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COMPARATIVE EFFECT OF FLAXSEED OIL AND FISH OIL IN ACETIC ACID- INDUCED COLITIS IN RATS

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Abstract

Objectives: The aim of the present study was to evaluate the possible protective effect of flaxseed oil and to compare this effect with fish oil in experimental ulcerative colitis (UC).Methods: Rats were equally divided into five groups of six animals each. Sham control group (corn oil, 1 ml), acetic acid group (normal saline, 1 ml), flaxseed oil group (FSO, 1 ml), fish oil group (FO, 1 ml) and mesalamine-treated group (3 ml ) as a positive control. All drugs were administered intrarectally (IR). One hour following treatment in the acetic acid group, FSO group, FO group and mesalamine group, 1 ml of 4% acetic acid was introduced as an enema. Rats were sacrificed after 24 hrs and histopathological scores of the all colonic specimens were assessed by microscope. Colonic weight/length ratio was also evaluated.Results: Microscopical improvement as manifested by the reduction in the inflammatory score and normalization of intestinal mucosal architecture was observed in fish oil pretreated rats compared to acetic acid group but there was no significant difference in flaxseed oil pretreated group. The decrease in weight/length ratio was statistically significant in fish oil-treated group compared with acetic acid group, but there was no significant difference between flaxseed oil-treated and acetic acid group.Conclusion: The results of this study suggest that fish oil but not flaxseed oil could ameliorate the mucosal damage in experimentally induced ulcerative colitis in rats when given in the form of an enema.
Copyright © 2012 LJPCP. This is an open access article distributed under the Creative Commons Attribution 3.0 License, which permits unrestricted use,
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Citation:Libyan J Pharm & Clin Pharmacol 2012, 1: 451372 -http://dx.doi.org/10.5542/ LJPCP.v3i0. 451372
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1
COMPARATIVE EFFECT OF FLAXSEED OIL AND FISH
OIL IN ACETIC ACID-INDUCED COLITIS IN RATS
Aisha Dugani1, Ahlam Elhelawi1,Aisha Edrah2,1) Department of Pharmacology and Clinical Pharmacy,
University of Tripoli, Tripoli, Libya,2) Department of Pharmacology, Faculty of Medicine, Tripoli University, Tripoli,
Libya.
Received: 26 April 2012, Accepted in revised form: 18 Jun 2012, Published: 7 July 2012
Corresponding author: Aisha Dugani, e- mail: duganiaisha@yahoo.com
ABSTRACT:
Objectives: The aim of the present study was to evaluate the possible protective effect of flaxseed oil and to
compare this effect with fish oil in experimental ulcerative colitis (UC).
Methods: Rats were equally divided into five groups of six animals each. Sham control group (corn oil, 1 ml),
acetic acid group (normal saline, 1 ml), flaxseed oil group (FSO, 1 ml), fish oil group (FO, 1 ml) and
mesalamine-treated group (3 ml ) as a positive control. All drugs were administered intrarectally (IR). One hour
following treatment in the acetic acid group, FSO group, FO group and mesalamine group, 1 ml of 4% acetic
acid was introduced as an enema. Rats were sacrificed after 24 hrs and histopathological scores of the all colonic
specimens were assessed by microscope. Colonic weight/length ratio was also evaluated.
Results: Microscopical improvement as manifested by the reduction in the inflammatory score and
normalization of intestinal mucosal architecture was observed in fish oil pretreated rats compared to acetic acid
group but there was no significant difference in flaxseed oil pretreated group. The decrease in weight/length ratio
was statistically significant in fish oil-treated group compared with acetic acid group, but there was no significant
difference between flaxseed oil-treated and acetic acid group.
Conclusion: The results of this study suggest that fish oil but not flaxseed oil could ameliorate the mucosal
damage in experimentally induced ulcerative colitis in rats when given in the form of an enema.
Keywords: Flaxseed oil; ulcerative colitis; fish oil; acetic acid induced colitis.
