 60°C bath for 30 min, cool and filter, and use immediately after preparation.

[0052] (2) Remove the frozen sections and air dry them at room temperature for 30 min.

[0053] (3) Dye with Oil Red O for 10 min at room temperature, covered and protected from light.

[0054] (4) Treat with 60% isopropanol solution for 4 s and 6 s respectively.

[0055] (5) Clean with three pure water tanks for 20s, 20s, and 10s respectively.

[0056] (6) Restain with hematoxylin for 3 minutes and wash in three cylinders of pure water for 10, 20, and 30 seconds respectively.

[0057] (7) Differentiation with 0.25% hydrochloric acid alcohol and washing with distilled water for 1 min.

[0058] (8) Treat with 0.3% ammonia water and then wash with water for 2 minutes. Pay attention to the cell morphology and nuclear status.

[0059] (9) Seal the sections with glycerol-gelatin mounting medium and take photos.

[0060] The results are as follows Figure 3The results showed that the control group had less red coloring; compared with the control group, the model group had larger plaque formation and more red blood vessel coloring, and compared with the model group, the plaque in the LncRNANORAD overexpression group was reduced. These results indicate that LncRNANORAD can alleviate AS aortic lipid accumulation.

[0061] 5. HE staining to observe AS aortic root plaque

[0062] In order to observe the changes in AS aortic root plaques in the four components A, B, C, and D of mice, HE was used to stain the above four components. The specific steps are as follows:

[0063] 1. Tissue paraffin embedding

[0064] (1) Tissue fixation: Take an appropriate amount of tissue, wash it with PBS, and then immerse it in 4% paraformaldehyde for 24 hours.

[0065] (2) Dehydration: The fixed tissue was immersed in the following concentrations of alcohol for dehydration: 70% ethanol (1 h), 80% ethanol (50 min), 95% ethanol (45 min), 100% ethanol I (40 min), and 100% ethanol II (40 min).

[0066] (3) Transparency: Soak the dehydrated tissue in xylene in the following order: 1 / 2 anhydrous ethanol + 1 / 2 xylene (35 min), xylene I (30 min), and xylene II (30 min).

[0067] (4) Wax immersion: Place the transparent tissue into paraffin and immerse it in paraffin I (25 min), paraffin II (25 min), and paraffin III (25 min).

[0068] (5) Embedding: Place the tissue block into a mold filled with paraffin, position the tissue block with the cut surface facing down, cover the mold with a plastic cover, fill it with paraffin, wait for the paraffin to cool, and then remove the paraffin block.

[0069] 2. Slicing

[0070] Sectioning: Fix the tissue block on the slicer and cut slices with a thickness of 5um. After cutting, put them in 20% alcohol for spreading, and then put them in a 47℃ water bath for spreading. After flattening, use cationic glass slides to stick them. After sticking, put them in a 64℃ oven for baking. After the paraffin melts, take out the glass slides and put them in the slide box.

[0071] 3. HE staining

[0072] (1) Dewaxing: Place the slides in xylene I (10 min) and xylene II (10, min);

[0073] (2) Hydration: Place in 100% alcohol I (5 min), 100% alcohol II (5 min), 95% alcohol (5 min), 80% alcohol (3 min), and 70% alcohol (2 min) in sequence; rinse with PBS three times, 5 min each time.

[0074] (3) Hematoxylin restaining: Place the slide in hematoxylin for 5 minutes, rinse with distilled water, place in an alcohol-hydrochloric acid solution for differentiation for 10 to 15 seconds, and place in tap water to return to blue, which should take at least 15 minutes.

[0075] (4) Eosin staining: Place the slide in eosin for 5 to 10 seconds, then wash once in distilled water.

[0076] (5) Dehydration: 95% alcohol (5-10 s), 100% alcohol I (5 min), 100% alcohol II (5 min).

[0077] (6) Transparent: Xylene I (10 min), Xylene II (10 min).

[0078] (7) Sealing: Use neutral gum to seal the slides.

[0079] (8) Scan: Scan the entire film.

[0080] The results are as follows Figure 4 The results showed that the cells in the control group were arranged neatly; compared with the control group, plaques were formed in the model group; compared with the model group tissue, the plaques in the LncRNANORAD overexpression group were reduced, so LncRNA NORAD helps to alleviate AS aortic root plaques.

