scholarly journals Effect of Arrabideae chica (crajiru) extract in a model of induced experimental colitis in rats

2021 ◽  
Vol 12 (2) ◽  
pp. 68-76
Author(s):  
Evelynne Silva ◽  
Ítalo Medeiros Azevedo ◽  
Irami Araújo Filho ◽  
Aldo Cunha Medeiros
Keyword(s):  
Experimental Colitis ◽  
Rectal Administration ◽  
Colon Perforation ◽  
Control Group ◽  
Trinitrobenzene Sulfonic Acid ◽  
Colon Tissue ◽  
Colon Wall ◽  
Tnf Α ◽  
Daily Dose ◽  
Underlying Mechanisms

Objective: This study aimed to investigate the effect of A. chica extract on the evolution of experimental rectocolitis in rats, and the expression of the pro-inflammatory cytokines TNF-a, IL-1β and IL-6 in colonic tissue. Methods: Wistar rats weighing 275±23g were distributed into 4 groups of 6 animals each. Rectocolitis was induced in rats by rectal administration of trinitrobenzene sulfonic acid (TNBS). Seventy-two hours after TNBS injection, animals were treated daily for 6 days. Groups: 1. Normal control group without induction of rectocolitis. Received 0.9% saline injection v.o. by gavage during treatment. 2. TNBS rectocolitis group, treated with normal saline (SN) by gavage (TNBS+SN); 3. TNBS rectocolitis group treated with A. chica extract (ACE), receiving a daily dose of 300 mg of A. chica extract by gavage (TNBS+ACE);4. TNBS rectocolitis group treated with mesalazine, receiving a daily dose of 100 mg/kg of mesalazine orally (TNBS+MEZ). Macroscopic examination of the colon and dosing of TNF-α, IL-1β and IL-6 in colon tissue were performed. Results: There was a reduction in weight in animals treated only with TNBS+NS. No difference in weight was observed comparing the animals treated with ACE and MEZ. In the control group no mucosal ulcers or edema of the colon wall were observed. Several mucosal ulcers, edema and hyperemia occurred in the colon of rats in the TNBS+SN group. In two of the animals in this group there was colon perforation, tamponated by omentum. A reduction of mucosal ulcers number in the TNBS+ACE (crajiru) group was seen, compared to the TNBS+SN and TNBS+MEZ group. There was a significant reduction of TNF-α, IL-1β and IL-6 in the colon tissue of animals treated with crajiru extract, TCBS+ACE group, when compared to the control group (p<0.001), TNBS+SN group, and TNBS+MEZ groups (p<0.001). Conclusion: This is the first study to show that A. chica extract positively influences the treatment of TNBS/induced rectocolitis through its antiinflamatory activity. More comprehensive studies are needed to understand the underlying mechanisms.

On the benefit of Teucrium in murine colitis through improvement of toxic inflammatory mediators

2010 ◽  
Vol 29 (4) ◽  
pp. 287-295 ◽  
Author(s):  
Amir Hossein Abdolghaffari ◽  
Amir Baghaei ◽  
Fariborz Moayer ◽  
Hadi Esmaily ◽  
Maryam Baeeri ◽  
...  
Keyword(s):  
Lipid Peroxides ◽  
Experimental Colitis ◽  
Rectal Administration ◽  
Colon Tissue ◽  
Antioxidant Power ◽  
Beneficial Effects ◽  
Tnf Α ◽  
Ferric Reducing Antioxidant Power ◽  
Anti Inflammatory ◽  
Factor Α

Regarding the role of free radicals in pathogenesis of inflammatory bowel disease (IBD), we were interested to investigate the effects of Teucrium persicum with approved antioxidant and anti-inflammatory properties in an experimental model of colitis. Immunologic colitis was induced by rectal administration of a mixture of 2,4,6-trinitrobenzene sulphonic acid (TNBS) and ethanol through rubber cannula into rats. Three different doses of Teucrium (100, 200, and 400 mg/kg) were gavaged in a duration of 10 days to rats. Endpoint markers of colitis included macroscopic and microscopic examination of colon tissue and measuring colonic cells concentrations of tumor necrosis factor-α (TNF-α), interlukin-1β (IL-1β), total antioxidant power as ferric reducing antioxidant power (FRAP), myeloperoxidase (MPO), and lipid peroxidation as thiobarbitoric acid-reactive substance (TBARS). Teucrium at all doses improved both macroscopic and histological damages of rats with colitis. Teucrium reduced colonic MPO activity and concentrations of cellular lipid peroxides, TNF-α, and IL-1β, with a concomitant increase in FRAP value in rats with colitis. It is concluded that beneficial effects of Teucrium in experimental colitis is mediated through its antioxidant and anti-inflammatory potentials. Examination of this herbal medicine in patients with IBD as a supplement would further reveal the potential of Teucrium.

