• Users Online: 72
  • Print this page
  • Email this page


 
 
Table of Contents
BASIC RESEARCH
Year : 2018  |  Volume : 8  |  Issue : 3  |  Page : 166-172

Diet containing seeds of Buchholzia coriacea accelerates healing of acetic acid induced colitis in rats


1 Laboratory for Gastrointestinal Secretion and Inflammation Research, Department of Physiology, College of Medicine, University of Ibadan, Oyo State; Department of Physiology, Federal University of Technology, Akure, Ondo State, Nigeria
2 Laboratory for Gastrointestinal Secretion and Inflammation Research, Department of Physiology, College of Medicine, University of Ibadan, Oyo State, Nigeria

Date of Submission12-Nov-2017
Date of Decision20-Dec-2017
Date of Acceptance10-Jan-2018
Date of Web Publication21-Mar-2018

Correspondence Address:
Samuel B Olaleye
Laboratory for Gastrointestinal Secretion and Inflammation Research, Department of Physiology, College of Medicine, University of Ibadan, Oyo State
Nigeria
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2221-1691.227998

Get Permissions

  Abstract 


Objective: To investigate the anti-colitic effects of diet containing seeds of Buchholzia coriacea (B. coriacea) on acetic acid induced ulcerative colitis. Methods: Male Wistar rats (70-100 g) were fed with standard diets (control group) or with same diet containing B. coriacea seeds at 12.5% or 25% for six weeks. At the sixth week, colitis was induced by intra-rectal administration of 1 mL/200 g 6% acetic acid. Animals were sacrificed at days 0 (before induction), 1, 3 and 7 post induction to assess disease severity via evaluation of stool consistency, haematological variables and histomorphometry of colon tissues. Results: A significant increase in body weight was observed in the 12.5% B. coriacea fed group compared to the control. B. coriacea significantly reduced stool consistency and microscopic scores. Histological evaluation revealed significantly decreased inflammatory aggregates in B. coriacea fed groups compared to control after colitis induction. There was a significant decrease in packed cell volume, red blood cell and haemoglobin concentration in the control group at day 1 post colitis induction compared to 12.5% B. coriacea fed groups. Neutrophils and white blood cell were also significantly increased after colitis induction in the control group while these were significantly decreased in the B. coriacea fed groups. Conclusions: The addition of B. coriacea seeds to diets promotes healing of acetic acid induced colitis by suppressing infiltration of inflammatory aggregates and ameliorating anemia.

Keywords: Buchholzia coriacea, Acetic acid, Ulcerative colitis, Diarrhea, Inflammatory aggregates


How to cite this article:
Omayone TP, Salami AT, Odukanmi AO, Olaleye SB. Diet containing seeds of Buchholzia coriacea accelerates healing of acetic acid induced colitis in rats. Asian Pac J Trop Biomed 2018;8:166-72

How to cite this URL:
Omayone TP, Salami AT, Odukanmi AO, Olaleye SB. Diet containing seeds of Buchholzia coriacea accelerates healing of acetic acid induced colitis in rats. Asian Pac J Trop Biomed [serial online] 2018 [cited 2018 Apr 19];8:166-72. Available from: http://www.apjtb.org/text.asp?2018/8/3/166/227998




  1. Introduction Top


Inflammatory bowel disease is an umbrella term used to describe ulcerative colitis and Crohn's disease. It is characterized by superficial infiltration of the bowel wall by inflammatory white blood cells, resulting in multiple mucosal ulceration and crypt abscesses[1]. Ulcerative colitis is a disease usually associated with the western developed countries such as United Kingdom, United States and Canada[2],[3], however, in recent times, cases of the disease are now being diagnosed in developing countries such as China[4], Nigeria[5] and this may be due to civilization and industrialization spreading across the world at a very fast rate.

The typical symptom of ulcerative colitis is diarrhoea which is usually associated with bloody stool. Bowel movements are frequent but small in volume as a result of rectal inflammation[6]. Other symptoms include fever and pain, which may be in either the lower quadrant or rectum. Systemic features, including fever, malaise, and weight loss are more common if a greater portion of the colon is affected[6]. Ulcerative colitis is an intermittent disease, with periods of exacerbated symptoms and periods that are relatively symptomfree. Symptoms sometimes however can diminish on their own but usually require treatment to go into remission[7].