[0081] VI. TUNEL detection of apoptosis in mouse aortic endothelial tissue

[0082] In order to observe the apoptosis of the aorta endothelial tissue in the four AS components of mice A, B, C, and D, tunel detection was performed on the four components. The specific steps are as follows:

[0083] 1. Sample preparation

[0084] (1) Soak the paraffin tissue sections in xylene at room temperature for 10 min, repeat twice; then soak in anhydrous ethanol for 5 min, repeat twice; finally soak in graded ethanol (95%, 80%, 70%) once, each for 5 min.

[0085] (2) Gently rinse the slices with PBS and remove excess liquid around the sample. Use a histochemical pen to draw a small circle 3 mm away from the tissue along the outer contour of the tissue to facilitate downstream permeability treatment and equilibrium labeling operations. During the experiment, do not let the sample dry. Place the processed sample in a humidified box to keep the sample moist.

[0086] (3) Preparation of Proteinase K working solution: Use PBS as diluent to dilute the Proteinase K (200 μg / mL) stock solution at a volume ratio of 1:9 to a final concentration of 20 μg / mL.

[0087] (4) Add 100 μL of the above-mentioned Proteinase K working solution to each sample to completely cover the tissue and incubate at 37°C for 20 min; (Note: Proteinase K treatment mainly helps the permeability of staining reagents in subsequent steps of tissues and cells. Incubation time that is too long or too short will affect the subsequent labeling efficiency. In order to obtain better results, the Proteinase K incubation time can be optimized).

[0088] (5) Wash the sample with PBS solution three times, 5 min each time (Protease K must be washed clean, otherwise it will interfere with the subsequent labeling reaction). Place the treated sample in a wet box to keep the sample moist.

[0089] (6) (Optional step) Remove excess liquid from the sample, add an appropriate amount of membrane permeabilization solution to the tissue, fully infiltrate the tissue, and treat at room temperature for 20 minutes; after the membrane permeabilization treatment is completed, rinse the sample with PBS solution for 3 times, each time for 5 minutes; the treated sample is placed in a wet box to keep the sample moist.

[0090] (7) Remove excess liquid from the sample, add an appropriate amount of 3% H2O2 (prepared in PBS) to the tissue to fully infiltrate the tissue, and treat at room temperature for 20 minutes (to inactivate endogenous peroxidase in the tissue. The incubation time should not be too long, otherwise hydrogen peroxide-induced DNA breakage will occur, resulting in false positives); then rinse the sample with PBS solution 3 times, 5 minutes each time; the treated sample is placed in a wet box to keep the sample moist.

[0091] 2. Labeling and detection

[0092] (1) Equilibration: Add 50 μL of Equilibration Buffer to each sample to cover the entire sample area and incubate at room temperature for 10 min.

[0093] (2) Preparation of labeling solution: Thaw Biotin-dUTP Labeling Mix and Equilibration Buffer on ice, and mix enough TdT incubation buffer for all experiments in the ratio of Recombinant TdT enzyme: Biotin-dUTP Labeling Mix: Equilibration Buffer = 1 μL: 5 μL: 50 μL (1:5:50). The volume of reagents used in a specific experiment can be adjusted in proportion according to the size of the slide.

[0094] (3) Negative control system: Prepare a control TdT incubation buffer without Recombinant TdT enzyme and replace it with ddH2O.

[0095] (4) Labeling: Remove as much equilibration buffer as possible, then add 56 μL of TdT incubation buffer to each tissue sample and incubate at 37°C for 1 h. Be careful not to dry the slides and keep the slides away from light.

[0096] (5) Immediately rinse the tissue sample with PBS, washing 4 times, 5 min each time.

[0097] (6) Use filter paper to gently wipe off the PBS solution around the sample.

[0098] (7) DAB staining: Add DAB staining solution to the tissue block for staining, and place the slide under a microscope to observe the staining. When the staining is obvious, rinse off the staining solution with PBS. Rinse with PBS three times, 5 minutes each time.

[0099] (8) Hematoxylin restaining: Place the slide in hematoxylin for 5 minutes, rinse with distilled water, place in an alcohol-hydrochloric acid solution for differentiation for 10 to 15 seconds, and place in tap water to return to blue, which should take at least 15 minutes.

[0100] (9) Dehydration: Dehydration was performed using 70% alcohol (2 min), 80% alcohol (3 min), 95% alcohol (5 min), 100% alcohol I (5 min), and 100% alcohol II (5 min) in sequence.

[0101] (10) Transparency: Use xylene I (10 min) and xylene II (10 min) for transparency.

[0102] (11) Sealing: Use neutral gum to seal the slides.

[0103] (12) Analysis: Full film scan.