scholarly journals Coix Seed Diet Ameliorates Immune Function Disorders in Experimental Colitis Mice

Nutrients ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 123
Author(s):  
Qilyu Zhou ◽  
Ruyang Yu ◽  
Tianlong Liu ◽  
Yeye Li ◽  
Jia Zhong ◽  
...  
Keyword(s):  
Immune Cell ◽  
Complete Blood Count ◽  
Experimental Colitis ◽  
Positive Control ◽  
Network Pharmacology ◽  
Control Group ◽  
Group Model ◽  
Colon Tissue ◽  
Coix Seed ◽  
Underlying Mechanisms

Coix seed is a functional food in the Chinese diet that possesses the ability to alleviate ulcerative colitis clinically. However, the underlying mechanisms remain ambiguous. In this study, we investigated the protective effect of the Coix seed diet on experimental colitis mice. The mice were randomly divided into four groups: control group, model group, Coix seed feed group, and positive control group. The maintenance feed of the mice was replaced with Coix seed feed 10 days before orally administering the mice 5% (w/v) dextran sulfate sodium drink. As a result, the Coix seed feed alleviated colitis symptoms, maintained the complete blood count at a normal level, reduced the pathological score, relieved inflammatory cytokine secretion, and alleviated oxidative stress. Network pharmacology analysis was used for further exploration of the targets of Coix seed feed. The results showed that T-cell regulation is one of the targets of Coix seed feed, and the analysis of the T-lymphocyte subset and innate immune cell distribution of the colon tissue supported the network pharmacology results. In conclusion, Coix seed, as a staple food, can alleviate experimental colitis, and the mechanism may be related to the immune regulation effect of Coix seeds.

scholarly journals The effect of progesterone in the prevention of the chemically induced experimental colitis in rats

2012 ◽  
Vol 27 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Oguzhan Karatepe ◽  
Merih Altiok ◽  
Muharrem Battal ◽  
Gulcin Kamali ◽  
Ahu Kemik ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Experimental Colitis ◽  
Control Group ◽  
Albino Rats ◽  
Trinitrobenzene Sulfonic Acid ◽  
Colon Tissue ◽  
Chemically Induced ◽  
Group 3 ◽  
Group 2 ◽  
Wistar Albino Rats

PURPOSE: To study the effects of progesterone on an experimental colitis model. METHODS: Wistar albino rats were treated subcutaneously with 2mg/kg once a day during seven days Colitis was induced by intrarectal administration of 5mg trinitrobenzene sulfonic acid (TNBS). Disease activities, macroscopic and microscopic scores were evaluated. To determine the response provoked by progesterone we measured Colonic malondialdehyde (MDA), TNF alfa, IL-6 and Nitric oxide (NO) levels in addition to the MPO (Myeloperoxidase) and caspase-3 activities. RESULTS: Progesterone ameliorated significantly the macroscopic and microscopic scores. TNBS-induced colitis significantly increased the colonic MDA levels and caspase-3 activities in group 2 in comparison to the control group. The results of the study revealed a decline in MDA, NO, IL6 and TNF-α levels in the colon tissue and in blood due to progesterone therapy in group 3 when compared to the group 2, a significant improvement. Progesterone treatment was associated with decreased MDA, MPO, TNF alfa and caspase-3 activity. CONCLUSION: Progesterone therapy decreased oxidative damage in the colonic mucosa.

Thiadiazolidinone-8 Ameliorates Inflammation Associated with Experimental Colitis in Mice

Pharmacology ◽  
2017 ◽  
Vol 101 (1-2) ◽  
pp. 35-42 ◽  
Author(s):  
Vanessa Mateus ◽  
João Rocha ◽  
Paula Alves ◽  
Hélder Mota-Filipe ◽  
Bruno Sepodes ◽  
...  
Keyword(s):  
Glycogen Synthase ◽  
Experimental Colitis ◽  
Trinitrobenzene Sulfonic Acid ◽  
Protective Actions ◽  
Tnf Α ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
Gsk 3Β ◽  
Necrosis Factor

