JP2007326830A - Cyclooxygenase activity inhibitor - Google Patents

Abstract

<P>PROBLEM TO BE SOLVED: To provide a highly safe extract exhibiting COX-inhibiting activities, preferably one exhibiting cyclooxygenase-inhibiting activities that strongly inhibits selectively cyclooxygenase-2 compared with cyclooxygenase-1, a cyclooxygenase activity inhibitor comprising the extract, and a composition comprising these. <P>SOLUTION: The extract is obtained by subjecting at least one selected from among Mesona chinensis, Echinacea angustifolia, Plantago lanceolata and Rosa rugosa to extraction with an organic solvent or an organic solvent aqueous solution and exhibits cyclooxygenase-inhibiting activities. The cyclooxygenase activity inhibitor comprises the extract. The composition comprises the extract or the cyclooxygenase activity inhibitor. <P>COPYRIGHT: (C)2008,JPO&INPIT

Description

  The present invention relates to an extract having cyclooxygenase inhibitory activity, a cyclooxygenase activity inhibitor, and a composition containing these obtained from herbs, echinacea, psyllium, hermanus, which are plants derived from natural products and conventionally used as foodstuffs. Related to things.

  Cyclooxygenase (hereinafter referred to as COX) is a rate-limiting enzyme of the arachidonic acid cascade that produces chemical mediators such as prostaglandins and thromboxanes from arachidonic acid. There are two COX isozymes in the living body, which are called cyclooxygenase type 1 (COX-1) and cyclooxygenase type 2 (COX-2), respectively. COX-1 is constitutively expressed in many cells such as platelets, stomach, and vascular endothelial cells, and has effects such as platelet aggregation, gastric acid secretion inhibitory action, and gastric mucosa protection, and is involved in the protection of living organisms. COX-2 is an inducible enzyme whose production is induced by inflammatory stimuli or hormonal stimuli, and is thought to produce prostaglandins responsible for reactions such as fever, pain, and inflammation such as edema.

Non-steroidal anti-inflammatory agents known to date such as aspirin and indomethacin well inhibit both COX-1 and COX-2. At this time, since not only COX-2 but also COX-1 is strongly inhibited, side effects such as peptic ulcer and dizziness occur. From these facts, development of a highly safe COX activity inhibitor with less side effects, that is, a highly selective COX activity inhibitor with respect to COX-2 is desired (for example, Patent Document 1, Non-Patent Document). 1).
JP 2006-76910 A FitzGerald GA. Nature Reviews 2: 879-890, 2003.

  An object of the present invention is to provide a highly safe extract having cyclooxygenase inhibitory activity having COX inhibitory activity, preferably selectively selectively inhibiting COX-2 as compared with COX-1, and cyclooxygenase activity containing the extract It aims at providing the inhibitor and the composition containing these.

From the viewpoint of safety, the present inventors conducted a search for COX inhibitors using an in vitro system for extracts of edible materials. As a result, it was found that Sengoku, Echinacea, Psyllium, Hermanus has high COX inhibitory activity, and the present invention has been completed.
That is, the gist of the present invention is as follows.
[1] An extract (hereinafter referred to as COX inhibitory activity) obtained by extracting from one or more species selected from Sengoku, Echinacea, Hera plana, and Hermanus with an organic solvent or an aqueous organic solvent solution, and containing COX inhibitory activity Extract)),
[2] The extract according to the above [1], which more strongly inhibits cyclooxygenase type 2 than cyclooxygenase type 1,
[3] A cyclooxygenase activity inhibitor comprising the extract according to [1] or [2],
[4] A composition comprising the extract according to [1] or [2] or the cyclooxygenase activity inhibitor according to [3].

  The COX inhibitory activity extract of the present invention is highly safe because it is derived from food. In addition, the COX activity inhibitor of the present invention has a selective inhibitory activity compared to COX-2, which has a relatively strong inhibitory activity in COX-2, while the inhibitory activity of COX-1 is moderate. It is expected that there are few side effects. The selectivity with respect to COX-2 here is a number in which the ratio (COX-1 / COX-2) of ICX values of COX-1 and COX-2 is 1.5 or more. In addition, IC50 value is a value measured by the method as described in the below-mentioned Example.

  Furthermore, the present invention can be applied to food compositions, external preparation compositions, pharmaceutical compositions, and quasi-drug compositions, and is based on COX activity inhibitory action, causing various diseases and functional declines associated with inflammation. Prevention and improvement effects are expected.

