KR20150024651A - Composition for preventing or treating neurodegenerative disease comprising loganin - Google Patents

Abstract

The present invention relates to a pharmaceutical composition for preventing or treating degenerative neuronal diseases comprising loganin as an active ingredient. The loganin of the present invention has excellent activity of inhibiting Aβ-inducing neurotoxity, thereby being used for a pharmaceutical composition, a functional food, etc for preventing or treating (alleviating) degenerative neuronal diseases including Alzheimer′s. The loganin of the present invention is a material derived from cornus fruit which is a natural product, and has stability without cytotoxicity so that the composition of the present invention comprising the same as an active ingredient has no side effects to a body and safety advantages in long-term use.

Description

[0001] The present invention relates to a composition for preventing or treating degenerative neurological diseases,

The present invention relates to a pharmaceutical composition for the prevention or treatment of degenerative neurological diseases comprising rogaine as an active ingredient.

Neurons are constantly killed in the process of reconstitution and synapse reconstitution, and stress and apoptotic cell apoptosis are major causes of degenerative brain diseases. Double oxidative stress is known to be associated with a number of causes of degenerative brain diseases such as Parkinson's disease, stress, aging, stroke and Huntington's disease. Recent studies have shown that chronic stress and oxidative stress It induces oxidative stress in the pituitary-adrenal, hippocampus, striatum, black and cortical areas, thereby increasing cell death and reducing neurons and growth factors, resulting in Parkinson's disease, stress, aging, stroke and Huntington's disease Is known to cause.

In particular, free radicals liberated from oxygen are known to be the main causes of tissue damage. The types of oxidative radicals associated with neurotoxicity include hydrogen peroxide, hydrogen peroxide anions, and hydroxyl groups, among which hydrogen peroxide is the most important precursor of highly reactive free radicals It is known to be a substance and is likely to cause apoptosis of the central nervous system.

When oxidative stress is given to neuronal cells, reactive oxygen species are triggered, resulting in activation of cytochrome C and activation of caspase-3 in mitochondria, leading to apoptosis. At the same time, ROS leads to the activation of glutamate, particularly the NMDA receptor, resulting in an increase of Ca ²⁺ ions by metabotrophical cascade, and the increase of intracellular Ca ²⁺ associated with ROS is also caused by the activation of caspase-2 Which leads to DNA damage.

In addition, the elderly population is increasing globally, and Korea has already entered an aging society in 2000, and in 2010, the proportion of the population over 65 years rose to 11%. It is anticipated that in 2018 it will become an aged society and in 2026 it will become a super-aged society. Therefore, the resolution of geriatric diseases in the elderly population is emerging as an urgent social problem.

In particular, Alzheimer's disease, which accounts for about half of the elderly dementia disease, is currently one of the most important neurological diseases to be solved in the aging society. .

Korean Patent No. 0838253

Accordingly, an object of the present invention is to provide a pharmaceutical composition useful for preventing or treating degenerative neurological diseases including Alzheimer, which is excellent in the activity of inhibiting Aβ-induced neurotoxicity in rogannin.

Another object of the present invention is to provide a health functional food useful for preventing or ameliorating a degenerative neurological disease including Alzheimer, which is excellent in the activity of inhibiting A.beta. Induced neurotoxicity in rogannin.

In order to accomplish the above object, the present invention provides a pharmaceutical composition for preventing or treating degenerative neurological diseases comprising a compound represented by the following formula (1) or a pharmaceutically acceptable salt thereof as an active ingredient.

[Chemical Formula 1]

.

.

 In one embodiment of the present invention, the compound may be contained at a concentration of 0.01 to 60 μM on the composition.

In one embodiment of the present invention, the compound can inhibit ROS production and / or apoptosis by A [beta] -induced toxicity.

In one embodiment of the present invention, the compound may inhibit or inhibit the activity of kappa-3 and / or TNF- by A [beta] -induced toxicity.