ﻲﺑرﻌﻟا صﺧﻠﻣﻟا:
ﻲﻓ لﺧﻟا ضﻣﺣ نﻋ ﺔﺋﺷﺎﻧﻟا تﺎﺑﺎﮭﺗﻟﻻا ﻰﻠﻋ كﻣﺳﻟا تﯾز رﯾﺛﺄﺗﺑ نﺎﺗﻛﻟا ةرذﺑ تﯾز رﯾﺛﺄﺗ ﺔﻧرﺎﻘﻣﻟ ﺔﺳارد
نارﺋﻔﻟا دﻧﻋ نوﻟوﻘﻟا
ﻲﻧﺎﺟوﺪﻟا ﺔﺸﺋﺎﻋ
*1
يوﻼﮭﻟا مﻼﺣأ ،
1
ﺔﺸﺋﺎﻋ و ،هارد
2
،ﺔﻟﺪﯿﺼﻟا ﺔﯿﻠﻛ ،ﺔﯾﺮﯾﺮﺴﻟا ﺔﻟﺪﯿﺼﻟاو ﺔﯾودﻷا ﻢﻠﻋ ﻢﺴﻗ2 ﺎﯿﺒﯿﻟ ،ﺲﻠﺑاﺮط ،ﺲﻠﺑاﺮط ﺔﻌﻣﺎﺟ ،ﺐﻄﻟا ﺔﯿﻠﻛ ،ﺔﯾودﻷا ﻢﻠﻋ ﻢﺴﻗ.
فدﮭﻟا :نارﺋﻔﻟا دﻧﻋ نوﻟوﻘﻟا تﺎﺑﺎﮭﺗﻟا نﻣ ﺔﯾﺎﻗوﻟا ﻲﻓ كﻣﺳﻟا تﯾز رﯾﺛﺄﺗﺑ ﮫﺗﻧرﺎﻘﻣو نﺎﺗﻛﻟا ةرذﺑ تﯾزﻟ رﯾﺛﺄﺗﻟا مﯾﯾﻘﺗ ﻰﻟإ ﺔﺳاردﻟا هذھ فدﮭﺗ.
قرطﻟا :نارﺋﻓ ﺔﺗﺳ ﺎﮭﻧﻣ لﻛﺑ ،ﺔﯾوﺎﺳﺗﻣ تﺎﻋوﻣﺟﻣ سﻣﺧ ﻰﻟإ نارﺋﻔﻟا تﻣﺳﻗ .تﯾز تﯾطﻋأ ،ﺔطﺑﺎﺿﻟا ﺔﻋوﻣﺟﻣﻟا رﺑﺗﻌﺗ ،ﻰﻟوﻷا ﺔﻋوﻣﺟﻣﻟا ةرذﻟا
)1 رﺗﻟ ﻲﻠﻣ .( ًﺎﯾﺣﻠﻣ ًﻻوﻠﺣﻣ تﯾطﻋﺄﻓ ،لﺧﻟا ضﻣﺣ ﺔﻋوﻣﺟﻣ ،ﺔﯾﻧﺎﺛﻟا ﺔﻋوﻣﺟﻣﻟا)1 رﺗﻟ ﻲﻠﻣ .( تﯾطﻋأ ،كﻣﺳﻟا تﯾز ﺔﻋوﻣﺟﻣ ،ﺔﺛﻟﺎﺛﻟا ﺔﻋوﻣﺟﻣﻟا
كﻣﺳﻟا تﯾز)1 رﺗﻟ ﻲﻠﻣ .(نﺎﺗﻛﻟا ةرذﺑ تﯾز نﻣ رﺗﻟ ﻲﻠﻣ دﺣاو تﯾطﻋﺄﻓ ،نﺎﺗﻛﻟا ةرذﺑ تﯾز ﺔﻋوﻣﺟﻣ ،ﺔﻌﺑارﻟا ﺔﻋوﻣﺟﻣﻟا . ﺎﻣأﻣﺎﺧﻟا ﺔﻋوﻣﺟﻣﻟا ،ﺔﺳ
تﯾطﻋﺄﻓ ،ﺔﺑﺟوﻣﻟا ﺔطﺑﺎﺿﻟا ﺔﻋوﻣﺟﻣﻟا3 نﯾﻣﻻازﯾﻣﻟا رﺎﻘﻋ نﻣ رﺗﻟ ﻲﻠﻣ mesalamine .جرﺷﻟا قﯾرط نﻣ ﺎھؤﺎطﻋإ مﺗ تﺎﻋرﺟﻟا لﻛ . ﺔﻋﺎﺳ دﻌﺑو