Thiadiazolidinone-8 (TDZD-8) is an effective thiadiazolidinone derivate that is able to suppress the expression of inflammatory cytokines; it also presents tissue protective actions by glycogen synthase kinase (GSK)-3β inhibition, promoting thus an anti-inflammatory effect. Since inflammatory bowel disease is a chronic disease with reduced quality of life, where currently available therapies are only able to induce or maintain the patient in remission, it is crucial to investigate new pharmacological approaches. The main objective of this study was to evaluate the effect of TDZD-8 in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis. Male CD-1 mice with TNBS-induced colitis were treated with a daily dose of TDZD-8 5 mg/kg/day IP during 4 days. The anti-inflammatory properties of TDZD-8 in the TNBS-induced colitis were confirmed by suppression of pro-inflammatory mediators, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β and myeloperoxidase, as well as by the significant increase of the anti-inflammatory cytokine, IL-10. These treated mice also presented a reduction in fecal hemoglobin and alkaline phosphatase, suggesting a beneficial effect of TDZD-8. Furthermore, renal and hepatic biomarkers remained stabilized after treatment. In conclusion, TDZD-8 reduces the inflammatory response associated with TNBS-induced colitis in mice, and modulation of GSK-3β seems to be an interesting pharmacological target in colitis.

scholarly journals The Arp2/3 Inhibitory Protein Arpin Is Required for Intestinal Epithelial Barrier Integrity

2021 ◽  
Vol 9 ◽  
Author(s):  
Sandra Chánez-Paredes ◽  
Armando Montoya-García ◽  
Karla F. Castro-Ochoa ◽  
Julio García-Cordero ◽  
Leticia Cedillo-Barrón ◽  
...  
Keyword(s):  
Protein Complexes ◽  
Experimental Colitis ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Colon Tissue ◽  
Inhibitory Protein ◽  
Α Subunit ◽  
Epithelial Monolayers ◽  
Tnf Α

The intestinal epithelial barrier (IEB) depends on stable interepithelial protein complexes such as tight junctions (TJ), adherens junctions (AJ), and the actin cytoskeleton. During inflammation, the IEB is compromised due to TJ protein internalization and actin remodeling. An important actin regulator is the actin-related protein 2/3 (Arp2/3) complex, which induces actin branching. Activation of Arp2/3 by nucleation-promoting factors is required for the formation of epithelial monolayers, but little is known about the relevance of Arp2/3 inhibition and endogenous Arp2/3 inhibitory proteins for IEB regulation. We found that the recently identified Arp2/3 inhibitory protein arpin was strongly expressed in intestinal epithelial cells. Arpin expression decreased in response to tumor necrosis factor (TNF)α and interferon (IFN)γ treatment, whereas the expression of gadkin and protein interacting with protein C-kinase α-subunit 1 (PICK1), other Arp2/3 inhibitors, remained unchanged. Of note, arpin coprecipitated with the TJ proteins occludin and claudin-1 and the AJ protein E-cadherin. Arpin depletion altered the architecture of both AJ and TJ, increased actin filament content and actomyosin contractility, and significantly increased epithelial permeability, demonstrating that arpin is indeed required for maintaining IEB integrity. During experimental colitis in mice, arpin expression was also decreased. Analyzing colon tissues from ulcerative colitis patients by Western blot, we found different arpin levels with overall no significant changes. However, in acutely inflamed areas, arpin was significantly reduced compared to non-inflamed areas. Importantly, patients receiving mesalazine had significantly higher arpin levels than untreated patients. As arpin depletion (theoretically meaning more active Arp2/3) increased permeability, we wanted to know whether Arp2/3 inhibition would show the opposite. Indeed, the specific Arp2/3 inhibitor CK666 ameliorated TNFα/IFNγ-induced permeability in established Caco-2 monolayers by preventing TJ disruption. CK666 treatment also attenuated colitis development, colon tissue damage, TJ disruption, and permeability in dextran sulphate sodium (DSS)-treated mice. Our results demonstrate that loss of arpin triggers IEB dysfunction during inflammation and that low arpin levels can be considered a novel hallmark of acute inflammation.

scholarly journals Study on the effect of Periplaneta americana on ulcerative colitis in rats induced by 2,4,6-trinitrobenzene sulfonic acid

2020 ◽  
Vol 18 ◽  
pp. 205873922094262
Author(s):  
Yi-Hao Che ◽  
Zhi-Bin Yang ◽  
Han-Chao Zhang ◽  
Xiu-Mei Wu ◽  
Min-Zhe Sun ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Sulfonic Acid ◽  
Periplaneta Americana ◽  
Treated Group ◽  
Normal Control Group ◽  
Control Group ◽  
Trinitrobenzene Sulfonic Acid ◽  
Tnf Α ◽  
Ifn Γ ◽  
Tgf Β1

