KR101940024B1 - A pharmaceutical composition for preventing or treating inflammasome mediated inflammatory disease comprising n-acyl homoserine lactone compounds - Google Patents

Abstract

The present invention relates to a composition for the improvement, prevention or treatment of inflammatory-mediated inflammatory diseases. In the case of using N-acyl homoserine lactone (AHL) -based compounds, adaptive protein apoptosis- inhibiting NLRP3 inflammation activity through the inhibition of polymer formation, thereby exerting an effect on the improvement, prevention or treatment of the above-mentioned diseases.

Description

TECHNICAL FIELD The present invention relates to a pharmaceutical composition for preventing or treating an inflammatory disease mediated by inflammatory disease comprising an N-acyl homoserine lactone compound as an active ingredient. The present invention relates to a pharmaceutical composition for preventing or treating an inflammatory mediator-

The present invention relates to a pharmaceutical composition for the prophylaxis or treatment of an inflammatory mediated inflammatory disease comprising an N-acyl homoserine lactone compound as an active ingredient.

Pseudomonas Aeruginosa is a relatively common bacterium that causes disease in mammals, including humans. The Pseudomonas aeruginosa is widely distributed in surrounding soil, water, and skin, and can be grown in a relatively low oxygen concentration. Animal infections can cause inflammation and sepsis, and can be fatal if infected with human organs such as the lungs and kidneys. It is rapidly recognized on wet surfaces and is frequently detected in medical facilities and devices, and thus is recognized as a major germ causing cross infection in hospitals. In the environmental field, it is also used as a microbial agent that removes tarballs when an oil spill accident occurs due to the ability to decompose hydrocarbons.

In addition, many other factors that are involved in virulence in P. aeruginosa have been reported to be regulated by an intercellular signaling mechanism called quorum sensing (QS), as in other Gram-negative bacteria (Fuqua et al., 2001; Welch et al., 2005; Coggan and Wolfgang, 2012). In general, the quorum sensing mechanism is controlled by a diffusible signaling substance, an enzyme that synthesizes it, and a receptor protein that accepts it (Henke and Bassler, 2004; Welch et al., 2005). The QS signaling substance is very different in structure and type depending on the bacteria. In the case of Gram-positive bacteria, a small peptide is used as a signal substance, and Gram-negative bacteria are mostly used as acyl homoserine lactone (acyl-HSL) , And some Vibrio and intestinal bacteria use furanone-based materials called AI-2 (Fuqua et al., 2001; Henke and Bassler, 2004; Reading and Sperandio, 2006).

In the meantime, inflammmasomes are substances that induce the maturation of inflammatory cytokines, such as IL-1, associated with innate immune defenses, such as cell infections or stress. And acquired inflammatory diseases have been emphasized in the immune response modulating mechanism, and there have been active developments of therapies targeted therewith.

It is an object of the present invention to provide a pharmaceutical composition for the prevention or treatment of an inflammatory mediated inflammatory disease comprising an N-acyl homoserine lactone (AHL) -based compound as an active ingredient.

It is an object of the present invention to provide a food composition for improving or preventing inflammomas-mediated inflammatory diseases comprising an N-acyl homoserine lactone (AHL) -based compound as an active ingredient.

However, the technical problem to be solved by the present invention is not limited to the above-mentioned problems, and other matters not mentioned can be clearly understood by those skilled in the art from the following description.

The present inventors have found that a compound containing N-acyl homoserine lactone (AHL) -based compounds in an auto-inflammatory disease, neuroinflammatory disease or metabolic disease mediated by NLRP3 inflammation activity It has been confirmed that when a pharmaceutical composition is administered, the above-mentioned diseases can be treated by inhibiting the NLRP3 activity effectively, thereby completing the present invention.

In one embodiment of the present invention, there is provided a pharmaceutical composition for preventing or treating inflammatory-mediated inflammatory diseases, comprising an N-acyl homoserine lactone (AHL) -based compound as an active ingredient.