Ulcerative colitis has been known as a clinical entity as early as 1859, however, the aetiological mystery is yet to be completely unraveled[8]. Various factors have been reported to be involved in the disease formation condition which include an increase in reactive oxygen species leading to oxidative stress[9],[10] and in pro- inflammatory cytokines such as IL-8, IL1 β and TNF- α [11],[12] as well as genetic and environmental factors[13].

Until recently, the clinical treatments for ulcerative colitis were relatively limited, essentially comprising of 5-aminosalicylic acid (ASA) compounds, steroids and azathioprine/ 6-mercaptopurine. In the 1990s, methotrexate and cyclosporine were included as immunoregulatory agents used in inflammatory bowel diseases. The approval of infliximab (Remicade; Centocor), a chimeric monoclonal antibody which targets tumor-necrosis factor- α , for the treatment of ulcerative colitis disease launched the era of biologic therapy for inflammatory bowel diseases[14]. These varieties of medications used in treatment of ulcerative colitis fall into two categories; maintenance drugs which are taken all the time to prevent flare-ups and fast- acting drugs which are taken occasionally to stop a flare up[15]. Many people who have ulcerative colitis turn to alternate therapies in addition to medical management of their disease[16]. This alternative therapy includes natural plant products and the use of plant extracts for the disease treatment. Some of the herbs and supplements that have been studied include Aloe vera, Boswellia, butyrate, licorice root, slippery elm, and omega-3 fatty acids. Some of these remedies have shown promise for ulcerative colitis but others have not been shown to have any value, and may actually be harmful[16].

Buchholzia coriacea (B. coriacea) is a forest tree belonging to the Capparaceae family[17]. It was named after R. W. Buchholz who collected plants in Cameroon in the late 19th century[18]. The seeds of the plant are edible, taste peppery and are known to have great medicinal value which gave the plant its common name ‘wonderful kola’[19]. Over the years, the plant has been used in different parts of African countries to treat various illnesses ranging from headache, nasal congestion, small pox, cough, fever and also used as an antihelmintic agent[20],[21],[22].

Recent studies on the seed extract of this plant have shown that it is a good source of energy[19]; it possesses antibacterial, anti-diabetic, hypolipidemic, antioxidant and anti-ulcer activities[23],[24],[25]. Despite the various reports on the plant use to treat various illnesses, information on the use of the seeds of the plant in gastrointestinal ulceration is scarce. However, there is no report on its effect on ulcerative colitis, thus the present study was undertaken to evaluate the effect of diet containing seeds of B. coriacea on healing experimentally induced ulcerative colitis.


  2. Materials and methods Top


2.1. Plant collection and preparation

The seeds of B. coriacea were purchased from Oje market in Ibadan, Oyo State. The seeds were washed, peeled, air dried and thereafter milled into powdery form. It was then incorporated into the feed of the animals at varying percentages.

2.2. Experimental design

The animals used in this study were male Wistar rats obtained from the central animal house, University of Ibadan. All protocols in this study were approved by the Gastrointestinal Research Group of the University of Ibadan, Ibadan, Nigeria and carried out in accordance with the guidelines of the National Institute of Health for laboratory animal care and use.

A total of 60 rats weighing between 70-100 g were used and divided into three groups of 20 rats each. Animals were fed with standard rat diet for the control group, and with same diet containing 12.5% B. coriacea and 25% B. coriacea for six weeks and all groups received water ad libitum. At the end of six weeks, 15 animals were randomly selected from each group for the induction of colitis and thereafter continued with same diet for the period of assessment.

2.3. Induction of colitis

Under light ether anaesthesia, a flexible plastic catheter (outer diameter of 2 mm) was inserted rectally into the colon 8 cm proximal to the anus. Colitis was then induced by administering 1 mL/200 g 6% acetic acid[26]. The animals were inspected and scored for the presence of diarrhoea and 5 rats from each group were sacrificed at day 0 (without colitis), days 1, 3 and 7 after colitis induction.