In one embodiment of the invention, the compound may inhibit or inhibit the activity of iNOS, COX-2 and / or NF-kB.

In one embodiment of the invention, the degenerative neurological disease is selected from the group consisting of Alzheimer's disease, Parkinson's disease, Lou Gehrig's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, immune system dysfunction, progressive neurodegenerative disease, Neuropsychiatric disorders, dementia due to Neemann-Pick disease, brain ischemia and cerebral hemorrhage.

The present invention also provides a health functional food for preventing or ameliorating a neurodegenerative disease, which comprises a compound represented by the following general formula (1) or a pharmaceutically acceptable salt thereof as an active ingredient.

[Chemical Formula 1]

.

.

The reorganin of the present invention is excellent in the activity of inhibiting Aβ-induced neurotoxicity, and thus can be effectively used for pharmaceutical medicines and functional foods for the prevention or treatment (improvement) of neurodegenerative diseases including Alzheimer's disease. In particular, the roganin of the present invention is a material derived from natural product, which is a natural product, and has stability without cytotoxicity. Therefore, the composition of the present invention containing it as an effective ingredient has safety advantages for long-term use without adverse effect on the human body.

FIG. 1 is a graph showing the cell survival rate of roganin against Aβ-induced toxicity.
Fig. 2 is a graph showing the inhibitory effect of roganin on ROS production on A [beta] -induced toxicity.
FIG. 3 is a graph showing the effect of rogaine on apoptosis against Aβ-induced toxicity.
4 is a graph showing the inhibitory effect of roganin on kappa-3 activity on A [beta] -induced toxicity.
Figure 5 is a graph showing the TNF-activity inhibitory effect of roganin on A [beta] -induced toxicity.
FIG. 6 is a graph showing the inhibitory effect of roganin against the A [beta] -induced toxicity by iNOS and COX-2 activity.
Fig. 7 is a graph showing the inhibitory effect of roganin against NF-κB activity on Aβ-induced toxicity.

The present invention relates to a novel use of lungan, and is characterized by providing a composition for preventing or treating a neurodegenerative disease comprising rogain as an active ingredient.

The 'loganin' of the present invention is known to have an effect on the regulation of immune function, anti-inflammation and anti-shock as a main constituent substance of gingkohwa, acidulous oil and fomica but it can be used for degenerative brain diseases such as Alzheimer's dementia Have not been reported so far.

Accordingly, the inventors of the present invention have found out that, while carrying out various studies for the treatment of Alzheimer's disease, it is possible to effectively inhibit Aβ-induced neurotoxicity in rogaine.

This fact can be confirmed by one embodiment of the present invention. To investigate whether _Roganin inhibits reactive oxygen species on Aβ _25-35 -induced toxicity, Aβ _25-35 was treated and then _rogainin subjected to a ROS assay targeted the control group not treated with the Aβ _25-35 and the group treated with different concentrations for each result, Aβ _25-35 treatment compared to controls not treated with Aβ _25-35 was increased when more than 25% ROS ( p < 0.001). On the other hand, the inhibition of ROS production by rogaine treatment was inhibited and the significant effects (74% ( p <0.05) and 52% ( p <0.001) were obtained at the concentration of 10 and 50 μM, It was found that ROS generation was more effectively inhibited (see Fig. 2).

In another embodiment of the present invention, the degree of apoptosis inhibition by _{rogaine on} the Aβ _25-35- induced toxicity was examined. As a result, in the Aβ _25-35 treatment group, cell membrane blebbing phenomenon, chromatin condensation (Fig. 3). However, it was found that apoptotic morphology such as apoptosis and condensation was observed, while that of the present invention was significantly reduced when treated with rogannin (see Fig. 3).