Preferably, the N-acyl homoserine lactone (AHL) -based compound is N-3-oxododecanoyl-L-homoserine lactone represented by the following formula (1). OdDHL); N-3-oxohexanoyl-L-homoserine lactone (OHHL) represented by the following formula (2); And N-hexanoyl-L-homoserine lactone (HHL) represented by the following general formula (3), preferably a compound represented by the following general formula But are not limited to:

[Chemical Formula 1]

(2)

(3)

In another embodiment of the present invention, an effective amount of an N-3-oxododecanoyl-L-homoserine lactone (OdDHL) A pharmaceutical composition for the prophylaxis or treatment of mediastinal inflammatory diseases is provided.

In the present invention, the N-acyl homoserine lactone (AHL) -based compound is a typical substance generated by quorum sensing for communication between bacteria of Pseudomonas aeruginosa, a gram-negative bacterium, Homoserine lactone-based compounds can easily pass through cell membranes as they are cell signaling molecules (Infect. Immun., 1998, vol. 66, No. 1 36-42, J. Bacteriol. 176: 269-275.) . According to the above features, the pharmaceutical composition comprising the N-acyl homoserine lactone compound according to the present invention can easily pass through the cell membrane and effectively inhibit the production of inflammation in the cell.

In one embodiment of the present invention, the pharmaceutical composition according to the present invention may inhibit the activity of inflammose.

However, in the present invention, the inhibition of the activation of the inflammase refers to a modification in vivo that causes a decrease in the activation of the inflammation of the target cell or the like. For the purpose of the present invention, Inhibition of cytokine production or inhibition of the formation of ASC (oligomer formation) of a caspase-recruitment domain (ASC) containing associated apoptosis-associated spec-like protein. Preferably, the pharmaceutical composition according to the present invention may inhibit, but is not limited to, inhibiting the activity of inflammation through the inhibition of the formation of the ASC polymer corresponding to the pre-inflammation stage.

In the present invention, the inflammasomes are caspase-1-activated complex protein complexes comprising 1) a sensory protein NLRP3 (NLRP3), 2) a linking protein (ASC), which is an adapter protein, and a pro-caspase-1, an effector protein. The above inflammase components are assembled when a microorganism infection or tissue injury occurs. The inflammation activated by assembly in cytosol activates caspase-1 to produce interleukin (IL) -1β or interleukin- 18, and performs the innate immune defense function of the host (Schroder K, Tschopp J, Cell 140: 821-832 (2010); Franchi L, Munoz-Planillo R, Nunex, Nat Immunol 13: 325-332 ). Preferably, the inflammase may be, but is not limited to, NLRP3 inflammoma.

In the present invention, the NLRP3 inflammase is capable of inducing and / or promoting the onset of inflammatory mediated inflammatory disease when it is excessively active (Henao-Mejia J, Elinav Em Thaiss CA, Flavell RA (2014) Inflammasomes and Metabolic disease. Annu Rev Physiol 76: 57-78; Wen H, TingJP, eil LA 2012) A role for the NLRP3 inflammasome in metabolic diseases-did Warburg miss inflammation Nat Immunol 13: 352-357.

However, in the present invention, the inflammation-mediated inflammatory disease is an abnormal disease that occurs when the inflammoma is abnormally overactivated, and is preferably selected from the group consisting of autoinflammatory diseases, neuroinflammatory diseases and metabolic diseases But it is not limited thereto.

In the present invention, the autoinflammatory disease is classified as a disease group in which systemic inflammation is frequently repeated in a state where no autoantibody or antigen-specific T cell is found, unlike autoimmune disease, 21. Muckle-Wells syndrome (MWS), adult-type delayed autoimmune disease (MWD), and autoimmune disease (MWD) (CFAS), cryopyrin-related periodic syndrome (CAPS), neonatal-onset manifestation inflammatory syndrome (NOMID), chronic infantile dermatomal joint (CINCA) syndrome, familial mediterranean fever (LADA), familial cold autoimmune inflammatory syndrome (FMF), and / or systemic onset pediatric idiopathic arthritis (SJIA), systemic onset pediatric idiopathic rheumatoid arthritis, and certain forms of pediatric rheumatoid arthritis And / or certain forms of adult rheumatoid arthritis, but are not limited thereto.