نﻣ رﺗﻟ ﻲﻠ دﺣاو ﻲﻟوﻷا ﺔﻋوﻣﺟﻣﻟا يدﻋ ﺎﻣ ﻊﯾﻣﺎﺟﻣﻟا ﻊﯾﻣﺟ ءﺎطﻋأ مﺗ4% جرﺷﻟا قﯾرط نﻣ لﺧﻟا ضﻣﺣ .دﻌﺑو 24 ﻊﯾﻣﺟ لﺗﻗ مﺗ ﺔﻋﺎﺳ
ذﺧأو ،تﺎﻧاوﯾﺣﻟا تارﯾﻐﺗﻠﻟ يرﮭﺟﻣﻟا مﯾﯾﻘﺗﻟا ﺎﺿﯾأ مﺗو ،ﺎﮭﻧزو ﻰﻟإ ﺔﻌطﻘﻟا لوط نﯾﺑ ﺔﺑﺳﻧﻟا بﺎﺳﺣو ﺎﮭﻧزو نﯾﯾﻌﺗو ﺎﮭﻟوط سﺎﯾﻘﻟ نوﻟوﻘﻟا نﻣ تﺎﻧﯾﻋ ت
تﺎﻧﯾﻌﻟا ﻊﯾﻣﺟﻟ نوﻟوﻘﻟا ﺞﯾﺳﻧ ﻰﻠﻋ ﺔﯾﺿرﻣﻟا ﺔﯾﺟﯾﺳﻧﻟا.
ﺞﺋﺎﺗﻧﻟا :ﻘﺗﻟا نوﻟوﻘﻟا بﺎﮭﺗﻟا ثادﺣﺗﺳا لﺑﻗ جرﺷﻟا قﯾرط نﻣ كﻣﺳﻟا تﯾز ءﺎطﻋإ نأ ﺔﺳاردﻟا هذھ تﻧﯾﺑ ضﺎﻔﺧﻧا ﻰﻟإ ىدأ ،لﺧﻟا ضﻣﺣ ﺔطﺳاوﺑ ﻲﺣر
أ نﺎﺗﻛﻟا ةرذﺑ تﯾزﻟ ﺔﯾﻌﺿوﻣﻟا ﺔﯾﺟرﺷﻟا ﺔﺟﻟﺎﻌﻣﻠﻟ نﻛﯾ مﻟ نﯾﺣ ﻲﻓ ،نوﻟوﻘﻠﻟ ﺔﯾﺿرﻣﻟا ﺔﯾﺟﯾﺳﻧﻟا ﺔﻟﺎﺣﻟا ﻲﻓ نﺳﺣﺗو ،نوﻟوﻘﻟا بﺎﮭﺗﻟا لدﻌﻣ ﻲ رﯾﺛﺄﺗ ي
نوﻟوﻘﻟا تﺎﺑﺎﮭﺗﻟا ﻰﻠﻋ.
تﺎﺟﺎﺗﻧﺗﺳﻻا :ذﺑ تﯾز سﯾﻟو ،كﻣﺳﻟا تﯾز نﻘﺣ نأ ﺔﺳاردﻟا هذھ ﺞﺋﺎﺗﻧ تﻧﯾﺑ ﻲﺗﻟا تﺎﺷرﺧﺗﻟا نﻣ لﯾﻠﻘﺗﻟا ﻲﻓ دﯾﺟ رﯾﺛﺄﺗ ﮫﻟ جرﺷﻟا قﯾرط نﻣ ،نﺎﺗﻛﻟا ةر
نارﺋﻔﻟا دﻧﻋ نوﻟوﻘﻟا رادﺟ ﻲﻓ لﺧﻟا ضﻣﺣ ﺎﮭﺛدﺣﯾ.
ﺔﯾﺣﺎﺗﻔﻣ تﺎﻣﻠﻛﻟا :لﺧﻟا ضﻣﺣ ،ﻲﺣرﻘﺗﻟا نوﻟوﻘﻟا بﺎﮭﺗﻟا ،كﻣﺳﻟا تﯾز ،نﺎﺗﻛﻟا ةرذﺑ تﯾز.