2.4. Diarrhoea scoring

The stool consistency of each rat was assessed daily for diarrhoea and presence of blood using a standard scoring method[27] stated as follows.

0 - Normal stool (No traces of blood)

1 - Soft stool, but still formed

2 - Very soft + traces of blood

3 - Bloody diarrhoea.

2.5. Haematological analysis

Blood samples were collected from each animal at the days of sacrifice via cardiac puncture into ethylene-diamine-tetra-acetic acid bottle. Complete blood count analysis was carried out; packed cell volume (PCV), haemoglobin (Hb) concentration, red blood cell (RBC) count, platelets, white blood cell (WBC) count, lymphocytes and neutrophils[28].

2.6. Assessment of colon weight

After quick decapitation of the animals, the distal colon (8 cm) was removed and opened longitudinally, washed to remove luminal contents with ice cold normal saline. The colon was weighed with an electronic weighing balance, model DT 1000 with capacity of 0.01 to 100 g.

2.7. Histological observations

Small section of the 8 cm distal colon was taken from each colon and fixed in 10% formalin for histological examination. Each tissue was fixed, cut longitudinally into 5 mm sections, stained with Haematoxylin and Eosin (H&E). The slides were coded to prevent observer bias and evaluated blindly by light microscope. The extent of tissue injury was scored using the following criteria;

0 – No evidence of inflammation; 1- Low level of inflammation with scattered infiltrating mononuclear cells (1-2 foci); 2- Moderate inflammation with multiple foci; 3- High level of inflammation with increased vascular density and marked wall thickening and 4- Maximal severity of inflammation with transmural leukocyte infiltration and loss of goblet cells.

2.8. Statistical analysis

All data were expressed as mean±SEM. Statistical comparison was performed across the groups using Graph Pad Prism6. Results were analyzed by Kruskal-Wallis test and Mann-Whitney for nonparametric variables while ANOVA and Student t-test were used for parametric variables. Significant differences were taken as P<0.05.


  3. Results Top


3.1. Effect of B. coriacea on weekly body weight changes

The results on body weight showed feeding animals with diets containing B. coriacea had no adverse effect on body weight profiles as all the animals had increased body weight with weeks of treatment. However, the group fed with 12.5% B. coriacea gained weight at a significantly higher level from the second week compared with the other groups [Figure 1].
Figure 1: Effect of B. coriacea on weekly body weight changes.
Values are expressed as mean±SEM. *P<0.05, compared to control group.


Click here to view


3.2. Effect of B. coriacea on diarrhoea score and colon weight

The stools of animals in all groups were normal at day 0 before the induction of colitis, with diarrhoea score of 0.00±0.00. On induction of colitis, all groups showed signs of diarrhoea. As shown in [Table 1], the diarrhoea score 24 h after inducing colitis was 0.40±0.16 in the control rats. The scores in the 12.5% and 25% B. coriacea diet groups were 0.67±0.19 and 0.24±0.13 respectively. Compared with the first day post-colitis, diarrhoea score in the control animals increased by 332.5%. Diarrhoea was however less frequent in the 12.5% B. coriacea (37.3%) and 25% B. coriacea (79.2%) fed rats. By day 7, the 12.5% B. coriacea diet had reduced diarrhoea score to levels below the 24-hour value (-25.3%), indicating that it had more significant anti-colitis effect.
Table 1: Diarrhoea score and colon weight in control rats and those fed with diets containing 12.5% and 25% B. coriacea diet before and after acetic acid induced colonic injury.

Click here to view


Colon weight was also significantly reduced in the B. coriacea fed group in a dose dependent manner by days 1, 3 and 7 after colitis induction compared to the control group as shown in [Table 1].

