Mushroom Science and Biotechnology, Vol. 28 (1) 7-14, 2020
Copyright © 2020, Japanese Society of Mushroom Science and Biotechnology

Regular Paper

7

Effects of dietary ethanol extract from fruiting
bodies of golden oyster mushroom (Pleurotus
citrinopileatus ) on chronic colon inflammation inmice treated with dextran sulfate sodium salt
Shinji YAMASHITA1), Kota AKADA1), Satoshi MATSUMOTO2)
and Mikio KINOSHITA1)*
1)

Department of Life and Food Science, Obihiro University of Agriculture andVeterinary Medicine, Inada-cho, Obihiro, Hokkaido 080-8555, Japan
2)
L/S Corporation, 5F, Kyodo Bldg. 13-4 Nihonbashi Kodenma, Chuo-ku, Tokyo
103-0001, Japan（Received 11 September 2019 / Accepted 25 December 2019）

Abstract
In recent years, the incidence of intestinal impairments, such as colon cancer and inflammatory bowel
disease (IBD), has been increasing in East Asian countries. Healthy dietary habits, as well as taking dietary
supplements, are seen as important to preventing these impairments. Mushrooms and the hydrophilic
fraction are commonly recognized for multiple nutritious functions, while the function of the lipophilic
fraction remains uncertain. In this study, we investigated the effects of the lipophilic fraction containing
sphingolipids, extracted from Pleurotus citrinopileatus (golden oyster mushroom), on mice suffering fromchronic colon inflammation by treatment of dextran sulfate sodium salt (DSS) as IBD models. In theexperiment, mice were fed with (1) control AIN-76 standard diet or (2) AIN-76 diet supplemented with 1%
ethanol extract from fruiting bodies of golden oyster mushroom (GOMEE) or (3) AIN-76 diet supplemented
with 5% GOMEE. Subsequent to experimental diets for 10 days, mice were drinking water ad libitum
supplemented with DSS. We found that in mice ingesting DSS for 26 days, dietary GOMEE suppressed the
body weight reduction and the spleen weight increase by administration of DSS. Dietary GOMEE decreased
DSS-induced chorionic crypt injury, and the ameliorative effect by 5% GOMEE diet was stronger whencompared to the 1% GOMEE diet. Moreover, we researched the impact of GOMEE on the early/middle stageof inflammation in colon mucosa, by assessing levels of inflammation-related cytokines in mice ingesting
DSS for 18 days. The levels of almost inflammatory cytokines and chemokines examined in the colon weresignificantly increased due to DSS ingestion. Dietary 5% GOMEE was correlated with a significant decreasein the levels of 5 inflammatory cytokines and 5 chemokines. These results suggested that dietary GOMEE
contributes to suppression of colon inflammation and the effect is dose-dependent.
Key words: Colitis, Cytokine, Golden oyster mushroom, Inflammatory bowel disease, Sphingolipid

Introduction
In recent years, the incidence rate of intestinal
impairments, such as colon cancer and inflammatory
bowel disease (IBD), has increased in East Asian countries,
including Japan, and remains alarmingly high in theWestern countries1, 2). IBD is a persistent disease difficult
to treat and achieve full recovery. Moreover, IBD patients
carry an increased risk of developing colon cancer3). It isbelieved that colon cancer in IBD patients can be induced
due to dedifferentiation-associated epigenetic regulations
by chronic inflammation4). Numerous epidemiologicalstudies indicate that colon cancer is strongly associatedwith diet. Subsequently, it is suggested that these inflammation-related diseases can be prevented by following
dietary habits and taking dietary supplements5).
In Japan in the 1960s, dietary mushrooms wereintroduced into the health food market, and there has been
increasing research interest in the properties of Agaricus*Corresponding author. E-mail: kinosita@obihiro.ac.jp