In the present invention, the neuroinflammatory disease refers to a disease caused by damage to nerve tissue by an inflammatory reaction. Preferably, the neuroinflammatory disease is Alzheimer's disease, Parkinson's disease, Huntington's disease, Lou Gehrig's disease, Creutzfeldt Jakob disease, multiple sclerosis, But is not limited to, any one or more diseases selected from the group consisting of lateral sclerosis, diffuse rheumatoid disease, white matter encephalitis, temporal lobe epilepsy and inflammatory spinal cord injury, more preferably Alzheimer's disease.

The above-mentioned Alzheimer's disease is reported to be an important mechanism of microglia activation of microglia, and in animal models of Alzheimer's disease, caspase-1 and IL, which are the cytokines generated by inflammation in the microglia, -1 is increased (Immunol Rev. 2015 May; 265 (1): 63-74.).

In the present invention, the metabolic diseases are collectively referred to as diseases caused by metabolic disorders in vivo, and are preferably selected from the group consisting of obesity, type 2 diabetes, hyperlipidemia, hypercholesterolemia, atherosclerosis and fatty liver May be any one or more diseases, and more preferably, it may be any one or more of type 2 diabetes and arteriosclerosis, but is not limited thereto.

As a result of recent researches on metabolic diseases, it was confirmed that NLRP3 protein expression was increased in adipocytes of obese patients. Cerimide synthesized in obese adipocytes not only activated NLRP3 inflammase but also NLRP3 gene deficient mice (Front Immunol 2013; 4: 50, Nat Med 2011; 17: 179-188, Nat Immunol 2011; 12: 408-415). In addition, the incidence of atherosclerosis is reported when inflammation of blood vessels occurs in patients with hyperlipidemia. Inflammatory cells recognize cholesterol crystals and induce the formation and synthesis of NLRP3 inflammase, thereby increasing the inflammatory response of blood vessels (Nature 2010; 464 : 1357-1361) NLRP3 inflammase plays a very important role in the induction and / or promotion of the metabolic diseases.

Recent studies have shown that compounds that inhibit NLRP3 inflammation formation, such as MCC950 or ketone metabolite beta-hydroxybutyrate, glibenclamide, Alzheimer's disease, inflammatory disease, and CNS damage, etc., have been reported to exert a therapeutic effect through a process of relieving the disease (Nature Medicine Volume: 21, Pages: 248-255 Year published: 2015) DOI: doi: 10.1038 / nm.3806 , Nature Medicine Volume: 21, Pages: 263-269 Year published: (2015) DOI: doi: 10.1038 / nm.3804). It has also been reported that NLRP3 knock out mice that artificially inhibit NLRP3 inflammation formation have therapeutic effects in metabolic diseases such as obesity, type 2 diabetes, atherosclerosis and Alzheimer's disease (Nat Med. 2011 Feb ; 17 (2): 179-88, doi: 10.1038 / nm.2279, Epub 2011 Jan 9, Nature. 2010 Apr 29, 464 (7293): 1357-61 doi: 10.1038 / nature08938., Nature. 31, 493 (7434): 674-8, doi: 10.1038 / nature11729, Epub 2012 Dec 19.). Thus, a pharmaceutical composition comprising a compound of the N-acyl homoserine lactone (AHL) family that inhibits NLRP3 inflammation formation according to the present invention significantly inhibits NLRP3 inflammation, thereby inhibiting NLRP3 inflammase mediated inflammatory disease , In particular, for the treatment of autoinflammatory diseases, neuroinflammatory diseases and metabolic diseases.