3.3. Effect of B. coriacea on hematological variables

[Table 2] and [Table 3] summarized the effect of B. coriacea on hematological variables. It was deduced that there was no significant difference in any of the parameters on day 0 prior to the induction of colitis. On induction of colitis, a significant decrease in PCV, RBC count and Hb concentration was observed in the control groups on days 1, 3 and 7. However, the 12.5% B. coriacea fed group had significantly higher PCV, RBC and Hb concentration compared to control group [Table 2]. There was also a corresponding significant increase in WBC count, neutrophils count and neutrophil/ lymphocyte ratio (NLR) in the control compared to B. coriacea groups on day 1 post colitis induction. On day 3, there was no significant difference in these variables between control group and B. coriacea fed groups, however, WBC was significantly higher in B. coriacea fed groups by day 7, while neutrophils and NLR were significantly increased in 25% B. coriacea group compared to control [Table 3].
Table 2: Effect of B. coriacea on RBC, PCV, Hb and platelet count.

Click here to view
Table 3: Effect of B. coriacea on WBC, neutrophils, lymphocytes and NLR.

Click here to view


3.4. Effect of B. coriacea on histological observation and score

There was no significant difference in the mean histological score between control group (0.00±0.00) and the B. coriacea fed groups; 12.5% (0.00±0.00) and 25% (0.25±0.25) on day 0 (pre- colitis). On induction of colitis, there was a marked increase in the influx of inflammatory aggregates as well as severe ulceration and inflammation in control group, nevertheless, mild to moderate erosion and influx of inflammatory aggregates were observed in the B. coriacea fed groups [Figure 2] leading to a significant increase in the histological scores. On day 1 post colitis induction, there was no significant difference in histological scores between control group (1.25±0.25) and B. coriacea fed groups; 12.5% (1.75±0.25) and 25% (1.50±0.29). Significantly low histological scores were recorded in the 12.5% B. coriacea group (1.60±0.24 and 1.40±0.24) and 25% B. coriacea group (2.20±0.37 and 2.40±0.24) on days 3 and 7 respectively compared to control group (3.00±0.31 and 3.60±0.24).
Figure 2: Photomicrograph collage of the colon of rats before (A, B, C) and after (A7, B7 and C7) acetic acid induced colitis.
A and B are control and 12.5% B. coriacea respectively showing intact epithelium. C represents 25% B. coriacea showing very mild erosion. A7i (× 100) and A7ii (× 400) show colon of control group (H&E) 7 d after colitis induction. U, ulceration and glandular degeneration. N, marked infiltration of inflammatory aggregates. B7i (× 100) and B7ii (× 400) show colon of 12.5% B. coriacea diet group 7 d after colitis induction. E, epithelial erosion. N, moderate infiltration of inflammatory aggregates. C7i (× 100) and C7ii (× 400) show colon of 25% B. coriacea diet group 7 d after colitis induction. E, moderate epithelial erosion and glandular degeneration. N, mild infiltration of inflammatory aggregates.


Click here to view



  4. Discussion Top


The dietary life style of an individual is very paramount to determining the health condition of the person. Various disease conditions including ulcerative colitis have been associated with poor dietary life style[29],[30]. In this study, the incorporation of seeds of B. coriacea into the diets of rats had ameliorative effect on experimentally induced ulcerative colitis.

The result on weekly body weight changes showed that B. coriacea fed groups gained considerable weight more than the control group which was noticed two weeks after consumption of B. coriacea .This result is supported by the report of Amaechi[19], where the nutritive and anti-nutritive value of seeds of B. coriacea were evaluated. It was reported that the seeds contain high carbohydrate and protein content and low fat content, thus they can serve as a good source of energy as well as an alternative source of protein. Haematological observation from this study also indicated that the animals were healthy as there was no substantial difference between the B. coriacea fed groups (12.5% B. coriacea and 25% B. coriacea) and control group prior to the induction of ulcerative colitis.

The use of acetic acid for the production of ulcerative colitis in rats is a standardized model[10]. Acetic acid model of induction of ulcerative colitis has been reported to have similar histological features to that of human. It is usually associated with deep ulceration and inflammation, enhanced vasopermeability as well as severe influx of neutrophils and macrophages to the site of injury[31],[32], hence, it is preferred in studying the healing potential of any proposed anti-colitic agent or drug. The influx of neutrophils and macrophages to the site of injury causes increase thickness of colonic wall with a resultant increase in colonic weight. In this study, the increased colon weight observed in the control group following the induction of colitis was decreased in the B. coriacea fed groups (12.5% B. coriacea and 25% B. coriacea). The apparent suppression of acetic acid induced colon weight by B. coriacea suggests its ability to prevent influx of neutrophils and macrophages to the site of injury. This result is buttressed by the histopathological observation, WBC and neutrophils count. Marked influx of inflammatory mediators into the submucosa layer was observed in the untreated group, while mild to moderate inflammatory mediators were observed in the submucosa layer in the B. coriacea fed groups. Likewise, the histological score further confirms these observations with the control group having a significantly increased histological scores compared to the B. coriacea fed groups.