blazei Murill (Almond mushroom)6), Hericium erinaceus(Monkey head mushroom)7), Grifola frondosa (Maitake)8, 9),
and Pleurotus citrinopileatus (Golden oyster mushroom)10-15).
Golden oyster mushroom recently became a popular
delicacy in East Asia, including China, Japan, and Taiwan,
due to its flavor and potential health benefits. Ingestion ofwhole fruiting bodies of golden oyster mushrooms, as well
as extracts obtained from them, have been demonstrated tohave a number of biological effects, including, antioxidative
effects10, 11), cardiovascular disease prevention11), reductionof blood sugar levels12), and immune regulation13, 14). In
addition, numerous bioactive components have been
isolated from the fresh fruiting bodies, e.g., novel lectinwith potent antitumor, mitogenic, and HIV-1 reverse
transcriptase inhibitory activities15).
Glucosylceramide (GlcCer) is a sphingolipid foundon the eukaryotic cell membrane, mainly in plants andfungi. The GlcCer molecule consists of a sphingoid basewith an amide-linked fatty acid (i.e., a ceramide) and one
glucose. Administration of GlcCer derived from plants
has been reported to prevent atopic dermatitis16) and8Vol. 28 No. 1

improve skin-barrier function17). Our previous studies
showed that dietary GlcCer from plant sources alleviates
colon inflammation in the IBD mice model treated withdextran sulfate sodium (DSS)18) and suppresses colon
aberrant crypt foci formation and inflammation-related
cytokine production induced by 1,2-dimethylhydrazine(DMH)19). In vitro experiments indicate the possibility
that GlcCer protects the colon surface from the harmful
effects of various drugs20). In addition, sphingoid bases
induce apoptosis in colon cancer cells in vitro21).
It has been shown that sphingolipids found in the
lipophilic fractions extracted from mushrooms aredifferent from those found in plants and mammals22).
The main difference is 9-methyl-4,8-sphingadienine
being the major sphingoid base in the structure of GlcCer
found in mushrooms. It is well-unknown how the specificchemical structure of GlcCer is related to its function.
Moreover, the main sterol found in the lipophilic
fractions extracted from fruiting bodies of mushrooms
is ergosterol, which is absent in plants or mammals23).
This motivated our interest in the food functions of thelipophilic fraction extracted from fruiting bodies ofgolden oyster mushrooms.
In this study, we investigated the effects of ethanol
extract from the fruiting bodies of golden oyster
mushroom (GOMEE) - lipophilic fraction - on colon
inflammation in DSS-treated mice, which served asa model of colitis. Prior to this experiment, we had
determined the optimal DSS concentration for inducing
chronic colon inflammation in mice. To research the roleof dietary GOMEE in initiation of inflammation in thecolon, we measured the expression of inflammation-related cytokines in colon mucosa at the early/middle stage ofinflammation, when blood is not present in feces.

Materials and Methods
Materials
GOMEE was purchased from Three-bee Corporation(Hokkaido, Japan). Briefly, golden oyster mushroom(culture strain Elm Mush 291) was cultured in a 850
mL-size polypropylene bottle with 450 g of medium(containing 65% of water, and dried wheat bran anddried sawdust from Larix kaempferi (Japanese larch)
mixed at 32 : 31 ratio). One culture bottle yielded 100 gof fruiting bodies. As shown in Fig. 1, after removing
the hydrophilic fraction from 30 kg of fruiting bodies
of golden oyster mushrooms, 210 g of GOMEE was
obtained from the residue by 3 series of extractions with150 L of ethanol. Lipid composition in GOMEE wasanalyzed on the silica gel thin-layer chromatography(TLC)24). We used the Folch procedure to extract total
lipids from GOMEE. The total lipids were saponified
with 0.4 M KOH in methanol at 38℃ for 2 h to obtain thealkali-resistant fraction. GlcCer, sterols, and ceramides
were determined by the position and the sterol-specificFig. 1. Preparation of ethanol extract from fruiting body of golden
oyster mushroom (GOMEE).