In the present invention, the pharmaceutical composition may be in the form of capsules, tablets, granules, injections, ointments, powders or beverages, and the pharmaceutical composition may be a human.

The pharmaceutical composition of the present invention may be formulated in the form of oral preparations such as powders, granules, capsules, tablets, aqueous suspensions, external preparations, suppositories and sterilized injection solutions according to a conventional method, have. The pharmaceutical compositions of the present invention may comprise a pharmaceutically acceptable carrier. The pharmaceutically acceptable carrier may be a binder, a lubricant, a disintegrant, an excipient, a solubilizing agent, a dispersing agent, a stabilizer, a suspending agent, a coloring matter, a perfume or the like in the case of oral administration. A solubilizing agent, an isotonic agent, a stabilizer and the like may be mixed and used. In the case of topical administration, a base, an excipient, a lubricant, a preservative and the like may be used. The formulation of the pharmaceutical composition according to the present invention can be variously prepared by mixing with a pharmaceutically acceptable carrier as described above. For example, oral administration may be in the form of tablets, troches, capsules, elixirs, suspensions, syrups, wafers, etc. In the case of injections, they may be formulated in unit dosage ampoules or in multiple dosage forms have. Other forms may be formulated as solutions, suspensions, tablets, capsules, sustained release formulations and the like.

Examples of suitable carriers, excipients and diluents for formulation include lactose, dextrose, sucrose, sorbitol, mannitol, xylitol, erythritol, maltoditol, starch, acacia rubber, alginate, gelatin, calcium phosphate, calcium silicate, Cellulose, methylcellulose, microcrystalline cellulose, polyvinylpyrrolidone, water, methylhydroxybenzoate, propylhydroxybenzoate, talc, magnesium stearate or mineral oil. Further, it may further include a filler, an anticoagulant, a lubricant, a wetting agent, a flavoring agent, an emulsifying agent, an antiseptic, and the like.

The route of administration of the pharmaceutical compositions according to the present invention may be, but is not limited to, oral, intravenous, intramuscular, intraarterial, intramedullary, intrathecal, intracardiac, transdermal, subcutaneous, intraperitoneal, intranasal, Sublingual or rectal. Oral or parenteral administration is preferred. The term "parenteral" as used herein includes subcutaneous, intradermal, intravenous, intramuscular, intraarticular, intrasynovial, intrasternal, intrathecal, intralesional and intracranial injection or infusion techniques. The pharmaceutical compositions of the present invention may also be administered in the form of suppositories for rectal administration.

The pharmaceutical composition of the present invention varies depending on various factors including the activity of the specific compound used, age, weight, general health, sex, diet, time of administration, route of administration, rate of excretion, drug combination and the severity of the particular disease to be prevented or treated. And the dosage of the pharmaceutical composition may be appropriately selected by a person skilled in the art depending on the condition of the patient, the body weight, the degree of disease, the type of administration, the route of administration and the period of time, and may be 0.0001 to 50 mg / kg or 0.001 to 50 mg / kg. The administration may be carried out once a day or divided into several times. The dose is not intended to limit the scope of the invention in any way. The pharmaceutical composition according to the present invention can be formulated into pills, dragees, capsules, solutions, gels, syrups, slurries, suspensions.

In another embodiment of the present invention, there is provided a food composition for improving or preventing inflammatory-mediated inflammatory diseases, which comprises an N-acyl homoserine lactone (AHL) -based compound as an active ingredient.

Preferably, the N-acyl homoserine lactone (AHL) -based compound is N-3-oxododecanoyl-L-homoserine lactone represented by the following formula (1). OdDHL); N-3-oxohexanoyl-L-homoserine lactone (OHHL) represented by the following formula (2); And N-hexanoyl-L-homoserine lactone (HHL) represented by the following general formula (3), preferably a compound represented by the following general formula But are not limited to:

[Chemical Formula 1]

(2)

(3)

In another embodiment of the present invention, an effective amount of an N-3-oxododecanoyl-L-homoserine lactone (OdDHL) There is provided a food composition for improving or preventing an inflammatory disease.