  The herbaceous plant used in the present invention is a plant belonging to the genus Lamiaceae native to China, and includes scientific names such as Mesona chinensis and Mesona procumbens. In China and Taiwan, stalks and leaves cooked with rice, added with sugar, become brown when they are cooled, and they become beverages (see, for example, World useful plant encyclopedia page 677). In China, the whole plant is medicinal and used for colds and arthritis pain, but its mechanism of action is not known.

  As the herbaceous material used in the present invention, a stalk or leaf crushed with a mixer or the like can be used. Whole grass may be used if necessary. In addition, the sample is preferably dried for pulverization, but the dry state is not limited.

  The echinacea used in the present invention is a plant belonging to the genus Echinacea that is distributed from the east coast of North America to Texas, and includes the scientific name Echinacea angustifolia. This plant has been used for a long time by Indians because it has been used by crushing roots to help cough and sore throat. However, the mechanism of action for this effect has not been investigated.

  As the extraction sample used in the present invention, a leaf pulverized with a mixer or the like can be used. Stems and flowers can also be included as extracted samples. The sample is preferably dried for pulverization, but the dry state is not limited.

  The plantain used in the present invention is a plant native to Europe and belonging to the genus Psyllidae, and includes the scientific name Plantago lanceolata. Since long ago, young leaves have been eaten as seasonings and tempura, and those that have been dried and roasted have been used as folk medicines such as cough, antipyretic, and anemia, but the mechanism of action has not been investigated.

  As the leafhopper sample used in the present invention, a leaf pulverized with a mixer or the like can be used. Stems and flowers can also be included as extracted samples. The sample is preferably dried for pulverization, but the dry state is not limited.

  Hermanus used in the present invention is a plant belonging to the genus Rosaceae, and its scientific name is Rosa rugosa. So far, astringent action, bile secretion promoting action, and α-glucosidase inhibitory activity have been known, but the relationship with COX has not been clarified (see JP 2005-306801 A). In China, it has been drunk for a long time as “Mayi Hanacha”, and it is known for its sufficient food experience.

  As the Hermanus sample used in the present invention, a flower part and stem crushed with a mixer or the like can be used. The sample is preferably dried for pulverization, but the dry state is not limited.

  As the extraction solvent, an organic solvent or an organic solvent aqueous solution is used. Examples of the organic solvent include, but are not limited to, lower alcohols such as methanol, ethanol, propanol, and butanol, and esters such as ethyl acetate. These organic solvents may be used alone or in combination of two or more, or may be used as an organic solvent aqueous solution which is a mixed solvent of an organic solvent and water. From the viewpoint of safety, it is preferable to extract with ethanol or an aqueous ethanol solution. In addition, the ratio of each solvent in the case of mixing organic solvents or organic solvent and water is not particularly limited.

  As an extraction method, for example, one or more plant samples selected from the above four types and the extraction solvent are mixed and extracted by stirring at room temperature for 1-5 hours or refluxing at the boiling temperature of the extraction solvent for 1-5 hours. After performing, the sample residue is removed from the extract by filtration or centrifugation, and the extract is concentrated by reduced pressure or ultrafiltration. Further, if necessary, the extraction solvent may be completely removed and dried by solidification or lyophilization.

  The COX inhibitory activity extract obtained as described above has COX inhibitory activity that selectively and strongly inhibits COX-2 as compared to COX-1. Here, the COX inhibitory activity is measured by the method described in Examples below.

  An oil layer (for example, an ethyl acetate layer or a 1-butanol layer) in which a COX inhibitory activity extract extracted from one sample of each of Sengoku, Echinacea, Hera plana, and Hermanus by the above method is distributed with a low polarity organic solvent. COX inhibitory activity was observed in the derived extract, and COX inhibitory activity was not observed in the extract derived from a highly polar solvent layer (eg, aqueous layer). By partitioning with the ethyl acetate layer or 1-butanol layer, a more purified COX inhibitory activity extract can be obtained.

  The COX inhibitory activity extract of the present invention can be used as a COX activity inhibitor. Therefore, the present invention relates to a COX activity inhibitor comprising the COX inhibitory activity extract.

  Since the COX activity inhibitor contains the COX inhibitory activity extract as an active ingredient, it inhibits COX-2 more strongly than COX-1. The COX activity inhibitor may be mixed with other components as long as the COX inhibitory activity of the extract is not impaired. There is no limitation in particular as another component.