dye. GlcCer standard was prepared from maize by
applying to a silica gel column and preparative-TLC, as
described previously18). All reagents used in the following
experiments were purchased from FUJIFILM Wako Pure
Chemical Co. (Osaka, Japan) unless stated otherwise.
Animals and their diet
Male BALB/c mice were obtained from Japan SLC,
Inc. (Shizuoka, Japan) at 4 weeks old and housed inisolator cages at 22℃ under a 12-hour light/dark cycle.
Mice were provided tap water and CE-diets (CLEA Japan,
Inc., Tokyo, Japan) ad libitum. After one-week acclimatization, mice were randomly divided into 4 groups (blank,
control, and two test groups), with 10 mice in each group.
The blank and control groups were fed control AIN-76
diet, which does not contain sphingolipids24). “1% GOMEE”
test group was fed with AIN-76 diet supplemented with
1% GOMEE and “5% GOMEE” test group was fed with
the AIN-76 diet supplemented with 5% GOMEE. After
feeding the experimental diet for 10 days, all groups,
except for the blank one, were administrated DSS using
drinking water as a vehicle. Samples for the cytokine
array assay were collected post mortem after 18 days ofingesting DSS, with 5 mice in each group. Samples for allother tests were collected after 26 days of ingesting DSS,
with 5 mice in each group. All protocols involving workon animals were approved by the Animal Care and Use
Committee and were conducted in accordance with the
Obihiro University Guidelines (Permit Number, 28-164).
Sample preparation for histological analysis
The large intestine was excised under anesthesia, and a
portion of the large intestine from the cecum to the vent was
isolated and rinsed with cold saline. Next, the histologicalsamples were fixed overnight with 4% paraformaldehydein phosphate-buffered saline (PBS). Subsequently, thespecimens were embedded in a paraffin wax, and transverse
sections were cut and stained with hematoxylin and eosin18).
Cytokine array assay
Cytokine secretion was examined using a commercial
cytokine array in accordance with the manufacturer’s
protocol (Mouse Cytokine Array Panel A; R&D Systems,
Minneapolis, MN). Briefly, the mucosa of the large
intestine was collected using a glass slide. Next, it
was homogenized with 1% Triton X-100 in PBS (pH日本きのこ学会誌
MUSHROOM SCIENCE AND BIOTECHNOLOGY

Results
Lipid profiles of GOMEE
Lipid composition of GOMEE was obtained by
TLC analysis for specimens obtained before and after
alkali-treatment. As presented in Fig. 2, the lipid
profiles of GOMEE from both conditions look alike, withsphingolipids (i.e., ceramides and GlcCer), sterylglycoside(SG) derivatives, and free and acyl sterols (alkali-resistantlipids) being the most abundant.
Effects of dietary GOMEE on weight gain associated with
DSS ingestion
Figure 3 shows a progression of weight gain in miceover the course of the experiment. In the initial phase,before DSS was administered, body weight increased
daily, and that was true for all groups. Within the initial
14 days of ingesting 1.5% DSS, the previously observed
pattern of body weight gain remained unaffected. In thelater phase of the experiment, weight loss was recorded
within the control group and the body weight of thecontrol group indicated significantly lower level whencompared to those of the blank group. On the other
hand, dietary 1% or 5% GOMEE suppressed this reduction

in body weight when compared to the control group.
Effects of dietary GOMEE on colon constriction andspleen swelling caused by DSS ingestion
It is widely agreed that acceleration of colon
inflammation induces other symptoms, such as colon
constriction and spleen swelling25). As shown in Fig. 4, after
treatment with DSS, the length of the large intestine was
reduced, and the weight of the spleen was significantly
higher. Respectively, ingesting dietary GOMEE

Fig. 2. Lipid profiles of GOMEE on silica thin-layer chromatography.
A: Lipid composition of GOMEE; B: Composition of alkali-resistant lipids in GOMEE.
To remove lipid components except for alkali-resistant lipids(sphingolipids and sterols), GOMEE was treated with alkali.
1, Maize GlcCer fraction; 2, GOMEE; 3, GOMEE treated byalkaline.
Mobile phase, Chloroform:Methanol (95:12, v/v); Detection,
50% H2SO4.
GlcCer, glucosylceramides; SG, sterylglycosides.