Aisha Dugani et al
Citation:Libyan J Pharm & Clin Pharmacol 2012, 1: 451372 -http://dx.doi.org/10.5542/ LJPCP.v3i0. 451372
2(Page number is not for citation purpose).
INTRODUCTION:
lcerative colitis (UC) is a form of
inflammatory bowel disease (IBD)
characterized by diffuse mucosal
inflammation of the colon and rectum and typically
involves only the innermost lining of the mucosa,
manifesting as continuous areas of inflammation and
ulceration with no segments of normal tissue [1].
The disease typically starts in the rectum, but
often extends to involve the whole length of the
colon [2].Despite the enormous research on the
pathogenesis of UC, the exact cause of the
condition remains not completely understood.
The disease appears to be related to combination
of genetic and environmental factors [1].The
pathological findings associated with UC include:
an increase in inflammatory mediators such as
prostaglandins (PG) and leukotrienes (LT), which
are produced from arachidonic acid. Clinical and
experimental studies have confirmed that the
levels of prostaglandin E2, thromboxane A2,
prostacyclin, and especially LTB4 during colonic
inflammation were highly increased [3]. Other
factors include: oxidative stress, altered colonic
milieu, abnormal mucosal content of
glycosaminoglycan (GAG), decreased oxidation
of short chain fatty acids (SCFAs), increased
intestinal permeability, increased sulfide
production, and decreased methylation
[1].Treatment of IBD including UC consists of
sulphasalazine (SSZ), 5-aminosalicylic acid (5-
ASA), corticosteroids, immunomodulator drugs
[azathioprine (AZA) and methotrexate (MTX)], 6
mercaptopurine (6-MP), calcineurin inhibitors
(cyclosporin and tacrolimus), and anti-TNF-alpha
antibodies (infliximab, adalimumab and
certolizumab). The choice of treatment depends
on the clinical goal (induction or maintenance of
remission), extent and severity of disease,
response to current or prior medication and the
presence of complications [4].Polyunsaturated
fatty acids (FA) of the omega-3 class, especially
eicosapentaenoic acid (EPA) and docosahexaenoic
acid (DHA) have attracted interest in recent years
because of their anti-inflammatory properties [5].
Several published research work have confirmed
the protective effect of fish oil supplemented in
diet or as enema in experimental induced colitis
[5-8] and also in clinical trials on patients with
IBD [9-13]. Thus it was thought worthwhile to
investigate the effect of other omega-3 rich oil
such as flaxseed oil and to study the comparative
effects of these
two oils in the protection against acetic acid
inducing colitis in rats.
MATERIALS AND METHODS:
ANIMALS.
Healthy Albino Wistar rats of either sex
weighing 200-250 g were used in this study.
They were randomly allocated to groups of 6
rats each. The animals were housed in the
animal care facility in the department of
Pharmacology and Clinical Pharmacy and
maintained at 23˚C with a 12 hour light and 12
hour dark cycle. All rats were fasted for 24
hours prior to the experimental procedure. The
study was approved by the Faculty of Pharmacy
and the experiments were done according to the
ethics guidelines of Tripoli University.
INDUCTION OF COLITIS AND TREATMENT
PROTOCOL:
Colitis was induced in rats by intrarectal (IR)
administration of acetic acid (AA). After
anesthetized with ketamine in a dose of 75
mg/kg injected intraperitoneally, a soft 6F
polypropylene catheter lubricated with jelly was
inserted 6-8 cm via the anal canal into the
colon. One ml of AA (4% vol./vol. in 0.9%
saline) was slowly infused into the distal colon
and rats were maintained in a head-down
position for 30 seconds to limit the expulsion of
the solution [5].
TREATMENT PROTOCOLS:
Rats were randomized into five groups. Group
1: Sham control group (SC). One ml of normal
saline was given IR after 1 hour from
administration of one ml corn oil enema. Group
2: Control colitis group (CC), one ml of 4% AA
was administered IR 1 hour following IR
administration of normal saline. Group 3: Fish
oil treatment group (FO-IR), one ml of FO was
administered as enema one hour before
induction of colitis. Group 4: Flaxseed oil
treatment group (FSO-IR), one ml of FSO was
administered as enema one hour before
induction of colitis. group 5: mesalazine
treatment group, the animals were given 3 ml of
mesalazine enema one hour before induction of
colitis.One hour following the above
treatments, colitis was induced in all animal in
groups 3, 4 and 5 by the administration of AA
IR (1.0 ml of 4%). All rats were scarified 24
hours following AA-treatment.