  The COX inhibitory activity extract or the COX activity inhibitor may be blended with various base materials to form a composition. The blending amount and the type of base material are not particularly limited, and may be set as appropriate. The base material is not particularly limited as long as it is a product used for foods, pharmaceuticals, quasi drugs, and the like, and examples of the oral administration base material include tablets, capsules, candy, gummi, and beverages. As a blending method for these various base materials, it can be produced by using known techniques in the fields of foods, pharmaceuticals, quasi drugs and the like.

  EXAMPLES Hereinafter, the present invention will be specifically described with reference to examples, but the present invention is not limited thereto.

Example 1
100 ml of ethanol was added to 10.0 g of Sengoku powder and stirred at room temperature for 1 hour. The extract was filtered through filter paper, and the filtrate was concentrated with a rotary evaporator under reduced pressure. From a 10.0 g sample, 0.10 g of extract was obtained. The extract was dissolved in dimethyl sulfoxide so as to have a concentration of 10 mg / ml and used in the following experiment.

(Test Example 1) COX Activity Inhibition Test A test was performed using Cayman chemical Cox Inhibitor Screening Assay (Cox Inhibitor Screening Assay, Catalog No. 560131).

(Sample solution)
As the sample solution, the sengakusa extract obtained in Example 1 was appropriately diluted with dimethyl sulfoxide so that the extract concentration was 10, 1.0, 0.1, or 0.01 mg / ml. . As a control, dimethyl sulfoxide containing no extract was used as a negative control. Moreover, what dissolved indomethacin (made by SIGMA), "NS-398" (made by CALBIOCHEM), and ibuprofen (made by Wako Pure Chemical Industries) in dimethylsulfoxide was used as a positive control.

(Method)
Arachidonic acid as a substrate was added to a COX solution as an enzyme solution to carry out a prostaglandin production reaction (hereinafter referred to as COX reaction). Each sample solution prepared at this time was added according to the test method of the kit, and the influence on the production amount of prostaglandins was examined. Prostaglandins produced by the COX reaction were quantified using an enzyme immunoassay (EIA method). At this time, the compound indomethacin used as a control is known as a compound that inhibits the activities of both COX-1 and COX-2. NS-398 is a compound that specifically inhibits COX-2, and ibuprofen is a compound that specifically inhibits COX-1. (See, for example, Timothy D. Warner. Et al. Proc. Natl. Acad. Sci. (1999); 96: 7563-68) The enzyme activity inhibition rate was calculated from the amount of prostaglandin produced in each sample solution relative to the control group. . Using this result, the IC50 value (inhibitor amount showing 50% activity inhibition) of each inhibitor was determined. The results are shown in Table 1.

  From Table 1, the herb extract which is the product of the present invention obtained in Example 1 showed inhibitory activity against COX-1 and COX-2. More specifically, as with NS-398, COX-1 / COX-2 showed a value of 1.5 or more. That is, the selectivity of COX-2 was recognized compared with COX-1. Therefore, it is expected that the product of the present invention tends to specifically suppress COX-2 expressed during inflammation.

(Example 2)
300 ml of ethanol was added to 30.0 g of Sengoku powder and stirred at room temperature for 1 hour. The extract was filtered through filter paper, and the filtrate was concentrated with a rotary evaporator under reduced pressure. 0.57 g of extract was obtained from a 30.0 g sample.

  The above Sengoku extract was distributed using water and ethyl acetate. The obtained extract was dissolved in a mixed solution of ethyl acetate (40 ml) and water (40 ml) and allowed to stand, and then the upper layer was collected as an ethyl acetate fraction. This operation was repeated a total of 3 times to obtain about 120 ml of an ethyl acetate layer fraction. Further, this solution fraction was dried by a rotary evaporator to obtain 0.17 g of an ethyl acetate extract fraction. For the aqueous layer, 1-butanol was further added, and partitioning was performed in the same manner to obtain 0.23 g of the aqueous layer extraction fraction and 0.15 g of the butanol layer extraction fraction. Further, each extract fraction was dissolved in dimethyl sulfoxide so that the concentration was 1 mg / ml.

(Test Example 2)
In the same manner as in Test Example 1, the COX activity inhibition rate of the herbaceous fraction extract obtained in Example 2 was calculated. Regarding COX-1, 93.04% inhibition was observed in the ethyl acetate layer (AcOEt) and 71.06% inhibition in the butanol layer (BuOH), but the aqueous layer was comparable to the negative control. Similarly, for COX-2, 96.42% inhibition was observed in the ethyl acetate layer and 97.17% inhibition in the butanol layer, but the aqueous layer was similar to the negative control (see FIG. 1).