Fig. 3. Effects of dietary GOMEE on weight gain in DSS-treatedmice.
After feeding experimental diets for 10 days, mice were
given 1.5% DSS in drinking water ad libitum. Numbers on thehorizontal axis indicate day when DSS treatment was terminated.
♦, Blank; ■, Control treated by DSS; ▲, 1% GOMEE treated by
DSS; ×, 5% GOMEE treated by DSS.
：Day of dissection; first for cytokine array; second for otheranalyses.
＊：Significant difference (p<0.05) vs Control.
→7.4), centrifuged at 10,000 × g for 1 minute, and thesupernatant was collected and examined using thecytokine array assay. Detected cytokines were denoted asfollows: B lymphocyte chemoattractant (BLC); chemokine(C-C motif) ligand 1 (I-309); complement component 5a(C5/C5a); eotaxin; granulocyte macrophage colony-stimulating factor (GM-CSF); interferon-γ (IFN-γ); interferon-γinduced protein 10 (IP-10); interleukin (IL)-1ra; IL-2; IL-3;
IL-4; IL-5; IL-6; IL-7; IL-10; IL-12; IL-13; IL-16; IL-17; IL-23;
IL-27; metallopeptidase inhibitor 1 (TIMP-1); monocyte
chemoattractant protein 2 (MCP-2); macrophage
inf la mmator y protei n-1β (MIP-1β); macrophageinflammatory protein-1α (MIP-1α); monokine induced
by gamma interferon (MIG); monocyte chemotactic
protein 5 (MCP-5); monocyte-specific cytokine MCP-1(JE); macrophage colony-stimulating factor (M-CSF);
neutrophil-activating protein 3 (KC); interferon-inducible T cell alpha chemoattractant (I-TAC); regulatedon activation, normal T cell expressed and secreted(RANTES); soluble intercellular cell adhesion molecule1(sICAM-1); stromal cell-derived factor 1 (SDF-1); thymus
and activation regulated chemokine (TARC); triggering
receptor expressed on myeloid cells 1 (TREM-1); andtumor necrosis factor-α (TNF-α).
Statistical analysis
The significance of data collected from all fourgroups was assessed using one-way ANOVA with Tukey’s
post hoc test. For the results to be considered significant,p values were set to be < 0.05. Further data analysis
was performed using BellCurve for Excel (Social Survey
Research Information Co., Ltd., Tokyo, Japan) and all of
the results are reported as means ± standard error of themean (SEM).

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Fig. 4. Effects of dietary GOMEE on colon length (A) and spleen weight (B) in DSS-treated mice.
＊：Significant difference (p<0.05) vs Control.

Fig. 5. Effects of dietary GOMEE on large intestinal villi in DSS-treated mice.
A & E, Blank; B & F, Control treated by DSS; C & G, 1% GOMEE treated by DSS; D & H, 5% GOMEE treated by DSS.
A-D, ×10 objective magnification. Scale bar = 100 μm.
E-H, ×40 objective magnification. Scale bar = 25 μm.

significantly suppressed the length reduction in the large
intestine and the increase in the spleen weight.
Effects of dietary GOMEE on colon villi damage caused
by DSS ingestion
We assessed the status of the colon by microscopic
examination of the histology samples stained withhematoxylin and eosin (Fig. 5). Colon samples from theblank group had normal morphology of crypts. Typical
histological changes associated with acute DSS-colitis
are mucin depletion and the disappearance of epithelial

cells. Similar morphological changes were observedin the histological samples collected from the control
group. Ingestion of dietary GOMEE limited damage ofthe chorionic crypts associated with DSS treatment andthe effect was more visible in samples collected from thegroup fed with diet supplemented with 5% GOMEE incomparison to the “1% GOMEE” group.
Effects of dietary GOMEE on colon cytokine induction
caused by DSS ingestion
Cytokine array assay was performed to determine日本きのこ学会誌
MUSHROOM SCIENCE AND BIOTECHNOLOGY

Fig. 6. Effects of dietary GOMEE on cytokine levels in the colonic mucosa of DSS-treated mice.
(A) Inflammatory cytokines. (B) Chemokines. (C) Antiinflammatory cytokines. (D) Others.
; 1% GOMEE treated with DSS,
; 5% GOMEE treated with DSS,
Control treated with DSS,
Each cytokine expression was adjusted the values to the blank group = 1.0.
#：Significant difference (p<0.05) between blank and control.
＊：Significant difference (p<0.05) vs control.

the influences of dietary GOMEE on production of
inflammation-related cytokine in DSS-treated mice inthe early/middle stage of inflammation (18th day of DSS
treatment). The cytokine array simultaneously detects
40 different cytokines. The suitability of this assay wasvalidated by comparing the densities of positive andnegative control spots in this array.
Figure 6 shows cytokine production levels in thecolon in the group treated with DSS in comparison to
the blank group. Levels of most inflammation-related

11.

cytokines examined were significantly increased by
DSS ingestion. In comparison to the control group,
ingestion of dietary 5% GOMEE significantly decreased
levels of 5 inflammatory cytokines and 5 chemokines
and significantly increased levels of IL-12p70. The levelsof anti-inflammatory cytokines were not altered byingesting dietary GOMEE. Other cytokines, i.e., adhesion
molecules, were stimulated by DSS intake and remained
unaffected by GOMEE intake.