Neutrophil recruitment is key in the onset and healing of ulcerative colitis. Neutrophil is a major source of reactive oxygen species, hence, plays a crucial role in the development of tissue damage[33]. Various studies have reported that activated neutrophils are capable of producing superoxide and a cascade of various species leading to a very reactive hydroxyl radical and peroxides[34],[35]. Prolonged production of these reactive hydroxyl radicals and peroxides may overwhelm the endogenous antioxidant defense mechanism, leading to oxidative stress. Agents that can mop up reactive oxygen species, act as an exogenous antioxidants as well as boost the endogenous antioxidants system, are likely beneficial in the treatment of chronic inflammatory disease. B. coriacea suppressed neutrophil infiltration noticed from histological observation as well as haematological parameters, hence can be proposed to have had a similar role in the level of free radicals. It has been reported[24] that methanol extract of B. coriacea significantly decreases serum malondialdehyde levels while increasing serum catalase and glutathione reductase activities in streptozotocin-induced diabetes.

Diarrhoea which is a major manifestation during ulcerative colitis leads to loss of body fluid associated with malabsorption of electrolytes[36]. Stool consistency evaluated in this study was used as a marker for diarrhoea. Diarrhoea with bloody stool was observed in the control group by day 3 post colitis induction unlike the B. coriacea fed groups which had soft but formed stool with no blood traces. Ulcerative colitis though affect the colon, may also have some extraintestinal manifestation of which anaemia is thus far the most common extraintestinal complication associated with it[37]. Treatment with B. coriacea was able to reverse and stabilize the levels of PCV, RBC and Hb which were decreased in the control group on induction of ulcerative colitis. Blood flow is very important in the healing process of inflammation for the supply of nutrients and growth factors[38]. The prevention of diarrhoea associated with bloody stool which could also result in anaemia as well as maintenance of the haematopoietic system further contributed to the mechanism by which B. coriacea enhanced the healing of experimentally induced colitis.

In conclusion, this investigation is only a preliminary study on the effect of B. coriacea on the healing of acetic acid induced colitis, we conclude base on the results that B. coriacea has a potent effect against various pathological changes caused by the administration of acetic acid. Inhibition of neutrophil infiltration as well as enhancing haematopoietic system by preventing anaemia could be likely mechanisms of action.

Conflict of interest statement

The authors of this publication declared that there is no conflict of interest.



 
  References Top

1.
Xavier RJ, Podolsky DK. Unravelling the pathogenesis of inflammatory bowel disease. Nature 2007; 448: 427-434.  Back to cited text no. 1
    
2.
Kaplan GG. The global burden of IBD: From 2015 to 2025. Nat Rev Gastroenterol Hepatol 2015; 12: 720-727.  Back to cited text no. 2
    
3.
Benchimol EI, Bernstein CN, Bitton A, Carroll MW, Singh H, Otley AR, et al. Trends in epidemiology of pediatric inflammatory bowel disease in Canada: Distributed network analysis of multiple population-based provincial health administrative databases. Am J Gastroenterol 2017; 112(7): 1120-1134.  Back to cited text no. 3
    
4.
Jiang XL, Lui HF. An analysis of 10218 ulcerative colitis cases in China. World J Gastroenterol 2002; 8(1): 158-161.  Back to cited text no. 4
    
5.
Ekanem EE, Ikobah JM, Ngim OE, Okpara HC. Ulcerative colitis in a Nigerian child: Case report. Niger J Paediatr 2016; 43(4): 291-294.  Back to cited text no. 5
    