(Test Example 3)
The herbaceous fraction extract obtained in Example 2 was adjusted with dimethyl sulfoxide so as to be 1.0, 0.1, 0.01 mg / ml. As a control, indomethacin dissolved in dimethyl sulfoxide was used.

  In the same manner as in Test Example 1, the COX activity inhibition rate of the above herb extract was calculated. IC50 value of each inhibitor was calculated | required using this result. The results are shown in Table 2.

  From Table 2, COX-2 inhibitory activity was observed in the ethyl acetate and butanol layer fractions of the herbaceous extract. In addition, the extract obtained from the sengaku butanol layer fraction showed an inhibitory activity of about 2.2 times that of the ethyl acetate layer fraction, but almost no activity was observed in the aqueous layer fraction. It was.

(Example 3)
100 ml of ethanol was added to 10.0 g of Echinacea powder and stirred at room temperature for 1 hour. The extract was filtered through filter paper, and the filtrate was concentrated with a rotary evaporator under reduced pressure. 0.13 g of extract was obtained from 10.0 g of sample. It was dissolved in dimethyl sulfoxide so that the extract concentration was 10 mg / ml, and used as an echinacea extract in the following experiments.

(Test Example 4)
In the same manner as in Test Example 1, the COX-1 and COX-2 activity inhibition rates of the Echinacea fraction extract were calculated. IC50 value of each inhibitor was calculated | required using this result. The results are shown in Table 3.

  From Table 3, the Echinacea extract which is the product of the present invention obtained in Example 3 showed inhibitory activity against COX-1 and COX-2. More specifically, as with NS-398, COX-1 / COX-2 showed a value of 1.5 or more. That is, the selectivity of COX-2 was recognized compared with COX-1. Therefore, it is expected that the product of the present invention tends to specifically suppress COX-2 expressed during inflammation.

Example 4
300 ml of ethanol was added to 30.0 g of Echinacea powder, and the mixture was stirred at room temperature for 1 hour. The extract was filtered through filter paper, and the filtrate was concentrated with a rotary evaporator under reduced pressure. 0.58 g of extract was obtained from 30.0 g of sample.

  The above Echinacea extract was partitioned using water and ethyl acetate. The obtained extract was dissolved in a mixed solution of ethyl acetate (40 ml) and water (40 ml) and allowed to stand, and then the upper layer was collected as an ethyl acetate fraction. This operation was repeated a total of 3 times to obtain about 120 ml of an ethyl acetate layer fraction. Further, this solution fraction was dried by a rotary evaporator to obtain 0.23 g of ethyl acetate extracted fraction. For the aqueous layer, 1-butanol was further added, and partitioning was performed in the same manner to obtain 0.13 g of an aqueous layer extraction fraction and 0.21 g of a butanol layer extraction fraction. Further, each extract fraction was dissolved in dimethyl sulfoxide so that the concentration was 1 mg / ml.

(Test Example 5)
In the same manner as in Test Example 1, the COX activity inhibition rate of the Echinacea fraction extract obtained in Example 4 was calculated. As for COX-1, 58.27% inhibition was observed in the ethyl acetate layer and 78.51% inhibition was observed in the butanol layer, but no inhibition activity was observed in the aqueous layer. Similarly, for COX-2, 99.40% inhibition was observed in the ethyl acetate layer and 98.16% inhibition in the butanol layer, but the aqueous layer was comparable to the negative control (see FIG. 2).

(Test Example 6)
The echinacea fraction extract obtained in Example 4 was adjusted with dimethyl sulfoxide so as to be 1.0, 0.1, 0.01 mg / ml. As a control, indomethacin dissolved in dimethyl sulfoxide was used.

  In the same manner as in Test Example 1, the COX activity inhibition rate of the Echinacea fraction extract was calculated. IC50 value of each inhibitor was calculated | required using this result. The results are shown in Table 4.

  From Table 4, COX-2 inhibitory activity was recognized in the ethyl acetate layer fraction and the butanol layer fraction of Echinacea extract. The extract obtained from the ethyl acetate layer fraction of Echinacea showed an inhibitory activity of about 2.8 times that of the butanol layer fraction, but almost no activity was observed in the aqueous layer fraction.