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Discussion
Dietary mushrooms and the hydrophilic fraction
extracted from dietary mushrooms are known to havenumerous food functions, e.g., antioxidative effects,
cardiovascular disease prevention, immune regulation,and reduction of blood sugar level6-15). However, there
is still little known about the functions of the lipophilic
fraction extracted from dietary mushrooms. In thisstudy, we investigated the impact of GOMEE (lipophilic
fraction extracted from fruiting bodies of mushrooms)
ingestion on chronic colon inflammation and the colon inflammation-related cytokines production in DSS-treatedmice. In this work, we demonstrated that in DSS-treatedmice, dietary GOMEE ingestion suppresses body weight
loss, colon constriction, and spleen swelling (Fig. 3 and4), as well as preventing colon villi damage and reducing
production of inflammation-related cytokines (Fig. 5 and
6). These findings are in line with our previous study on
DSS-treated mice, where we demonstrated that dietaryplant GlcCer ingestion limited colon villi damage anddecreased the levels of inflammatory cytokines andchemokines18). Because mushroom GlcCer, which possessa different sphingoid base than plant GlcCer, is a major
type of lipid found in the GOMEE (Fig. 2), we hypothesizethat suppression of colon inflammation by GOMEE isrelated to the presence of mushroom GlcCer.
In our previous study, we examined the anti-inflammatory effects of dietary plant GlcCer in mice treatedwith 2% DSS18). This method has the benefit of yielding
results within a short time, but it is not suitable forlong-term estimation because of the heavy symptoms ofcolon inflammation. To examine the long-term effects of
dietary functional food products, the dose-dependencyof the effect of DSS was examined. DSS was investigatedin mice at concentrations ranging from 0% to 1.5%. The
effects of DSS were only observed at the highest 1.5%
dose, where body weight gain was stopped, and blood infeces was observed, but there were no heavy symptoms
of inflammation such as bleeding from the vent (data notshown).
In this study, we reported that an intake of 5%
GOMEE suppresses the production of inflammation-related cytokines (Fig. 6) and limits the colon villi damage (Fig.
5) when ingestion of 1% dietary GOMEE is not sufficient
to trigger these effects. In contrast, there were no
significant differences in body weight, colon length, andspleen weight in samples collected from groups fed diets
supplemented with both 5% and 1% dietary GOMEE (Fig.
3 and 4). The mechanism of DSS action remains unclear.
Probably, DSS has a direct toxic impact on epithelial
cells of the basal crypts, causing the surfactant effect,
induction of colon inflammation, decreasing intestinal
barrier activity, and worsening of colon injury andinflammation. This result in changes of body parameters(e.g., body weight loss, colon constriction, and spleenswelling)25). Therefore, it is believed that ingesting 5%
GOMEE can have a strong protective effect in the earlystages of damage caused by DSS treatment. The next
logical step would be to study the dose-dependent effectsof GOMME on suppression of body weight gain. However,
because DSS is a potent inducer of colon inflammation,
continuous GOMEE intake, even small doses, is expected
to decrease the risk of colon inflammation in our life.
The lipophilic fraction of GOMEE cont a ins
considerable amounts of mushroom GlcCer, as well as
several lipids such as ergosterol and SG. Moreover, in thecontext of inflammation suppression by the lipophilic
fraction, the n-6/n-3 ratio in the fatty acid composition in
the diet has been widely discussed26). The most common
fatty acid in fruiting bodies of golden oyster mushrooms
is linoleic acid (C18:2n-6)27), which has the potential tostimulate inflammation26). In addition, the fatty acidcontent in GOMEE is lower than that in corn oil used inexperimental diets (corn oil: 50 g/kg diet, n-6/n-3 ratio= 69)24). Therefore, it is unlikely that the observed antiinflammatory effects of GOMEE are related to fatty acidcomposition.
The anti-cancer and anti-inflammatory effects
of dietary mushrooms and the hydrophilic fractions
extracted from the dietary mushroom have beenreported previously28, 29). It has been demonstrated that
dietary fruiting bodies of mushrooms can prevent and/or treat DSS-induced ulcerative colitis by modulation of
immune function, e.g., downregulation of cytokines suchas TNF-α, IL-10, and IFN-γ29). Dietary GOMEE suppresses
the increase in chemokine production in inflammatory
tissues. In our previous study, we demonstrated that
dietary GlcCer extracted from plants suppresses the
production of inflammatory cytokines and chemokines
in DSS-treated mice18). Therefore, we speculated thatmushroom GlcCer having a specific sphingoid basepresent in GOMEE also suppresses inflammation by
regulation of inflammatory cytokine and chemokine
levels. However, there are slight differences between
GOMEE and plant GlcCer; e.g., dietary GOMEE increased
levels of IL-12p70 while dietary plant GlcCer had noeffect on IL-12p70 levels. Differences between structuresof plant and mushroom GlcCer might influence themodulation of cytokines. In addition, candidates for antiinflammatory components in GOMEE also included otherlipophilic components. This is supported by the fact that
fungal sterols such as ergosterol and their glycosides
have several unique functions in comparison to sterols
found in plants and mammalians30-32). Further studies
are required to separate the lipid classes and this could
be achieved by using solvent distribution methods toidentify the active compounds.
It has been reported that in humans, GlcCer (which
is a component of the cell membrane) as well as othernutrients in plants and mushrooms are not able todisplay complete activity in the colon during digestion,

