• Title/Summary/Keyword: TNBS-induced colitis

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Changes of colonic endocrine cells in trinitrobenzene sulfonic acid (TNBS)-induced rat colitis

  • Back, Young-Doo;Lee, Hyeung Sik;Chung, In-Kwon;Cheon, Woo-Hyun;Ku, Sae Kwang
    • Korean Journal of Veterinary Research
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    • v.51 no.2
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    • pp.83-91
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    • 2011
  • In this study, immunohistochemistry was used to examine the changes in the density of colonic endocrine cells - argyrophil and argentaffin cells, chromogranin A (CGA), serotonin, somatostatin and glucagon-containing cells in trinitrobenzene sulfonic acid (TNBS)-induced rat colitis. Ulcerative colitis was induced by the instillation of 10 mg of TNBS into the colonic lumen through the anus. To confirm the inducement of ulcerative colitis, the macroscopic and microscopic scores as well as the colonic myeloperoxidase (MPO) activities were monitored for 8 days after TNBS instillation in the colonic lumens. In addition, the number of argyrophil and argentaffin cells, CGA, serotonin, somatostatin and glucagon-immunoreactive cells were counted in the colonic mucosa, respectively. After TNBS instillation into the lumen of the colon from the anus in rats, increases in macroscopic and microscopic scores in the colon tissues were observed along with increases in the colonic MPO activities. Therefore, ulcerative colitis was relatively well induced by the TNBS instillations. Marked decreases in the number of colonic endocrine cells were detected in the TNBS-treated animal compared to the sham control. These results suggest that colonic endocrine cells were also disrupted by TNBS-induced ulcerative colitis.

Effects of Ginseng Radix herbal acupuncture on TNBS-induced colitis in rats (TNBS 유발 대장염(大腸炎)에 의한 체중 및 혈액상 변화에 대한 인삼(人蔘) 약침(藥鍼)의 효과)

  • Kim Jong-Sung;Chun Sang-Woo;Park Sang-Yeon;Park Sung-Ik;Kim Kyung-Sik;Kim Jae-Hyo;Koo Sung-Tae;Sohn In-Chul
    • Korean Journal of Acupuncture
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    • v.23 no.4
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    • pp.147-156
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    • 2006
  • Objectives : The purpose of the present study is to evaluate the effects of herbal acupuncture with Ginseng Radix for the treatment to intestinal disease in the rat with 2, 4, 6-trinitrobenzenesulfonic acid (TNBS) induced colitis. Methods : All animals were subjected to the injection of saline $(300{\mu}{\ell},\;500{\mu}{\ell})$ for a study control or TNBS $(300{\mu}{\ell},\;500{\mu}{\ell})$ into the lumen of the colon, 8cm proximal to the anus through the intestine. Ginseng Radix herbal acupuncture ($20mg/m{\ell},\;0.4m{\ell}$) were injected to the both $Hapgok(LI_4)$ acupoints at 2nd injection of TNBS in rats. Thus, the body weight, RBC count, WBC count, total protein, IgG levels and IgM levels were observed to study the effects of Ginseng Radix herbal acupuncture. Results : Ginseng Radix herbal acupuncture on $Hapgok(LI_4)$ for TNBS-induced colitis inhibited the body weight loss rate but did not affect RBC and WBC counts. Furthermore, it inhibited the reduction of total protein concentration and serum IgG and IgM levels in TNBS induced colitis were recovered. Conclusions : Herbal acupuncture with Ginseng Radix helps recover the TNBS-induced colonic damage and may be an important method for treatment of the colitis.