In the food composition of the present invention, the N-acyl homoserine lactone (AHL) -based compound, inflammatory-mediated inflammatory diseases, may overlap with those described in the above-mentioned pharmaceutical composition, It is omitted.

In the present invention, the term " improvement "in the present invention can include, without limitation, any action that improves or alleviates symptoms of auto-inflammatory disease, neuroinflammatory disease or metabolic disease using the food composition of the present invention have.

The composition according to the present invention may be manufactured in the form of various foods such as beverage, gum, tea, vitamin complex, powder, granule, tablet, capsule, confection, rice cakes, bread and the like. When the compound of the present invention is contained in the food composition, the amount thereof may be added in a proportion of 0.1 to 50% of the total weight.

Herein, when the food composition is prepared in a beverage form, there is no particular limitation other than that the food composition is contained at the specified ratio, and it may contain various flavors or natural carbohydrates as an additional ingredient such as ordinary beverages. That is, natural carbohydrates include monosaccharides such as glucose, disaccharides such as fructose, sucrose and the like and sugar sugars such as polysaccharide, dextrin and cyclodextrin, and sugar alcohols such as xylitol, sorbitol and erythritol can do. Examples of the above-mentioned flavors include natural flavors (such as tau martin and stevia extract (for example, rebaudioside A and glycyrrhizin) and synthetic flavors (for example, saccharine and aspartame).

In addition, the food composition of the present invention can be used as a flavoring agent such as various nutrients, vitamins, minerals (electrolytes), synthetic flavors and natural flavors, colorants, pectic acid and its salts, alginic acid and its salts, , a pH adjusting agent, a stabilizer, a preservative, a glycerin, an alcohol, a carbonating agent used in a carbonated drink, and the like.

These components may be used independently or in combination. The proportion of these additives is not a key element of the present invention, but is generally selected in the range of 0.1 to about 50 parts by weight per 100 parts by weight of the food composition of the present invention.

In addition, the food composition of the present invention may be ingested as food or nutritional products such as milk or dairy fermented milk products, or as food supplements or health functional foods. Specifically, examples include foods such as dairy products, beverages, juices, soups or foods for children, but are not limited thereto. The dairy product means any liquid or semi-solid milk or liquid product having various fat contents. The milk product may be, for example, milk, goat's milk, positive milk, cream, full-fat milk, whole milk, low-fat milk or skim milk, Dyfiltered milk, microfiltered milk, recombinant milk obtained from milk powder or whey through any processing, processed products such as yoghurt, curd, milk oil, sour whole milk, , Buttermilk, other fermented milk products, e.g., viili, filling of snack bars, and the like. Another important group may include milk-based foods such as milk beverages, such as whey drinks, fermented milk, concentrated milk, infant and baby milk, ice cream, and sweets.

In the case of using a compound of the N-acyl homoserine lactone (AHL) system as a composition according to the present invention, the formation of ASC (adapter protein apoptosis-associated spec-like protein containing a caspase-recruitment domain) Inflammatory disease or metabolic disease by promoting the inhibition of the activity of inflammation by inhibiting the activity of the compound of the present invention.

FIG. 1 shows changes in protein expression in Western blot analysis after administering N-acyl homoserine lactone (AHL) -based compounds to bone marrow-derived macrophages in Experimental Example 1. FIG.
FIG. 2 shows the results of ELISA for the release of interleukin (IL) -1β after administration of N-acyl homoserine lactone (AHL) -based compounds to bone marrow-derived macrophages in Experimental Example 2 The results are shown.
FIG. 3 is a graph showing changes in protein polymerization by Western blot analysis after administering N-acyl homoserine lactone (AHL) -based compounds to bone marrow-derived macrophages in Experimental Example 3. FIG.

Hereinafter, the present invention will be described in more detail with reference to Examples. It will be apparent to those skilled in the art that these embodiments are only for describing the present invention in more detail and that the scope of the present invention is not limited by these embodiments in accordance with the gist of the present invention .