Ulcerative colitis (UC) is a chronic inflammatory disease of intestinal tract, and Periplaneta americana has been found to be effective in the treatment for UC. The purpose of the study was to investigate the therapeutic effect of Periplaneta americana extract Ento-A on UC in rats induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) and to explore its mechanism. The Sprague-Dawley (SD) rats were randomly divided into normal control group; TNBS-treated group; sulfasalazine (SASP) treated group; Ento-A low- (50 mg/kg), medium- (100 mg/kg), and high-dose (200 mg/kg) groups, respectively. The UC model of rats was induced via TNBS. Disease activity index (DAI) was used to evaluate the severity of UC in rats. The macroscopic and microscopic damages of colon were accessed by colon mucosa damage index (CMDI) and histopathological score (HS), respectively. The levels of interleukin-4 (IL-4), interleukin-17 (IL-17), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) in serum and the contents of myeloperoxidase (MPO), transforming growth factor-β1 (TGF-β1), and epidermal growth factor (EGF) in colonic mucosa were measured by enzyme-linked immunosorbent assay (ELISA). Compared with the normal control group, the TNBS-treated group showed increase in DAI, CMDI, HS, IL-17, TNF-α, IFN-γ as well as MPO and decrease in the levels of IL-4, EGF, and TGF-β1. However, Ento-A-administrated groups reversed the changes in the DAI, CMDI, HS, and the cytokines caused by TNBS. The study indicates that Periplaneta americana extract Ento-A can effectively alleviate the inflammation in TNBS-induced UC of rats, and the mechanism of that may be related to restoring the balance of T helper 1 (Th1)/Th2/Th17/T regulatory (Treg) cytokines.

scholarly journals Boehmeria niveaAttenuates the Development of Dextran Sulfate Sodium-Induced Experimental Colitis

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Eun Ju Shin ◽  
Mi Jeong Sung ◽  
Hye Jeong Yang ◽  
Myung Sunny Kim ◽  
Jin-Taek Hwang
Keyword(s):  
Activity Index ◽  
Disease Activity Index ◽  
Ethanol Extract ◽  
Experimental Colitis ◽  
Control Group ◽  
Untreated Control Group ◽  
Colon Tissue ◽  
Chemotactic Protein ◽  
Cox 2 ◽  
Histopathological Score

We examined the therapeutic effect of an ethanol extract derived fromBoehmeria nivea(Linn.) Gaudich in a mouse model of experimental colitis. Treatment with 70% ethanol extract derived fromB. nivea(EBN) at a dose of 100, 200, or 500 mg/(kg·d) improved colon shortening, body weight, the disease activity index (DAI), and histopathological score of DSS-induced colitis mice. DSS significantly increased the levels of cyclooxygenase-(COX-) 2 in colon tissue relative to that of the untreated control group. EBN administered at 100, 200, or 500 mg/(kg·d) reduced COX-2 levels in the DSS-treated mice. In addition, EBN decreased the DSS-induced secretion of the inflammatory cytokine interleukin-6 (IL-6) and chemokine monocyte chemotactic protein-1 (MCP-1). Taken together, these data suggest thatB. niveaextract is effective in preventing colitis.

scholarly journals Anti-inflammatory effect of elemental diets with different fat composition in experimental colitis

2013 ◽  
Vol 111 (7) ◽  
pp. 1213-1220 ◽  
Author(s):  
E. Papada ◽  
A. C. Kaliora ◽  
A. Gioxari ◽  
A. Papalois ◽  
A. Forbes
Keyword(s):  
Oxidative Stress ◽  
Experimental Colitis ◽  
Rectal Administration ◽  
Intercellular Adhesion Molecule ◽  
Control Group ◽  
Intercellular Adhesion Molecule 1 ◽  
Tissue Samples ◽  
Tnbs Colitis ◽  
Anti Inflammatory ◽  
Gst Activity

The aim of the present study was to evaluate the effectiveness of two isoenergetic elemental formulae with different fat content in the rat model of trinitrobenzene sulphonic acid (TNBS) colitis that mimics human inflammatory bowel disease. A total of forty-five male Wistar rats were assigned to five groups: (1) control group; (2) TNBS-induced colitis group; (3) TNBS-induced colitis group fed a long-chain TAG (LCT)-rich diet; (4) TNBS-induced colitis group fed a medium-chain TAG (MCT)-rich diet; (5) TNBS-induced colitis group fed a baseline diet and administered infliximab. Nutritional management lasted 12 d before and 4 d after rectal administration of TNBS. Subsequently, the rats were killed, and colonic tissue samples were collected for the assessment of histology, inflammation and oxidative stress. The MCT-rich diet decreased IL-6, IL-8 and intercellular adhesion molecule-1 (ICAM-1) levels and glutathione S-transferase (GST) activity, while the LCT-rich diet reduced only ICAM-1 levels and GST activity (P< 0·05). Neither elemental formula affected IL-10 levels. Infliximab reduced IL-8 and ICAM-1 levels and GST activity and increased IL-10 levels (P< 0·05). No significant differences were detected in oxidative stress. Histological damage scores differed significantly only between the control and the TNBS-induced colitis group. A MCT-rich formula seems to exert stronger anti-inflammatory effects than a LCT-rich formula in TNBS colitis.