In another embodiment of the present invention, in order to investigate whether capsaicin-3 activity is inhibited by Aβ _25-35- induced toxicity, Aβ _{25-35 was} treated with trypsin-EDTA The cells were removed and reacted on ice for 10 minutes with the addition of lysis buffer. Cell lysate obtained by separating the reaction product centrifugation (cell lysate) is then transferred to a 96 well plate, DDT solution and DEVD- p NA and allowed to react for one hour, and then a microplate reader (microplate reader) truncated at 405 nm using an p As a result of measuring the OD value of NA, kappa-3 was activated 1.6 times by Aβ _25-35 ( p <0.001), but when 1, 10 and 50 μM of the present invention was treated with roganin of the present invention, -3 activity was significantly inhibited ( p < 0.01) (see Fig. 4).

In another embodiment of the present invention, the morphology and nuclear fragmentation degree of the cells were observed by fluorescence microscopy in order to examine whether the effect of roganin on the inhibition of iNOS and COX-2 expression on Aβ _25-35 induced toxicity , cytokine (cytokine), including TNF-, but is is to their generation is also known that inhibiting iNOS and COX-2 expression amount is increased significantly in case of processing the Aβ _{25- 35} through inhibition of iNOS and COX-2 (Fig. 5 and Fig. 6). The results are shown in Fig.

Furthermore, the present inventors have western blotted on the expression amount of p65, a subunit of NF-κB, which is a transcription factor mediating the action of iNOS and COX-2. As a result, when Aβ _25-35 was treated with PC12 cells The activity of NF-κB was significantly increased ( p <0.05), but the concentration-dependent decrease of rogaine treatment was observed ( p <0.01). In addition, it was found that NF-κB expression suppression effect was higher than that of the control group in all the sections (see FIG. 7).

Therefore, the present inventors have experimentally proved that rogaine can partially inhibit apoptosis by deactivation of kappa-3 and effectively inhibit A [beta] -induced neurotoxicity.

Therefore, the composition of the present invention containing roggan as an active ingredient can effectively prevent or treat degenerative neurological diseases.

In the present invention, the organolin may be a compound represented by the following general formula (1).

&Lt; Formula 1 >

The compound represented by formula (I) according to the present invention can be used in the form of a salt, preferably a pharmaceutically acceptable salt. The salt is preferably an acid addition salt formed by a pharmaceutically acceptable free acid, and the free acid may be an organic acid or an inorganic acid. The organic acids include, but are not limited to, citric, acetic, lactic, tartaric, maleic, fumaric, formic, propionic, oxalic, trifluroacetic, benzoic, gluconic, methosulfonic, glycolic, succinic, Glutamic acid and aspartic acid. The inorganic acid includes, but is not limited to, hydrochloric acid, bromic acid, sulfuric acid, and phosphoric acid.

Roganine represented by formula (1) according to the present invention may be commercially available or may be prepared from a natural product or produced by a chemical synthesis method known in the art.

The composition of the present invention may be prepared by using pharmaceutically acceptable and physiologically acceptable adjuvants in addition to the above-mentioned effective ingredients as the pharmaceutical composition containing the leganin as an active ingredient. Examples of the adjuvant include excipients, , A sweetener, a binder, a coating agent, a swelling agent, a lubricant, a lubricant or a flavoring agent.

The pharmaceutical composition may be formulated into a pharmaceutical composition containing at least one pharmaceutically acceptable carrier in addition to the above-described active ingredients for administration.