Example

[ Preparation Example ] mouse Bone marrow origin  Macrophage isolation and culture

(AIM2), which is the most potent inhibitor of innate immunity to Francisella turalrensis, was obtained from C57BL / 6 mice (Fernandes-Alnemri T, et al. 385-393.). All mice were grown under specific disease-free conditions. Protocols for animal experiments were approved by the Ethics Committee of Yonsei University. All BMDMs were cultured in L929-regulated DMEM supplemented with 10% FBS and 100 U / ml penicillin / streptomycin at 37 ° C, 5%, in a CO ₂ incubator.

[ Experimental Example  1] mouse Bone marrow origin  In macrophages Inflammase  Active inhibition

The NLRP3 inflammation activity inhibitory effect of N-acyl homoserine lactone (AHL) -based compounds was confirmed by the following method.

L-homoserine lactone (hereinafter referred to as' C12 ') and N-butyryl-L-homoserine lactone (hereinafter referred to as' LPS (0.25 ㎍ / ml, 3 h) and ATP (2.5 mM, 40 min) were pre-treated for 30 min each with 40 μM of lactone (N-butyryl-L-homoserine lactone; RTI ID = 0.0 > NLRP3 < / RTI > After the culture supernatant was obtained, western blot analysis was performed to confirm protein changes in the cell lysate and supernatant after protein precipitation using the methanol / chloroform method.

The preparation method of the cell lysate protein used in the Western blot analysis is as follows. The BMDMs were harvested by treatment with PBS, washed with PBS, and then dissolved in a RIPA buffer, which is a cell lysis buffer containing a protein degradation inhibitor. The whole solution was fractionated using a centrifuge, and only the protein-containing solution was extracted. The supernatant and cell lysate proteins were quantified by the Bradford method. Proteins at the same concentration obtained by quantification were separated by performing SDS-polyacrylamide gel electrophoresis and then transferred to a PVDF membrane. The membranes from which the proteins were transferred were blocked with TBS-T (Tris-buffered saline / 0.1% Tween-20) solution containing 5% non-fat milk for 1 hour at room temperature to reduce non-specific binding Subsequently, the primary antibody diluted in 5% BSA solution was reacted at 4 ° C for at least 12 hours, and the secondary antibody (1: 5000 dilution) was reacted at room temperature for 1 hour. An enhanced chemiluminescence system was used for visualization.

Western blot analysis was performed to determine the expression levels of pro-caspase-1, p20 which is an activated caspase-1, interleukin (IL) -1β and pro-interleukin-1β, Is shown in Fig.

As shown in FIG. 1, when LPS and ATP were treated together, secretion of the activated forms of interleukin-1? And caspase-1 p20 into the supernatant was increased, indicating that NLRP3 inflammase activity . When the NLRP3 inflammase was induced, it was confirmed that when C12 was treated, the secretion was remarkably suppressed in the supernatant of interleukin-1 ?. In addition, it was confirmed that secretion was also remarkably suppressed by the supernatant of p20. On the other hand, when C4 was treated, secretion of interleukin-1β and p20 by LPS and ATP stimulation did not decrease.

From the above results, it can be seen that C12 according to the present invention significantly inhibits NLRP3 inflammase activity compared to C4.

[ Experimental Example  2] mouse Bone marrow origin  Interleukin- 1β  Confirmation of secretion inhibition

In order to confirm the NLRP3 inhibition of the activity of C12 by NLRP3, IL-lβ secreted by LPS and nigericin stimulation was quantitatively analyzed by ELISA (enzyme-linked immunosorbent assay).

The BMDMs of the preparations were pretreated with C4 and C12 (40 μM) for 30 minutes, treated with LPS (0.25 μg / ml for 3 hours), treated with Nigericin (5 μM, 40 minutes), and treated with NLRP3 After activating moss, each supernatant was obtained.