6.
Yamada S, Kanazawa Y, Nakamura N, Masutani K, Esaki M, Kitazono T, et al. Ulcerative colitis presented as fever and bloody diarrhea at initiation of dialysis in an elderly patient with end-stage kidney disease. Case Re Med 2015; 2015: 725205.  Back to cited text no. 6
    
7.
Moss AC. Residual inflammation and ulcerative colitis in remission. Gastroen Hepatol 2014; 10(3): 181-183.  Back to cited text no. 7
    
8.
Wilks S. The morbid appearance of the intestine of Miss Banks. Med Times Gazette 1859; 2: 264.  Back to cited text no. 8
    
9.
Tanideh N, Jamshidzadeh A, Sepehrimanesh M, Hosseinzadeh M, Koohi- Hosseinabadi O, Najibi A, et al. Healing acceleration of acetic acid- induced colitis by marigold (Calendula officinalis) in male rats. Saudi J Gastroenterol 2016; 22(1): 50-56.  Back to cited text no. 9
    
10.
Sadraei H, Asghari G, Khanabadi M, Minaiyan M. Anti-inflammatory effect of apigenin and hydroalcoholic extract of Dracocephalum kotschyi on acetic acid-induced colitis in rats. Res Phar Sci 2017; 12(4): 322-329.  Back to cited text no. 10
    
11.
Dileep R, Usharani M, Gopu B, Reddy AG, Kumar MV, Venkat CS, et al. Ameliorative effect of ginger extract in acetic acid induced ulcerative colitis in rats. Asian J Anim Vet Adv 2016; 11: 130-136.  Back to cited text no. 11
    
12.
Kim, JJ, Shajib, MS, Manocha, MM, Khan WI. Investigating intestinal inflammation in DSS-induced model of IBD. J Vis Exp 2012; 60: e3678.  Back to cited text no. 12
    
13.
O' Neill S, Brault J, Stasia MJ, Knaus UG. Genetic disorders coupled to ROS deficiency. Redox Biology 2015; 6: 135-156.  Back to cited text no. 13
    
14.
Feagan BG, MacDonald JK. Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis. Cochrane Database Syst Rev 2012; 10(1): CD000543.  Back to cited text no. 14
    
15.
Wirtz S, Neufert C, Weigmann B, Neurath FM. Chemically induced mouse models of intestinal inflammation. Nature Protocols 2007; 2(3): 541-546.  Back to cited text no. 15
    
16.
Ke F, Yadav PK, Ju LZ. Herbal medicine in the treatment of ulcerative colitis. Saudi J Gastroenterol 2012; 18(1): 3-10.  Back to cited text no. 16
    
17.
Mbata TI. Duru CM, Onwumelu HA. Antibacterial activity of crude seed extracts of Buchholzia coriacea E. on some pathogenic bacteria. J Dev Biol Tissue Eng 2009; 11(1): 1-5.  Back to cited text no. 17
    
18.
Keay RWJ. Trees of Nigeria. London, UK: Claredon Press; 1989, p. 42-44.  Back to cited text no. 18
    
19.
Amaechi NC. Nutritive and anti-nutritive evaluation of wonderful kola (Buchholzia coriace) seeds. Pak J Nutr 2009; 8(8): 1120-1122.  Back to cited text no. 19
    
20.
Adjanohun E, Assi LA. Ivory coast pharmaceutical plants. Ministry of Scientific Research of Côte d’ivoire; 1972, pp.78, 81.  Back to cited text no. 20
    
21.
Burkill, HM. The useful plants of West Tropical Africa, Vol. 1-3. 2nd edition. Richmond, UK: Royal Botanic Gardens, Kew; 1985, p. 319.  Back to cited text no. 21
    
22.
Eze JI, Ekelozie CF, Nweze NE. Immunomodulatory activity of Buchholzia coriacea seed methanol extract on Trypanosoma brucei brucei infected mice. Phar Biol 2016; 55(1): 636-640.  Back to cited text no. 22
    
23.
Ezekiel OO, Onyeoziri NF. Preliminary studies on the antimicrobial properties of Buchholzia coriacea (wonderful kola). Afr J Biotechnol 2009; 8(3): 472-474.  Back to cited text no. 23
    