The pharmaceutical composition may be in the form of granules, powders, tablets, coated tablets, capsules, suppositories, liquids, syrups, juices, suspensions, emulsions, drops or injectable solutions. For example, for formulation into tablets or capsules, the active ingredient may be combined with an oral, non-toxic pharmaceutically acceptable inert carrier such as ethanol, glycerol, water, and the like. Also, if desired or necessary, suitable binders, lubricants, disintegrants and coloring agents may also be included as a mixture. Suitable binders include, but are not limited to, natural sugars such as starch, gelatin, glucose or beta-lactose, natural and synthetic gums such as corn sweeteners, acacia, tracker candles or sodium oleate, sodium stearate, magnesium stearate, sodium Benzoate, sodium acetate, sodium chloride, and the like. Disintegrants include, but are not limited to, starch, methyl cellulose, agar, bentonite, xanthan gum and the like. Acceptable pharmaceutical carriers for compositions that are formulated into a liquid solution include sterile water and sterile water suitable for the living body such as saline, sterile water, Ringer's solution, buffered saline, albumin injection solution, dextrose solution, maltodextrin solution, glycerol, One or more of these components may be mixed and used. If necessary, other conventional additives such as an antioxidant, a buffer, and a bacteriostatic agent may be added. In addition, diluents, dispersants, surfactants, binders, and lubricants may be additionally added to formulate into injectable solutions, pills, capsules, granules or tablets such as aqueous solutions, suspensions, emulsions and the like. Further, it can be suitably formulated according to each disease or ingredient, using the method disclosed in Remington's Pharmaceutical Science, Mack Publishing Company, Easton PA as an appropriate method in the field.

In one embodiment of the present invention, the rogannin of the present invention may be included in the composition at a concentration of 0.01 to 60 μM.

Degenerative neurological diseases for which the pharmaceutical composition of the present invention can exhibit a therapeutic effect include Alzheimer's disease, Parkinson's disease, Lou Gehrig's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, immune system dysfunction, , Metabolic brain disease, neemann-pick disease, brain ischemia, and dementia due to cerebral hemorrhage, but is not limited to, Alzheimer's disease in detail, and more specifically, Alzheimer's Dementia Lt; / RTI &gt;

The present invention also provides the use of a composition comprising roganin as an active ingredient for the manufacture of a medicament for the prevention or treatment of degenerative neurological diseases. The composition of the present invention comprising the above-mentioned leganin as an active ingredient can be used for the manufacture of a medicament for the prevention or treatment of degenerative neurological diseases.

The present invention also provides a method of preventing or treating degenerative neurological diseases comprising administering rogain to a mammal.

The term "mammal " as used herein refers to a mammal that is the subject of treatment, observation or experimentation, preferably a human.

The term "therapeutically effective amount " as used herein refers to the amount of active ingredient or pharmaceutical composition that elicits a biological or medical response in a tissue system, animal or human, as contemplated by a researcher, veterinarian, The amount that induces the relief of the symptoms of the disease or disorder being treated. It will be apparent to those skilled in the art that the therapeutically effective dose and the number of administrations of the active ingredient of the present invention will vary depending on the desired effect. The optimal dosage to be administered can therefore be readily determined by those skilled in the art and will depend upon the nature of the disease, the severity of the disease, the amount of active and other ingredients contained in the composition, the type of formulation, and the age, , Sex and diet, time of administration, route of administration and rate of administration of the composition, duration of treatment, concurrent administration of the drug, and the like. In the treatment method of the present invention, in the case of an adult, it is preferable to administer the rogannin of the present invention at a dose of 0.01 mg / kg to 250 mg / kg once to several times a day.

In the therapeutic method of the present invention, the composition comprising the roganin of the present invention as an active ingredient can be administered orally, rectally, intravenously, intraarterially, intraperitoneally, intramuscularly, intrasternally, transdermally, topically, And can be administered in a conventional manner.

The present invention also provides a health functional food for preventing or ameliorating a degenerative neurological disease comprising roganin as an active ingredient.

The health functional food of the present invention can be manufactured and processed in the form of tablets, capsules, powders, granules, liquids, and circles for the purpose of preventing and improving degenerative neurological diseases.

In the present invention, the term &quot; health functional food &quot; refers to foods manufactured and processed using raw materials or ingredients having useful functions in accordance with Law No. 6727 on Health Functional Foods. Or to obtain a beneficial effect in health use such as physiological action.