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Mechanisms of Motility Change on Trinitrobenzenesulfonic Acid-Induced Colonic Inflammation in Mice

  • Cheon, Gab Jin;Cui, Yuan;Yeon, Dong-Soo;Kwon, Seong-Chun;Park, Byong-Gon
    • The Korean Journal of Physiology and Pharmacology
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    • v.16 no.6
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    • pp.437-446
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    • 2012
  • Ulcerative colitis is an inflammatory bowel disease (IBD) characterized by recurrent episodes of colonic inflammation and tissue degeneration in human or animal models. The contractile force generated by the smooth muscle is significantly attenuated, resulting in altered motility leading to diarrhea or constipation in IBD. The aim of this study is to clarify the altered contractility of circular and longitudinal smooth muscle layers in proximal colon of trinitrobenzen sulfonic acid (TNBS)-induced colitis mouse. Colitis was induced by direct injection of TNBS (120 mg/kg, 50% ethanol) in proximal colon of ICR mouse using a 30 G needle anesthetized with ketamin (50 mg/kg), whereas animals in the control group were injected of 50% ethanol alone. In TNBS-induced colitis, the wall of the proximal colon is diffusely thickened with loss of haustration, and showed mucosal and mucular edema with inflammatory infiltration. The colonic inflammation is significantly induced the reduction of colonic contractile activity including spontaneous contractile activity, depolarization-induced contractility, and muscarinic acetylcholine receptor-mediated contractile response in circular muscle layer compared to the longitudinal muscle layer. The inward rectification of currents, especially, important to $Ca^{2+}$ and $Na^+$ influx-induced depolarization and contraction, was markedly reduced in the TNBS-induced colitis compared to the control. The muscarinic acetylcholine-mediated contractile responses were significantly attenuated in the circular and longitudinal smooth muscle strips induced by the reduction of membrane expression of canonical transient receptor potential (TRPC) channel isoforms from the proximal colon of the TNBS-induced colitis mouse than the control.

A Review on Chemical-Induced Inflammatory Bowel Disease Models in Rodents

  • Randhawa, Puneet Kaur;Singh, Kavinder;Singh, Nirmal;Jaggi, Amteshwar Singh
    • The Korean Journal of Physiology and Pharmacology
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    • v.18 no.4
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    • pp.279-288
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    • 2014
  • Ulcerative colitis and Crohn's disease are a set of chronic, idiopathic, immunological and relapsing inflammatory disorders of the gastrointestinal tract referred to as inflammatory bowel disorder (IBD). Although the etiological factors involved in the perpetuation of IBD remain uncertain, development of various animal models provides new insights to unveil the onset and the progression of IBD. Various chemical-induced colitis models are widely used on laboratory scale. Furthermore, these models closely mimic morphological, histopathological and symptomatical features of human IBD. Among the chemical-induced colitis models, trinitrobenzene sulfonic acid (TNBS)-induced colitis, oxazolone induced-colitis and dextran sulphate sodium (DSS)-induced colitis models are most widely used. TNBS elicits Th-1 driven immune response, whereas oxazolone predominantly exhibits immune response of Th-2 phenotype. DSS-induced colitis model also induces changes in Th-1/Th-2 cytokine profile. The present review discusses the methodology and rationale of using various chemical-induced colitis models for evaluating the pathogenesis of IBD.

Lactobacillus plantarum C29 Alleviates TNBS-Induced Memory Impairment in Mice

  • Lee, Hae-Ji;Jeong, Jin-Ju;Han, Myung Joo;Kim, Dong-Hyun
    • Journal of Microbiology and Biotechnology
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    • v.28 no.1
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    • pp.175-179
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    • 2018
  • In a preliminary study, Lactobacillus plantarum C29 was found to suppress 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in mice. Therefore, to understand whether an anti-colitic probiotic C29 could attenuate memory impairment, we examined the effects of C29 on TNBS-induced memory impairment in mice. Orally administered Lactobacillus plantarum C29 attenuated TNBS-induced memory impairment in mice in the Y-maze, noble object, and passive avoidance task tests. C29 treatment increased TNBS-suppressed hippocampal brain-derived neurotrophic factor expression and inhibited TNBS-induced hippocampal NF-${\kappa}B$ activation and blood LPS levels. Moreover, C29 restored the TNBS-disturbed gut microbiota composition. These findings suggest that C29 can alleviate memory impairment presumably by restoring the gut microbiota composition.