scholarly journals Effect of Silymarin on Cathepsin Activity and Oxidative Stress in TNBS-induced Colitis in Rats

2019 ◽  
pp. 1-9
Author(s):  
Gokhan Bayramoglu ◽  
Hakan Senturk ◽  
Gungor Kanbak ◽  
Mediha Canbek ◽  
Aysegul Bayramoglu ◽  
...  
Keyword(s):  
Cathepsin L ◽  
Experimental Colitis ◽  
Control Group ◽  
Trinitrobenzene Sulfonic Acid ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Cathepsin Activity ◽  
Bowel Diseases ◽  
Treatment Agent ◽  
Group 2

The purpose of the this study was to defined protective effects of silymarin on the experimental colitis induced by intra-colonic application of 2,4,6-trinitrobenzene sulfonic acid (TNBS).  The twenty eight Sprague-Dawley rats were randomly seperated into four groups, each group containing seven rats represent as follows: group 1 determined as control; group 2 determined as colitis-untreated; group 3 determined as colitis rats administered silymarin (50 mg/kg) and group 4 determined as colitis rats administered silymarin (100 mg/kg). Doses of 50 mg/kg and 100 mg/kg silymarin decreased tissue levels of malondialdehyde (MDA), cathepsin L and cathepsin B and activity of myleperoxidase (MPO) enzyme with respect to the colitis group (p<0.05). Based on the results of the study, it can be said that silymarin can be used as an effective treatment agent in inflammatory bowel diseases.

scholarly journals Sex- and corticotropin-releasing factor receptor 2- dependent actions of urocortin 1 during inflammation

2016 ◽  
Vol 310 (11) ◽  
pp. R1244-R1257 ◽  
Author(s):  
Burcu Hasdemir ◽  
Pallavi Mhaske ◽  
Sreenivasan Paruthiyil ◽  
Elizabeth A. Garnett ◽  
Melvin B. Heyman ◽  
...  
Keyword(s):  
Immune Cell ◽  
Experimental Colitis ◽  
Mapk Signaling ◽  
Corticotropin Releasing Factor ◽  
Receptor Expression ◽  
Trinitrobenzene Sulfonic Acid ◽  
Plasma Extravasation ◽  
Tnf Α ◽  
Urocortin 1 ◽  
Inflammatory Bowel

We investigated whether corticotropin-releasing factor receptor 2 (CRF2) and its high-affinity agonist urocortin 1 (Ucn1) mediate sex-specific signaling and immune responses. Intrarectal trinitrobenzene sulfonic acid was used to induce experimental colitis in wild-type, CRF2 knockout (CRF2KO), and heterozygous (CRF2Ht) mice of both sexes. Changes in plasma extravasation, organ weight, survival, immune cell numbers, inflammatory cytokines, and the MAPK signaling pathway were assessed. Stored intestinal biopsies from patients with Crohn's disease (CD) and age- and sex-matched individuals without inflammatory bowel disease (IBD) were examined by immunofluorescence and confocal microscopy to characterize Ucn1 and CRF receptor expression. CRF2Ht mice of both sexes showed decreased survival during colitis compared with other genotypes. Ucn1 improved survival in male mice alone. Ucn1 restored colon length and spleen and adrenal weight and decreased colonic TNF-α, IL-6, and IL-1β levels in male CRF2Ht mice alone. CRF2Ht mice of both sexes showed decreased phosphorylation of MAPK p38 and heat shock protein 27 (Hsp27) levels. Ucn1 restored p-Hsp27 levels in male CRF2Ht mice alone. Expression of the chaperone protein Hsp90 decreased during colitis, except in male CRF2Ht mice. Taken together, our data indicate that sex shows significant interaction with genotype and Ucn1 during colitis. Human duodenal and colonic biopsies revealed that sex-specific differences exist in levels of CRF receptors and Ucn1 expression in patients with CD compared with the matched non-IBD subjects. To conclude, Ucn1 mediates sex-specific immune and cellular signaling responses via CRF2, emphasizing the need for inclusion of females in preclinical studies.

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