The health functional foods of the present invention may contain conventional food additives and, unless otherwise specified, whether or not they are suitable as food additives are classified according to the General Rules for Food Additives approved by the Food and Drug Administration, Standards and standards.

Examples of the items listed in the above-mentioned "food additives" include chemical compounds such as ketones, glycine, calcium citrate, nicotinic acid, and cinnamic acid; Natural additives such as persimmon extract, licorice extract, crystalline cellulose, high color pigment and guar gum; L-glutamic acid sodium preparations, noodle-added alkalis, preservative preparations, tar coloring preparations and the like.

For example, a health functional food in the form of tablets may be prepared by granulating a mixture of roganin, an active ingredient of the present invention, with an excipient, a binder, a disintegrant, and other additives by a conventional method, Or the mixture can be directly compression molded. In addition, the health functional food of the tablet form may contain a mating agent or the like if necessary.

The hard capsule of the capsule type health functional food can be prepared by filling a normal hard capsule with a mixture of rogaine, which is an effective ingredient of the present invention, with an additive such as an excipient, and soft gelatin capsules, And filling the mixture with a capsule base such as gelatin. The soft capsule may contain a plasticizer such as glycerin or sorbitol, a coloring agent, a preservative and the like, if necessary.

The ring-shaped health functional food can be prepared by molding a mixture of roganin, which is an effective ingredient of the present invention, excipient, binder, disintegrant, and the like, according to a conventionally known method, and if necessary, Or it may be coated with a material such as starch, talc.

The granular health functional food may be prepared by granulating a mixture of roganin, an active ingredient of the present invention, an excipient, a binder, a disintegrant, and the like into a granule by a known method. If necessary, a flavoring agent, And the like.

The health functional food may be a beverage, a meat, a chocolate, a food, a confectionery, a pizza, a ramen, a noodle, a gum, a candy, an ice cream, an alcoholic beverage, a vitamin complex and a health supplement food.

Hereinafter, the present invention will be described in more detail with reference to Examples. These examples are for further illustrating the present invention, and the scope of the present invention is not limited to these examples.

< Example  1>

Preparation for experiment

<1-1> Materials and reagents

And in a non-Aβ _25-35 are from Sigma-Aldrich (USA), the cell culture medium of RPMI 1640, PBS, FBS and penicillin-streptomycin (penicillin-streptomycin) solution was purchased from Hyclone Laboratories, Inc.. CH ₂ DCF-DA and Hoechst 33342 dye were purchased from Molecular Probes (USA), and Caspase-3 / CPP32 colorimetric assay kit was purchased from Bio Vision (USA). In addition, iNOS, COX-2, TNF-, β-actin, p65, anti-rabbit IgG and anti-mouse IgG were purchased from Cell signaling (USA).

<1-2> Statistical analysis

All results were expressed as mean ± standard deviation. One way analysis of variance was performed using SAS (Statistical Analysis System), and statistically significant at p <0.05 was considered. All analyzes were repeated three times.

< Example  2>

Cell culture

PC12 cells were cultured in RPMI 1640 medium containing 10% horse serum and 5% FBS in a 5% CO ₂ incubator at 37 ° C.

< Example  3>

Cell survival analysis

The present inventors have found that the effect of _{rogaine on A} [beta] _25-35 induced toxicity Cell viability was measured by MTT assay in order to analyze neuronal viability. PC12 cells were seeded in a 96-well plate at a density of 1 × 10 ⁴ , and then cultured at 37 ° C. for 24 hours. Thereafter, a sample was treated and after 1 hour incubation, A [beta] _25-35 was added.

After 24 hours, 5 mg / mL of MTT solution was added and reacted for 3 hours. After removing all media from the plate, the formed formazan was completely dissolved using DMSO and the absorbance was measured at 570 nm And was calculated by the following equation.

Cell viability (%) = (OD ₅₇₀ of control / A) x 100

The survival rate of PC12 cells treated with Aβ _25-35 was significantly lowered from 100% to 65% ( p <0.001), but 81% ( p <0.01) p < 0.001) (Fig. 1).