24.
Nwaehujor CO, Ode OJ, Nwinyi FC, Udeh NE. Effects of methanol extract of Buchholzia coriacea fruit in streptozotocin-induced diabetic rats. J Pharm Toxicol 2012; 7(4): 181-191.  Back to cited text no. 24
    
25.
Owonikoko M, Salami AT, Odukanmi AO, Olaleye SB. Gastric ulcer- healing properties of diets containing seeds of Buccholzia coriacea Englar in rats. Arch Bas App Med 2015; 3: 113-118.  Back to cited text no. 25
    
26.
Jagtap AG, Shirke SS, Phadkef AS. Effect of polyherbal formulation on experimental models of inflammatory bowel disease. J Ethnopharmacol 2004; 90: 195-204.  Back to cited text no. 26
    
27.
Masonobu F, Osamu K, Yoshio A, Akira A, Kehchi M, Kohsuke T, et al. Prebiotic treatment of experimental colitis with germinatedbarley food stuff: A comparison with probiotic or antibiotic treatment. Int J Mol Med 2002; 9: 65-70.  Back to cited text no. 27
    
28.
Dacie, JV, Lewis SM. Practical haematology. 7th edition. UK: ELBS with Churchill Livingstone; 1994, p. 5-82, 160-175.  Back to cited text no. 28
    
29.
Geerling BJ, Dagnelie PC, Badart-Smook A, Russel MG, Stockbrügger RW, Brummer RJ. Diet as a risk factor for the development of ulcerative colitis. Am J Gastroenterol 2000; 95: 1008-1013.  Back to cited text no. 29
    
30.
Larsson JK, Sonestedt E, Ohlsson B, Manjer J, Sjöberg K. The association between the intake of specific dietary components and lifestyle factors and microscopic colitis. Eur J Clin Nutr 2016; 70(11): 1309-1317.  Back to cited text no. 30
    
31.
Kandhare AD, Patil A, Guru A, Mukhrjee A, Sarkar S, Sengupta A, et al. Ameliorative effect of ferulic acid against acetic acid induced ulcerative colitis: Role of HO-1 and Nrf2. Pharmacologia 2016; 7: 114-124.  Back to cited text no. 31
    
32.
Bitar VAL, Laham DRS. Methylsulfonylmethane and green tea extract reduced oxidative stress and inflammation in an ulcerative colitis. Asian J Pharm Clin Res 2013; 6(2): 153-158.  Back to cited text no. 32
    
33.
Harputluoglu MM, Demirel U, Yücel N, Karadag N, Temel I, Firat S, et al. The effects of Gingko biloba extract on acetic acid-induced colitis in rats. Turk J Gastroenterol 2006; 17(3): 177-182.  Back to cited text no. 33
    
34.
McGuinness AJA, Sapey E. Oxidative stress in COPD: Sources, markers, and potential mechanisms. J Clin Med 2017; 6: 21.  Back to cited text no. 34
    
35.
Tian T, Wang Z, Zhang J. Pathomechanisms of oxidative stress in inflammatory bowel disease and potential antioxidant therapies. Oxid Med Cell Longev 2017; 2017(3): 1-18  Back to cited text no. 35
    
36.
Kockerling A, Sorgenfrei D, Fromm M. Electrogenic Na+ absorption of rat distal colon confined to surface epithelium: a voltage-scanning study. Am J Physiol 1993; 264(5 Pt 1): C1285-C1293.  Back to cited text no. 36
    
37.
Gisbert JP, Gomollon F. Common misconceptions in the diagnosis and management of anaemia in inflammatory bowel disease. Ann J Gastroenterol 2008; 103: 1299-1307.  Back to cited text no. 37
    
38.
Serra MB, Barroso WA, da Silva NN, Silva SD, Borges ACR, Abreu IC, et al. From inflammation to current and alternative therapies involved in wound healing. Int J Inflam 2017; 2017(11): 3406215.  Back to cited text no. 38
    


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  2. Materials and...
  In this article
Abstract
1. Introduction
3. Results
4. Discussion
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed95    
    Printed3    
    Emailed0    
    PDF Downloaded17    
    Comments [Add]    

Recommend this journal