U
Aisha Dugani et al
Citation:Libyan J Pharm & Clin Pharmacol 2012, 1: 451372 -http://dx.doi.org/10.5542/ LJPCP.v3i0. 451372
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ASSESSMENT OF COLONIC DAMAGE:
After midline laparotomy, the colon was
removed, cleaned from fat and mesentery, and
blotted on a filter paper. Each specimen was
weighed and its length measured under a
constant weight (2 g) and expressed as colon
weight (mg)/length (cm) ratio. The distal 2-
3cm segment of the colon was isolated from the
rest of the tissue samples and opened
longitudinally, rinsed with saline to remove
luminal content and fixed in 10% formalin and
embedded in paraffin, and 5µm sections were
prepared. Tissues were routinely stained with
hematoxylin and eosin and were evaluated for
the appearance of muscle layers by a light
microscopy by a pathologist who was not
informed about the treatment protocols.The
degree of colonic inflammation was evaluated
by histologic scoring (from 0 to 3) as previously
describe [14], where normal histologic
appearance = 0; 1= inflammation on mucosa
and submucosa; 2= inflammation on entire wall
of the bowel, and 3 = ulcer and necrosis of the
entire wall.
STATISTICAL ANALYSIS:
Data are expressed as mean +S.E.M. Statistical
calculations were done with SPSS 11.0 software
package. Comparison between two groups was
performed using Student’s t-test and
comparison between more than two groups was
carried using one-way analysis of variance
(ANOVA). Differences were considered
significant when the degree of confidence was
95% or better (P<0.05).
RESULTS:
The intracolonic administration of 1.0 ml of 4%
AA produced a severe and significant inflammatory
response in rat colon 24 hrs after injection. This
response is evidenced by the significant increase
in weight of 5 cm distal colonic segment and an
increase in the histopathological score as
compared to control group treated with normal
saline (Figure 1 and Figure 2B). All rats in the
acetic acid treatment group developed diarrhea, in
some animals bloody diarrhea was observed.
Figure1.Effect of pretreatment with fish oil, flaxseed
oil and mesalamine on colon weight/length ratio in
acetic acid-induced colitis in rats. Values are mean +
SEM, n = 6. #,P<0.001 significantly higher than sham
control (normal saline-treated);*, P<0.05 and **, P<0.01
significantly lower from colitis group (acetic acid-
treated group) respectively.
EFFECTS OF FISH OIL AND
FLAXSEED OIL ON COLONIC
WEIGHT/ LENGTH RATIO IN ACETIC
ACID-INDUCED COLITIS.
The colonic tissue segment weight/length
ratio was significantly higher in the AA-
group as compared to SC group (37.0 +1.0
vs 23.12 +0.9 respectively, P< 0.001, Figure
1. Pretreatment of rats with one ml of FO-
IR, showed a significant mucosal protection
effect against AA-induced colitis as
evidenced by the decrease in the colon
weight/length ratio in comparison with SC-
treatment groups (32.97 +1.02 vs 37.00 +
1.01, P< 0.05). FSO pretreatment, on the
other hand, has a slight but insignificant
reduction in the colonic tissue weight/length
ratio in comparison with AA-control group
(36.00 +1.9 vs 37.00 +1.01 respectively
Figure 1.
EFFECT OF FISH OIL AND
FLAXSEED OIL ON COLONIC
HISTOLOGICAL
DAMAGE INDUCED BY ACETIC ACID.
Representative histological segments of the
colon in the control, AA-treatment group
and in group of rats treated with FO, FSO
and mesalamine enemas are shown in figure
2. AA produced a significant inflammatory
response and prominent lesions in the
mucosa and submucosa, with invasion of
inflammatory cells mainly macrophages and
neutrophils and dilation of capillaries and
lymphatics,Figures 2B and 3.