(Example 5)
100 ml of ethanol was added to 10.0 g of Psyllium powder and stirred at room temperature for 1 hour. The extract was filtered through filter paper and concentrated on a rotary evaporator under reduced pressure. 0.50 g of extract was obtained from 10.0 g of sample. The extract was dissolved in dimethyl sulfoxide so that the concentration of the extract was 10 mg / ml, and used as the leafhopper extract in the following experiment.

(Test Example 7)
In the same manner as in Test Example 1, the inhibition rate of COX-1 and COX-2 activities of the above-mentioned extract of the plantain extract was calculated. IC50 value of each inhibitor was calculated | required using this result. The results are shown in Table 5.

  From Table 5, inhibitory activity was recognized with respect to COX-1 and COX-2 in the extract of Psyllium which is the product of the present invention obtained in Example 5. More specifically, as with NS-398, COX-1 / COX-2 showed a value of 1.5 or more. That is, the selectivity of COX-2 was recognized compared with COX-1. Therefore, it is expected that the product of the present invention tends to specifically suppress COX-2 expressed during inflammation.

(Example 6)
300 ml of ethanol was added to 30.0 g of psyllium powder and stirred at room temperature for 1 hour. The extract was filtered through filter paper, and the filtrate was concentrated with a rotary evaporator under reduced pressure. 1.24 g of extract was obtained from 30.0 g of sample.

  The above-mentioned extract of psyllium was distributed using water and ethyl acetate. The obtained extract was dissolved in a mixed solution of ethyl acetate (40 ml) and water (40 ml) and allowed to stand, and then the upper layer was collected as an ethyl acetate fraction. This operation was repeated a total of 3 times to obtain about 120 ml of an ethyl acetate layer fraction. Further, this solution fraction was dried by a rotary evaporator to obtain 0.40 g of an ethyl acetate extract fraction. For the aqueous layer, 1-butanol was further added, and partitioning was performed in the same manner to obtain 0.49 g of an aqueous layer extraction fraction and 0.33 g of a butanol layer extraction fraction. Further, each extract fraction was dissolved in dimethyl sulfoxide so that the concentration was 1 mg / ml.

(Test Example 8)
In the same manner as in Test Example 1, the COX activity inhibition rate of the extract of the extract of the leafhopper obtained in Example 6 was calculated. Regarding COX-1, inhibition of 60.59% was observed in the ethyl acetate layer and 37.03% in the butanol layer, but the aqueous layer was comparable to the negative control. Similarly, for COX-2, 97.81% inhibition was observed in the ethyl acetate layer and 78.97% inhibition in the butanol layer, but the aqueous layer was comparable to the negative control (see FIG. 3).

(Test Example 9)
The leafhopper extract obtained in Example 6 was adjusted with dimethyl sulfoxide so as to be 1.0, 0.1, 0.01 mg / ml. As a control, indomethacin dissolved in dimethyl sulfoxide was used.

  In the same manner as in Test Example 1, the COX activity inhibition rate of the above-mentioned extract of the plantain extract was calculated. IC50 value of each inhibitor was calculated | required using this result. The results are shown in Table 6.

  From Table 6, COX-2 inhibitory activity was recognized in the ethyl acetate layer fraction and the butanol layer fraction of Psyllium extract. The extract obtained from the ethyl acetate layer fraction of Psyllium was found to have an inhibitory activity of about 8.2 times that of the butanol layer fraction, but almost no activity was observed in the aqueous layer fraction.

(Example 7)
100 ml of ethanol was added to 10.0 g of Hermanus powder and stirred at room temperature for 1 hour. The extract was filtered through filter paper, and the filtrate was concentrated with a rotary evaporator under reduced pressure. 0.22 g of extract was obtained from 10.0 g of sample. The extract was dissolved in dimethyl sulfoxide so as to have a concentration of 10 mg / ml and used in the following experiment.

(Test Example 10)
In the same manner as in Test Example 1, the inhibition rate of COX-1 and COX-2 activity of the above-mentioned Hermanus fraction extract was calculated. IC50 value of each inhibitor was calculated | required using this result. The results are shown in Table 7.

  From Table 7, the Hermanus extract, which is the product of the present invention obtained in Example 7, showed inhibitory activity against COX-1 and COX-2. More specifically, as with NS-398, COX-1 / COX-2 showed a value of 1.5 or more. That is, the selectivity of COX-2 was recognized compared with COX-1. Therefore, it is expected that the product of the present invention tends to specifically suppress COX-2 expressed during inflammation.