Therefore, it can be seen that rogannin increases cell viability by Aβ _25-35 in a concentration-dependent manner.

< Example  4>

Active oxygen species  Analysis of inhibition effect

The present inventors conducted the following experiment using the ROS assay in order to determine whether Roganin inhibits reactive oxygen species on Aβ _25-35 -induced toxicity.

The degree of production of ROS in cells was measured by fluorescence of dichlorofluorescein (DCF) produced by oxidation of CH ₂ DCF-DA, an oxidative sensitive probe. Samples and A [beta] _25-35 were added to PC12 cells in the same manner as the MTT assay After the treatment, CH ₂ DCF-DA solution was added to the medium and cultured at 37 ° C for 30 minutes. The formation of DCF was measured by a microfluorescence reader (excitation: 485 nm / emission: 510 nm).

As a result, the Aβ _25-35 treatment resulted in an increase in ROS of 25% or more ( p <0.001) compared to the control without Aβ _25-35 treatment. On the other hand, the inhibition of ROS production by rogaine treatment was inhibited and the significant effects (74% ( p <0.05) and 52% ( p <0.001) were obtained at the concentration of 10 and 50 μM, It was found that ROS generation was more effectively inhibited (see Fig. 2).

< Example  5>

Analysis of inhibition of cell death

The inventors of the present invention conducted the following experiment to determine whether or not there is an effect of inhibiting the apoptosis of _{roganin on} Aβ _25-35 -induced toxicity.

First, PC12 cells were plated at 1x10 &lt; ⁶ &gt; concentration in a cover slip (Coverslips). After 24 hours, rogannin was treated with 1, 10, and 50 μM, incubated for 1 hour, treated with 50 μM Aβ _25-35, and reacted for 24 hours. After 24 hours, formaldehyde (4% formaldehyde) was fixed for 20 minutes at room temperature and stained with 1 μg / mL Hoechst 33342 dye for 20 minutes at room temperature. The cells were then observed with a fluorescent microscope (x400 magnification) by washing with cold PBS.

As a result, typical apoptotic morphology such as blebbing of cell membrane and chromatin condensation could be observed in Aβ _25-35 treated group, while in the treatment with rogaine of the present invention, Lt; RTI ID = 0.0 &gt; (Fig. 3). &Lt; / RTI &gt;

< Example  6>

Kappaase -3 activity inhibition assay

The present inventors conducted the following experiment to determine whether there is an inhibitory effect of roganin on kappa-3 activity of Aβ _25-35 -induced toxicity.

PC12 cells were seeded in a 6-well plate at a density of 1 × 10 ⁶ , treated with a sample, and treated with Aβ _25-35 one hour later. After 24 hours, the cells were removed with trypsin-EDTA, lysis buffer was added, and reacted on ice for 10 minutes. Cell lysate obtained by separating the reaction product centrifugation (cell lysate) is then transferred to a 96 well plate, DDT solution and DEVD- p NA and allowed to react for one hour, and then a microplate reader (microplate reader) truncated at 405 nm using an p The OD value of NA was measured.

As a result, kappa-3 was 1.6-fold activated by Aβ _25-35 ( p <0.001), but when the rogaine of the present invention was treated at 1, 10 and 50 μM, ( P < 0.01) (see Fig. 4).

Therefore, it can be seen from the above results that roganin can partially inhibit apoptosis by deactivation of kappa-3.

< Example  7>

iNOS Wow COX -2 expression inhibition assay

The present inventors conducted the following experiment to determine whether or not the effect of roganin on the inhibition of iNOS and COX-2 expression on Aβ _25-35- induced toxicity was examined.