In the ELISA, 100 μl of the supernatant was added to each well in a 96-well plate coated with an interleukin-1β antibody, and reacted at room temperature for 1 hour. After washing with PBS for 4 times, the reaction mixture was incubated with a secondary antibody conjugated with an enzyme for coloring for 1 hour at room temperature. Subsequently, a substrate buffer solution (3,3 ', 5,5'-Tetramethylbenzidine (TMB ) And hydrogen peroxide) was added, coloring was stopped, color development was stopped with 2N sulfuric acid, and absorbance was measured at 450 nm. The results are shown in Fig.

As shown in FIG. 2, the values of interleukin-1? Increased to about 500 pg / ml when LPS and nigerisin were treated together were significantly reduced to about 50 pg / ml or less when C12 was administered, The amount of interleukin-1 beta secretion in the supernatant was not changed.

From the above results, it can be seen that C12 inhibits interleukin-1 beta release and effectively inhibits NLRP3 inflammase activity.

[ Experimental Example  3] mouse Bone marrow origin  In macrophages ASC  Confirm polymerization inhibition

The following Western blot analysis was carried out to confirm that N-acyl homoserine lactone (AHL) compounds inhibited NLRP3 inflammation activity through inhibition of ASC polymerization. The ASC polymerization is known to be essential for NLRP3 inflammation activation.

The BMDMs of the preparations were pretreated with C4 and C12 (40 μM) for 30 minutes, treated with LPS (0.25 μg / ml for 3 hours), treated with Nigericin (5 μM, 40 minutes), and treated with NLRP3 After activation of the moxa, the cell lysate induces cross-linking of bound proteins present in the lysate using DSS (disuccinimidyl suberate), followed by western blotting as in the method of Experimental Example 1 Respectively.

Western blot analysis confirmed the polymerization of the ASC protein, and the results are shown in FIG.

As shown in FIG. 3, the production of ASC polymer (dimer, oligomer) is increased in cell lysate by LPS and nigerian stimulation, and the production of ASC polymer (oligomer) . On the other hand, when C4 was treated, the production of ASC polymer was not significantly different from that of the control group.

From the above results, it can be seen that C12 effectively inhibits NLRP3 inflammase activity, which is important for the induction of autologous inflammatory diseases or neuroinflammatory diseases by inhibiting ASC polymer production. On the other hand, it can be seen that C4 does not effectively inhibit the production of ASC polymer relative to C12, and thus does not effectively inhibit NLRP3 inflammase activity.

While the present invention has been particularly shown and described with reference to exemplary embodiments thereof, it is to be understood that the scope of the present invention is not limited to the disclosed exemplary embodiments, but various changes and modifications may be made without departing from the scope of the invention. It will be obvious to those who have knowledge of

Claims (6)

1. A pharmaceutical composition for the prevention or treatment of inflammatory mediated inflammatory diseases comprising as an active ingredient a compound represented by the following formula (1)
[Chemical Formula 1]

Wherein said inflammus-mediated inflammatory disease is Parkinson's disease, Huntington's disease, Lou Gehrig's disease, multiple sclerosis, amyotrophic lateral sclerosis, or inflammatory spinal injuries.
The method according to claim 1,
Wherein said compound inhibits inflammose activity.
3. The method of claim 2,
Wherein the inflammase is NLRP3 (NOD-like receptor family, pyrin domain-containing 3).
1. A food composition for improving or preventing an inflammatory disease mediated inflammatory disease comprising, as an active ingredient, a compound represented by the following formula (1)
[Chemical Formula 1]

Wherein said inflammus-mediated inflammatory disease is Parkinson's disease, Huntington's disease, Lou Gehrig's disease, multiple sclerosis, amyotrophic lateral sclerosis, or inflammatory spinal injury.
5. The method of claim 4,
Wherein said compound inhibits inflammose activity.
6. The method of claim 5,
Wherein the inflammase is NLRP3 (NOD-like receptor family, pyrin domain-containing 3).

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