Lactobacillus sakei S1 Improves Colitis Induced by 2,4,6-Trinitrobenzene Sulfonic Acid by the Inhibition of NF-κB Signaling in Mice

  • Jang, Se-Eun;Min, Sung-Won
    • Journal of Microbiology and Biotechnology
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    • v.30 no.1
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    • pp.71-78
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    • 2020
  • Lactobacillus sakei S1 strongly inhibits the expression of interleukin (IL)-6 and IL-1β in lipopolysaccharide-induced peritoneal macrophages by a mechanism for which lactic acid bacteria from kimchi that inhibit tumor necrosis factor-alpha (TNF-α) were isolated. Therefore, we further evaluated the protective effect of this strain on the colitis mouse model induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). TNBS significantly elevated myeloperoxidase (MPO) expression, macroscopic scores, and colon shortening. Oral L. sakei S1 administration resulted in reduction of TNBS-induced loss in body weight, colon shortening, MPO activity, expression of cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-κB). L. sakei S1 inhibited the expression of inflammatory cytokines IL-1β, IL-6 and TNF-α, induced by TNBS, but enhanced IL-10 expression. L. sakei S1 showed resistance to artificial digestive juices and adherence to intestinal epithelial Caco-2 cells. Thus, L. sakei S1 may inhibit the NF-κB pathway and be used in functional food to treat colitis.

Gliotoxin Protects Trinitrobenzene Sulfonic Acid-Induced Colonic Damage through Induction of Heme Oxygenase-1

  • Oh, Jaemin;Hur, Jungmu;Kim, Yourim;Kwon, Young-Mi;Kim, Kyungsuk;Chung, Yeuntai;Choi, Minkyu
    • Toxicological Research
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    • v.20 no.4
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    • pp.293-298
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    • 2004
  • Background: Crohn's disease is characterized by a chronic relapsing inflammation of the bowel. Gliotoxin has been known to play strong immunosuppressive properties, while mechanisms for its anti-inflammatory actions are not completely understood. Here, we investigated the effects of gliotoxin in trinitrobenzene sulfonic acid (TNBS) induced mouse colitis, an animal model of Crohn's disease. Results: Gliotoxin dramatically improved clinical and histopathological symptoms in accompanied with reduced expression of TNF-$\alpha$, IL-1$\beta$, and ICAM-1 protein levels in TNBS induced colitis. Interestingly Gliotoxin induced Heme oxygenase-1 (HO-1) and the HO-1 inducer cobalt protoporphyrin IX (CoPPIX) completely mimicked the protective effects of gliotoxin in TNBS induced colitis mice. In contrast, the HO-1 inhibitor zinc protoporphyrin IX (ZnPPIX) could reverse the anti-inflammatory effects of gliotoxin and CoPPIX. Conclusions: Gliotoxin is a potential therapeutic agent targeting for the treatment of Crohn's disease by inducing HO-1.

Effects of Moxi-tar Herbal Acupuncture at LI4 (HapGok) on TNBS-induced Colitis in Rats (합곡의 구진약침이 흰쥐의 염증성 대장염에 미치는 치료 효과)

  • Song, Jae-Soo;Yang, Beum-Sik;Kim, Sun-Young;Hong, Jeong-A;Song, Jeong-Bang;Kim, Kyung-Sik;Kim, Jae-Hyo;Kwon, Oh-Sang;Sohn, In-Chul
    • Korean Journal of Acupuncture
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    • v.24 no.2
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    • pp.217-230
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    • 2007
  • Objectives : Ulcerative colitis or Crohn's disease has been recognized as Ha-ri (下痢) or Jang-Byok in Korean oriental medicine. A purpose of the present study is to investigate the anti-inflammatory effect of moxi-tar herbal acupuncture at LI4 (HapGok) on 2,4,6-trinitrobenzene sulphonic acid (TNBS) induced colitis in rats and further elucidate the possibility of herbal acupuncture on ulcerative colitis which is chronic inflammatory disease of the gastrointestinal tract. Methods : Sprague-Dawley rats, weighing $170{\sim}190$ g, were subjected to intrarectal injection of either saline (300 ${\mu}l$, 500 ${\mu}l$) for a control or 2,4,6-trinitrobenzene sulphonic acid (TNBS) (300 ${\mu}l$, 500 ${\mu}l$) for a colitis, Moxi-tar (20 mg/ml) were subcutaneously injected to the LI4 just after the secondary injection time of TNBS in rats. To study the effects of Moxi-tar acupuncture in LI4, body weight, RBC count, WBC count, total protein, Paw edema rate, rate of protein leakage into CMC-pouch fluid, IgG levels and IgM levels were observed. Results: Moxi-tar acupuncture in LI4 on TNBS-induced colitis inhibited the body weight lose rate but not effect RBC, WBC count. In addition, it inhibited the reduction of total protein concentration, paw edema, rate of protein leakage into CMC-pouch fluid, IgG levels and IgM levels. Conclusions : It is suggested that moxi-tar herbal acupuncture at LI4 helps to recover TNBS-induced colitis and plays an important role for an treatment of the irritable bowel syndrome (IBS).