Aisha Dugani et al
Citation:Libyan J Pharm & Clin Pharmacol 2012, 1: 451372 -http://dx.doi.org/10.5542/ LJPCP.v3i0. 451372
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Figure2.Examples of photomicrographs of rat colonic
mucosa. (A) Sham negative control rat (saline-treated),
(B) Acetic acid-treated rat, (C) Fish oil-treated rat, (D)
Flaxseed oil-treated rats, (E) Mesalamine treated group.
Arrows and circle indicate ulcerated epithelium.
EFFECT OF FISH OIL AND FLAXSEED
OIL ON COLONIC HISTOLOGICAL
DAMAGE INDUCED BY ACETIC ACID
Representative histological segments of the
colon in the control, AA-treatment group and
in group of rats treated with FO, FSO and
mesalamine enemas are shown in figure 2. AA
produced a significant inflammatory response
and prominent lesions in the mucosa and
submucosa, with invasion of inflammatory cells
mainly macrophages and neutrophils and
dilation of capillaries and lymphatics,Figures
2B and 3. FO treatment resulted in correction of
the morphological disturbances associated with
AA administration. The hisopathological score
was significantly reduced from 3.7 +0.2 in the
AA colitis group to 1.2 +0.4 in the FO-
treatment group respectively, (P< 0.01) (Figure
2 C). FSO, on the other hand, has no effect on
tissue damage caused by AA, the histological
damage score in this group was 3.2 +0.5 versus
3.7 +0.2 in AA control group and the reduction
was not significant. Comparing the results of
FO group with the standard drug mesalamine,
the reduction in histological score was slight
and insignificant (1.2 +0.4 vs 1.5 +0.6). The
findings at microscopy were consistent with
macroscopic appearance and changes in colonic
weight and the weight/length ratio in the
different treatment groups. These results are
summarized in,figure 4.
Figure3. Higher magnification of rat colon treated with
acetic acid showing in A, B and C: large number of mucosal
glands with hyperplastic (1) and dysplastic (2) changes with
some of them lined by one or more layers and others seen
completely obstructed with cystic formation (3) or papillary
cystic formation. The submucosal blood vessels are severely
dilated and hyperemic (4)
Figure 4.Effect of pretreatment with fish oil, flaxseed oil
and meselamine on histological damage score in acetic acid-
induced colitis model in rats. Values are mean +SEM, n = 6.
$, P<0.01 significantly higher than normal saline (negative
control) group. #, P<0.05 significantly higher than fish oil ;
**,P<0.01 significantly lower than acetic acid (control colitis
group).
DISCUSSION:
The present study was planned to compare the
protective effects of two omega-3 rich oils; the
plant derived FSO and the marine derived FO on
AA colitis in rats. Induction of colitis by AA is
one of the standard methods to produce a model
with the characteristics of human ulcerative
colitis [15]. It affects the distal colon portionand
induces non-transmural inflammation, massive
necrosis of mucosal and submucosal layers,
mucosal edema, neutrophil infiltration of mucosal
and submucosal ulceration [16]. The
inflammatory response initiated by AA includes
activation of cyclooxygenase and lipooxygenase
pathways [17]. The reason behind investigating
the protective effects of FSO in this study and to
compare its effects with FO, is the fact that FSO
by far is the richest source of Omega-3 fatty acid
alpha-linolenic acid (ALA) at roughly 57%, six
times richer than most fish oil, in n-3 [18,19]. Its
Aisha Dugani et al
Citation:Libyan J Pharm & Clin Pharmacol 2012, 1: 451372 -http://dx.doi.org/10.5542/ LJPCP.v3i0. 451372
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omega6:omega3 ratio is very desirable at 0.3:1.