(Example 8)
300 ml of ethanol was added to 30.0 g of Hermanus powder and stirred at room temperature for 1 hour. The extract was filtered through filter paper and concentrated on a rotary evaporator under reduced pressure. 1.36 g of extract was obtained from a 30.0 g sample.

  The above Hermanus extract was partitioned using water and ethyl acetate. The obtained extract was dissolved in a mixed solution of ethyl acetate (40 ml) and water (40 ml) and allowed to stand, and then the upper layer was collected as an ethyl acetate fraction. This operation was repeated a total of 3 times to obtain about 120 ml of an ethyl acetate layer fraction. Further, this solution fraction was dried by a rotary evaporator to obtain 0.87 g of an ethyl acetate extract fraction. For the aqueous layer, 1-butanol was further added, and partitioning was performed in the same manner to obtain 0.24 g of an aqueous layer extraction fraction and 0.24 g of a butanol layer extraction fraction. Further, each extract fraction was dissolved in dimethyl sulfoxide so that the concentration was 1 mg / ml.

(Test Example 11)
In the same manner as in Test Example 1, the COX activity inhibition rate of the Hermanus fraction extract obtained in Example 8 was calculated. For COX-1, 96.66% inhibition was observed in the ethyl acetate layer and 19.04% inhibition in the butanol layer. Similarly, COX-2 was found to have 97.10% inhibition in the ethyl acetate layer and 43.81% inhibition in the butanol layer (see FIG. 4).

(Test Example 12)
The Hermanus fraction extract obtained in Example 8 was adjusted with dimethyl sulfoxide so as to be 1.0, 0.1, 0.01 mg / ml. As a control, indomethacin dissolved in dimethyl sulfoxide was used.

  In the same manner as in Test Example 1, the COX activity inhibition rate of the above-mentioned Hermanus fraction extract was calculated. IC50 value of each inhibitor was calculated | required using this result. The results are shown in Table 8.

  From Table 8, COX-2 inhibitory activity was recognized in the ethyl acetate layer fraction and the butanol layer fraction of Hermanus. The extract obtained from the ethyl acetate layer fraction of Hermanus showed 17 times or more inhibitory activity compared to the butanol layer fraction, but almost no activity was observed in the aqueous layer fraction.

  The COX activity inhibitory extract of the present invention can be suitably used as a highly safe COX activity inhibitor, preferably a highly safe COX activity inhibitor that inhibits COX-2 more strongly than COX-1. .

FIG. 1 is a graph showing the results of an analysis of COX activity inhibition conducted by the same method as in Test Example 1 using each extract of sengaku by the partitioning operation of Example 2. The vertical axis shows the activity when no inhibitor is contained as 100, and the activity obtained when the compound or extract is added is subtracted from 100 as the inhibition rate (%). FIG. 2 is a graph showing the results of an analysis of COX activity inhibition conducted in the same manner as in Test Example 1 using each extract fraction of Echinacea by the partitioning operation of Example 4. The vertical axis shows the activity when no inhibitor is contained as 100, and the activity obtained when the compound or extract is added is subtracted from 100 as the inhibition rate (%). FIG. 2 is a graph showing the results of analyzing and analyzing the COX activity inhibition experiment in the same manner as in Test Example 1, using each extract fraction of Psyllium by the partitioning operation of Example 6. The vertical axis shows the activity when no inhibitor is contained as 100, and the activity obtained when the compound or extract is added is subtracted from 100 as the inhibition rate (%). FIG. 4 shows the results of analyzing and analyzing COX activity inhibition experiments in the same manner as in Test Example 1 using each of the extracted fractions of Hermanus by the partitioning operation of Example 8. The vertical axis shows the activity when no inhibitor is contained as 100, and the activity obtained when the compound or extract is added is subtracted from 100 as the inhibition rate (%).

Claims (4)

  An extract obtained by extraction from one or more selected from Sengoku, Echinacea, Hera plantain, and Hermanus with an organic solvent or an organic solvent aqueous solution, and containing cyclooxygenase inhibitory activity.   The extract according to claim 1, which inhibits cyclooxygenase type 2 more strongly than cyclooxygenase type 1.   A cyclooxygenase activity inhibitor comprising the extract according to claim 1 or 2. A composition comprising the extract according to claim 1 or 2 or the cyclooxygenase activity inhibitor according to claim 3.

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