First, PC12 cells were seeded on a cover slip at a density of 1x10 &lt; ⁶ &gt; cells, and samples and A [beta] _25-35 were treated. After 24 hours, the cells were fixed with 4% formaldehyde and stained with 1 μg / mL Hoechst 33342 solution. Cell morphology and nuclear fragmentation were observed under a fluorescence microscope.

As a result, cytokine (cytokine), including TNF- is known that the generation is inhibited through inhibition of the expression of iNOS and COX-2 Aβ _{25- 35} the amount of iNOS and COX-2 expression was increased significantly in case of processing into When treated with ganin, showed a stronger inhibitory effect than the control (see FIGS. 5 and 6).

< Example  8>

Western Blotting  analysis

PC12 cells were seeded at a density of 2x10 &lt; ⁶ &gt; density in a 6-well plate, treated with a sample, and treated with A [beta] _25-35 after 1 hour. After 24 hours, the cultured cells were harvested, washed twice with PBS, and lysed with buffer. The supernatant was centrifuged at 13,000 rpm for 10 minutes, and protein concentration was quantitated by BCA protein assay.

40 μg of the lysate was electrophoresed on a 10% SDS-polyacrylamide gel to separate the proteins. The separated proteins were transferred to a polyvinylidene fluoride (PVDF) membrane at 130 mA for 2 hours and then blocked with TTBS (Tris buffered saline containing 0.1% + Tween 20) containing 5% skim milk at room temperature After washing with PBST, primary antibodies such as iNOS, COX-2, p-65 and TNF- were treated and reacted at room temperature, followed by washing with PBS.

Anti-rabbit IgG and anti-mouse IgG were used as secondary antibodies for 1 hour at room temperature. The membrane was then washed three times with PBST and then exposed to ECL (enhanced chemiluminescence) substrate for 5 to 10 minutes and then sensitized to x-ray film.

The expression level of p65, a subunit of NF-κB, a transcription factor mediating the action of iNOS and COX-2, was examined. As a result, the activity of NF-κB in PC12 cells treated with Aβ _25-35 was significantly ( P <0.05), but it was decreased in concentration - dependent treatment with rogaine treatment ( p <0.01). In addition, it was found that NF-κB expression suppression effect was higher than that of the control group in all the sections (see FIG. 7).

The present invention has been described with reference to the preferred embodiments. It will be understood by those skilled in the art that various changes in form and details may be made therein without departing from the spirit and scope of the invention as defined by the appended claims. Therefore, the disclosed embodiments should be considered in an illustrative rather than a restrictive sense. The scope of the present invention is defined by the appended claims rather than by the foregoing description, and all differences within the scope of equivalents thereof should be construed as being included in the present invention.

Claims (7)

A pharmaceutical composition for preventing or treating degenerative neurological diseases comprising a compound represented by the following formula (1) or a pharmaceutically acceptable salt thereof as an active ingredient;
[Chemical Formula 1]

. The method according to claim 1,
Wherein the compound is contained at a concentration of 0.01 to 60 μM with respect to the composition. The method according to claim 1,
Wherein said compound inhibits the production of active oxygen (ROS) and / or apoptosis by A? -Induced toxicity. The present invention also provides a pharmaceutical composition for preventing or treating degenerative neurological diseases. The method according to claim 1,
Wherein said compound inhibits or inhibits the activity of kappa-3 and / or TNF- by A [beta] -induced toxicity. The method according to claim 1,
Wherein said compound inhibits or inhibits the activity of iNOS, COX-2 and / or NF-kB. 6. The method according to any one of claims 1 to 5,
The degenerative neurological diseases are selected from the group consisting of Alzheimer's disease, Parkinson's disease, Lou Gehrig's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, immune system dysfunction, progressive neurodegenerative disease, metabolic brain disease, Or a dementia caused by dementia caused by dementia. A health functional food for preventing or ameliorating a degenerative neurological disease comprising a compound represented by the following formula (1) or a pharmaceutically acceptable salt thereof as an active ingredient;
[Chemical Formula 1]

.

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