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MUSHROOM SCIENCE AND BIOTECHNOLOGY

because of the lack of cellulase which digests the cellwall composed of cellulose23, 33). Mushroom GlcCer andother lipophilic compounds in GOMEE have already beenreleased from mushroom fruit bodies; therefore, GOMEE
is thought to have higher bioavailability in comparison
to lipophilic compounds existing in the cell when
consuming the whole fruiting bodies.
In conclusion, dietary GOMEE is rich in sphingolipids,
and it exerts anti-inflammatory effects in DSS-treatedmice. The present results suggest that the dietary
lipophilic fraction extracted from fruiting bodies ofgolden oyster mushrooms displays the potential toregulate colon homeostasis and that the benefits ofingesting GOMEE are dose-dependent. Continuous
dietary GOMEE intake, even small doses, is expected
to alleviate colon injuries caused by common weak
stressors.
Acknowledgement We thank Dr. Yoshihiko Tokuji,
Department of Human Science, Obihiro University ofAgriculture and Veterinary Medicine, for helping withthe preparation of microscopic slides.

和文摘要
DSS 誘導潰瘍性大腸炎モデルマウスにおけるタモギタケ（Pleurotus citrinopileatus）子実体
エタノール抽出物摂取の効果
山下慎司1)・赤田康太1)・松本 聡2)・木下幹朗1)*
1)

帯広畜産大学 生命・食料科学研究部門〒080-8555 北海道帯広市稲田町2)

株式会社エル・エスコーポレーション〒103-0001 東京都中央区日本橋小伝馬町 13-4
共同ビル 5 階

近年，日本を含む東アジアにおいて過敏性腸炎や潰瘍性大腸炎に代表される炎症性腸疾患の増加は深刻になりつつある．これら慢性的な腸管炎症の継続は，下痢等による生活の質の低下だけでなく，大腸ガン発症リスクを上昇させる可能性が報告されている．タモギタケを含むきのこ類，またその水溶性画分において，抗腫瘍活性などの機能性が報告されおり，その摂取による腸疾患予防が期待されている．本
研究では，きのこ子実体の脂溶性画分の腸疾患に対する機能性を明らかにするために，タモギタケ脂溶性画分としてタモギタケ子実体エタノール抽出物（GOMEE）を用い，食餌性 GOMEE が慢性大腸炎モデルマウスに及ぼす影響を調査した．1.5% デキストラン硫酸ナトリウム（DSS）飲水により誘導された慢性大腸炎に対し，食餌性 GOMEE は，飼育期間後期の体重減少を抑制するとともに，DSS 飲水 26 日
目では脾臓重量の増加並びに大腸の収縮を有意に抑制した．

13

また，GOMEE 摂取は DSS により誘導される大腸絨毛の損
傷を摂取量依存的に抑制することが観察された．DSS 飲水
18 日目の炎症初期・中期においては，GOMEE 摂取は大腸
粘膜の炎症関連サイトカインレベルの上昇を摂取量依存的に抑制した．以上の結果は，タモギタケの脂溶性成分には，抗炎症活性を有する腸管保護成分が存在する可能性を示唆する．
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