[0104] The results are as follows Figure 5The results showed that compared with the control group, the model group had increased endothelial tissue apoptosis; compared with the model group, the LncRNA NORAD overexpression group had reduced endothelial tissue apoptosis, indicating that LncRNA NORAD plays a certain role in regulating aortic endothelial tissue apoptosis.

[0105] VII. Immunohistochemical detection of changes in inflammatory factors MCP-1 and IL-10

[0106] Immunohistochemistry refers to the application of the principle of specific binding of immunological antigens and antibodies, through chemical reactions, the color of the labeled antibody (fluorescein, enzyme, metal ion, isotope) is developed to determine the antigen (peptide and protein) in the tissue or cell, and to perform localization, qualitative and relative quantitative examinations. In order to explore the expression of MCP-1 and IL-10, immunohistochemistry was used to detect them. The specific steps are as follows:

[0107] (1) Dewaxing and rehydration of paraffin sections: In order of concentration, the sections were placed in xylene I for 15 min, xylene II for 15 min, xylene III for 15 min, xylene I and II for 3 min, 95% ethanol, 85% ethanol, and 75% ethanol for 1 min respectively, and finally rinsed with distilled water for 3 times, each time for 5 min. Subsequently, 3% H2O2 was added and incubated at 4°C for 10 min to remove the activity of endogenous peroxidase and then rinsed with distilled water for 3 times.

[0108] (2) Antigen repair: First wash with PBS, then add 0.05% trypsin and react at 37°C for 20 min, 0.01 M citrate buffer and immerse the tissue sections in it, or use a microwave oven for antigen repair.

[0109] (3) Blocking endogenous peroxidase: Place the sections in 3% H2O2 and incubate at room temperature in the dark for 25 min. Place the slides in PBS (pH 7.4) and wash them three times on a decolorizing shaker, each time for 6 min.

[0110] (4) Serum blocking: Add 3% BSA evenly on the tissue and block at room temperature for 30 minutes. (If the primary antibody is from a source other than the primary antibody, use rabbit serum for blocking. If the primary antibody is from a source other than the primary antibody, use BSA for blocking.)

[0111] (5) Primary antibody incubation: Gently aspirate the blocking solution and add primary antibody dilution solution (1:1000) prepared in PBS onto the sections. Gently place the sections flat in a humidified chamber and incubate at 4°C overnight.

[0112] (6) Secondary antibody incubation: After gently shaking dry, add a secondary antibody (labeled with HRP) of the same species as the primary antibody to the tissue, covering the entire tissue surface, and incubate at room temperature for about 50 min.

[0113] (7) DAB color development: After drying, add freshly prepared DAB color development solution to the tissue and observe under a microscope. Strictly control the color development time. Positive expression is brown. Rinse the tissue section with water to stop color development.

[0114] (8) Re-staining of cell nuclei: Re-stain with hematoxylin for about 3 minutes, rinse with tap water, differentiate with hematoxylin differentiation solution for a few seconds, rinse with tap water, then reverse-bluing with hematoxylin anti-blue solution, and finally rinse with running water.

[0115] (9) Dehydration and sealing: Place the slices in 75% alcohol for 5 min, 85% alcohol for 5 min, anhydrous ethanol I for 5 min, anhydrous ethanol II for 5 min, and xylene I for 5 min to dehydrate and make them transparent. Then, gently remove the slices from the xylene solution, air dry, and seal with neutral gum.

[0116] (10) Film analysis: Observe under an optical microscope and take the mean value for analysis.

[0117] like Figure 6 and Figure 7 As shown, Figure 6 As shown, compared with the control group, the model group showed high expression of IL-10; compared with the model group, the LncRNA NORAD overexpression group showed low expression of IL-10. Figure 7 The results showed that compared with the control group, the model group had a high expression of MCP-1; compared with the model group, the LncRNANORAD overexpression group had a low expression of MCP-1. Therefore, the LncRNANORAD gene can alleviate the inflammatory response caused by atherosclerosis.

[0118] From the above experimental results, it can be seen that LncRNANORAD improves the symptoms of atherosclerosis, so the LncRNANORAD gene can be used to prepare drugs for treating and alleviating atherosclerosis.

Claims

1. A long non-coding RNA, characterized in that: The non-coding RNA is LncRNA NORAD, and the nucleotide sequence is shown in SEQ ID NO:

1.

2. Use of the long non-coding RNA according to claim 1 in the preparation of a drug for treating or alleviating atherosclerosis.

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