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The Preventive and Curative Effect of Cyanidin-3β-D-Glycoside and Its Metabolite Protocatechuic Acid Against TNBS-induced Colitis in Mice

  • Jang, Se-Eun;Choi, Jong-Ryul;Han, Myung Joo;Kim, Dong-Hyun
    • Natural Product Sciences
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    • v.22 no.4
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    • pp.282-286
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    • 2016
  • Cyanidin-$3{\beta}$-D-glycoside (C3G), which is widely distributed in herbal medicines and functional foods, exhibits anti-inflammatory, anti-oxidant, and anti-scratching behavioral effects. Orally administered C3G is metabolized to protocatechuic acid (PA) by gut microbiota. Therefore, we compared the anti-colitic effect of C3G to that of PA in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Orally administered C3G and PA preventively and curatively ameliorated TNBS-induced colitis parameters, including macroscopic colitis score, colon shortening, and increase of myeloperoxidase activity. Treatment with C3G or PA also inhibited the expression of cyclooxygenase-2, inducible NO synthatase, $IL-1{\beta}$, IL-6, and $TNF-{\alpha}$ and the activation of $NF-{\kappa}B$ in the colon of mice with TNBS-induced colitis. Furthermore, these also inhibited lipopolysaccharide-induced $NF-{\kappa}B$ activation and $TNF-{\alpha}$ expression in peritoneal macrophages. The anti-colitic effect of PA was more effective than C3G. Orally administered PA more potently attenuate colitis than C3G by inhibiting $NF-{\kappa}B$ activation and the anti-colitic efficacy of C3G may be dependent on the biotransformation of C3G to PA by gut microbiota.

Lactic Acid Bacteria Isolated from Human Breast Milk Improve Colitis Induced by 2,4,6-Trinitrobenzene Sulfonic Acid by Inhibiting NF-κB Signaling in Mice

  • Kyung-Joo Kim;Suhyun Kyung;Hui Jin;Minju Im;Jae-won Kim;Hyun Su Kim;Se-Eun Jang
    • Journal of Microbiology and Biotechnology
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    • v.33 no.8
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    • pp.1057-1065
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    • 2023
  • Inflammatory bowel disease (IBD), a chronic inflammatory disease, results from dysregulation of the immune responses. Some lactic acid bacteria (LAB), including Lactobacillus, alleviate IBD through immunomodulation. In this study, the anti-colitis effect of LAB isolated from human breast milk was investigated in a mouse model induced acute colitis with 2,4,6-trinitrobenzene sulfonic acid (TNBS). TNBS remarkably increased weight loss, colon shortening, and colonic mucosal proliferation, as well as the expression levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin (IL)-1β. Oral administration of LAB isolated from human breast milk resulted in a reduction in TNBS-induced colon shortening, as well as induced cyclooxygenase (COX)-2, nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-κB). In addition, LAB suppressed inflammatory cytokines such as TNF-α, IL-6, and IL-1β, and thus showed an effect of suppressing the level of inflammation induced by TNBS. Furthermore, LAB alleviated gut microbiota dysbiosis, and inhibited intestinal permeability by increasing the expression of intestinal tight junction protein including ZO-1. Collectively, these results suggest that LAB isolated from human breast milk can be used as a functional food for colitis treatment by regulating NF-κB signaling, gut microbiota and increasing expression of intestinal tight junction protein.