The ALA is converted by metabolism in vivo into
the longer chain omega 3’s EPA and DHA. To our
knowledge, there have been no reports on the
effects of the plant derived FSO either as
supplement or in the form of enema in
experimental colitis. Our results have
demonstrated that intracolonic administration of
4% AA caused a substantial degree of
inflammation and tissue injury in the rat colon as
evidenced microscopically by the increase in
cellular infiltration, muscle thickness and loss of
architectural structure and macroscopically by the
increase in weight of colon segment compared
with SC-group. The degree of tissue damage was
markedly attenuated by intrarectal treatment with
FO. These results are in accordance with other
studies, which demonstrated that FO enema
provided a protective effect against ethanol, AA
and trinitrobenzene-induced colitis models in rats
[5, 6].The protective effect was reported to be
associated with a significant reduction in the
levels of leukotriene B4 and myeloperoxidase
activity in the colonic tissue [5]. On the other
hand, we were unable to detect any protective
effect of FSO in AA-induced colitis. Clinical
reports [9-13] have indicated that in patients with
UC, supplementation with FO was effective in
reducing both the symptoms and the dose of
corticosteroid required to control the disease and
in reducing rate of relapse. In a case report study,
FO enema produced a significant improvement in
symptoms, normal-appearing colonic mucosa on
colonoscopy and on histopathology [20]. The
exact mechanism of omega-3 fatty acids (n-3
FAfatty acids) involved in the attenuation of
inflammations is not well understood. However,
they n-3 FA are believed to reduce inflammation
through reduction of the incorporation of EPA
and DHA into the arachidonic acid with
increased production of 3-series PGs and
thromboxanes and 5-series LTs, thus reduce the
inflammatory potential [21, 22]. Interleukin-1α
and tumor necrosis factor production may also be
reduced by the presence of n-3 FAfatty acids
[23]. Thus, the propagation of inflammatory
pathways is diminished. The n-3 FAfatty acids
from FO have been found to inhibit cytokine and
eicosanoid formation. Prolonged treatment with
FO in patients with rheumatoid arthritis (RA),
resulted in a significant decrease in LTB4 and
TNF-[24] Eicosapentaenoic acid EPA is the
precursor of the PG3 series of prostaglandins and
resolvins, which have anti-inflammatory effects.
Docosahexaenoic acid DHA is the precursor of
the docosanoids, termed 'resolvins' or 'protectins',
which are analogous to the eicosanoids and have
potent anti-inflammatory and immune-regulatory
actions [25, 26]. Docosahexaenoic acid DHA is
believed to have beneficial effects upon
inflammatory disorders of the intestine and in
reducing the risk of colon cancer, which may be
mediated through associations with specific
signaling proteins in membranes [25]. Flaxseed
oil FSO ccontains 50-60% omega-3 fatty acids in
the form of ALA and this amount are roughly
double that contained in FO. However, the results
obtained in this study using FSO in the form of
enema showed that it didn’t provide any
significant protective effect against AA-inducing
colonic injury. This may be attributed to the fact
that ALA present in FSO is a precursor and has to
be converted in vivo into two major metabolites;
the long chain omega-3 fatty acids,
eicosapentaenoic acid epa and docasahexaenoic
acid dha [18], such conversion require systemic
and not local treatment. Therefore, further
investigations are needed to explore the effect of
changing the route of administration of FSO
using oral feeding.
CONCLUSION:
The results presented in this article reflect that
FO but not FSO is beneficial in the prevention
of UC induced by AA when given in the form
of enema. This data reinforce the previous
reports on the beneficial effects of omega-3 rich
compounds on IBD. However,we could not
completely rule out any beneficial effects of
FSO in UC until further investigations using the
oral route of administration are completed.
A CKNOWLEDGMENT AND SOURCE
FUNDING:
This research received no specific grant from any
funding agency in the public, commercial, or not-
for-profit sectors.
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high α-linolenic acid flaxseed (linum usitatissimum): some nutritional properties in humans
cunnane sc, ganguli s, menard c, liede ac, hamadeh mj, chen zyliede ac, hamadeh mj, chen zy, et al. high α-linolenic acid flaxseed (linum usitatissimum): some nutritional properties in humans. br j nutr; 49:443-453, 1993. 19) thomas bartram (1998). bartram's encyclopedia of herbal medicine. pp. 271.
gram it, thelle, d. effects of eicosapentaenoic and docosahexaenoic acids on blood pressure in hypertension. a population-based intervention trial from the tromso study
bonna kh, bjerve ks, straume b, gram it, thelle, d. effects of eicosapentaenoic and docosahexaenoic acids on blood pressure in hypertension. a population-based intervention trial from the tromso study. n. engl. j. med. 322: 795-801, 1990.