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@#To investigate the pharmacodynamic effects and mechanism of Zhuling Jianpi capsule(Zhuling) on 2,4, 6-trinitrobenzene sulfonic acid (TNBS)-induced experimental colitis in rats.The experimental colitis model was established by enema with 2.5% TNBS.The rats were randomly divided into normal group,model group,Changyanning (180 mg/kg) group and Zhuling low-dose (40 mg/kg) group and Zhuling high-dose (120 mg/kg) group.After modeling,the rats were executed after 7 days of drug treatment.During this period,the disease activity status of the rats was observed,and the body weights of the rats were recorded daily.At the end of the experiment,the colonic tissues were obtained for the analysis of the expression of hematoxylin-eosin(HE) staining.The myeloperoxidase (MPO) enzyme activity,mRNA expression levels of inducible nitric oxide synthase (iNOS) and inflammatory cytokines (IL-6, IL-1β, IFN-γ, IL-10) were determined, and the levels of intestinal tight junction proteins and serum inflammatory factor levels were measured.The results showed that compared with model group, the administration of Zhuling significantly alleviated the weight loss and elevated the disease activity index (DAI) caused by TNBS, relieved the shortening, edema and pathological damage of colonic tissue, reduced inflammatory cell infiltration, destruction of crypt and loss of goblet cells, decreased the MPO enzyme activity of colonic tissue, iNOS and pro-inflammatory cytokines in colon, increased the levels of colonic tight junction protein (occludin, ZO-1), and decreased serum levels of inflammatory factors (IL-6,IL-1β).The results suggest that Zhuling administration ameliorates TNBS-induced experimental colitis in rats by decreasing the level of inflammatory factors and increasing the expression of intestinal tight junction proteins.This experiment could provide a theoretical basis for the clinical application of Zhuling.
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AIM: To investigate the effects of manganese superoxide dismutase mimic (MnSODm) on 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) induced ulcerative colitis (UC) in rats and to probe into its underlying mechanism. METHODS: Wistar rats were randomly divided into blank group, model group, sulfasalazine (SASP, 500 mg/kg) group, and different doses of MnSODm (10, 20 and 40 mg/kg) groups. Ulcerative colitis was induced in rats by rectal administration of 100 mg/kg TNBS dissolved in 50% ethanol. Rats were killed after SASP and different doses of MnSODm treatment 7 days. The disease activity index (DAI) was recorded, and then the colonic injury and inflammation were assessed by the colon weight/length ratio and microscopic damage scores. The serum and colon tissues activities myeloperoxidase (MPO) were detected by biochemistry method. The activities of glutathione peroxidase (GSH-Px), inducible nitric oxide synthase (iNOS), and the levels of glutathione (GSH) and NO in colon tissues were also detected. The levels of TNF-α, IL-4 and IL-10 in the colon tissues were measure by ELISA. Western blot was undertaken to determine the phosphorylation levels of AKT and PI3K. RESULTS: Compared with the model group, the colonic weight/length ratios, microscopic damage scores and colon tissues and serum MPO activity were significantly decreased in MnSODm groups (P<0.05 or P<0.01). INOS, NO, TNF-α, PI3K, p-AKT levels in colon tissues were also significantly decreased in MnSODm treatment groups; while the activity of GSH-Px and the concentration of GSH, IL-4 and IL-10 obviously increased (P<0.05, P<0.01). CONCLUSION: MnSODm is protective against colitis via antioxidant activity and by inhibiting inflammatory mediators and then down-regulating PI3K/AKT signaling pathways.
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Objective: To investigate effect of Shaoyaotang on intestinal mucosal immune barrier induced by 2,4,6-trinitrobenzene sulphonic acid (TNBS) in rats with ulcerative colitis.Method: Sixty SD rats were randomly divided into normal group,model group,mesalazine group (0.067 mg·kg-1),low,medium and high-dose Shaoyaotang groups (1.8,3.6,7.2 g·kg-1).In the TNBS-induced ulcerative colitis model,saline,mesalazine,peony soup were administered by gavage for 7 days.Hematoxylin-eosin (HE) staining was used to detect the histopathological changes of colon tissue.The number of CD4+T lymphocytes and the expression of secretory immunoglobulin A (SIgA) in intestinal mucosa were detected by immunohistochemistry and Western blot.Result: Compared with normal group,the scores of intestinal mucosal injury and the pathological scores in model group increased significantly (P+T lymphocytes and SIgA in the intestinal mucosa of model group decreased significantly (PP+T lymphocytes and SIgA in the intestinal mucosa of rats in each group elevated significantly (PPP+T lymphocytes and SIgA protein in the intestinal mucosa of rats in middle and high doses Shaoyaotang groups increased significantly (PConclusion: Shaoyaotang can reduce the intestinal mucosal damage and protect the intestinal mucosal immune barrier by increasing the number of CD4+T cells and the expression of SIgA secretion in the intestinal mucosa.
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Background:As the empirical studies on human body are restricted extremely,the establishment and selection of suitable animal models are important for researches on ulcerative colitis( UC ). Aims:To compare the symptoms and colonic pathology of rat models with experimental colitis induced by dextran sulfate sodium( DSS ) and trinitrobenzene sulfonic acid( TNBS),so as to provide a reference for selecting animal models in UC-related studies. Methods:Drinking 4% DSS freely for 7 days or intrarectal administration of single dose 100 mg/kg TNBS-50% ethanol were used to establish experimental colitis model in Sprague-Dawley rats. The disease activity index( DAI)was assessed dynamically during the course of experiment. The whole colon was removed in batches for measurements of colonic damage score and activity of myeloperoxidase(MPO)at different time points. Results:The DAI score reached the peak at the 7th day and the 2nd day in DSS group and TNBS group,respectively,and decreased gradually afterwards. Six and one deaths occurred during the experimental course in DSS and TNBS groups,respectively. In DSS group,the duration of inflammation was short,the colonic injury was moderate and recovered after drug withdrawal. At the 18th day,the colonic damage score and MPO activity was 0. 25 ± 0. 50 and(0. 80 ± 0. 33)U/g,respectively,and no significant differences were seen between DSS group and normal control group. In TNBS group,the duration of inflammation was longer and the colonic injury was more severe. At the 21st day,the colonic damage score and MPO activity was 3. 60 ± 0. 55 and( 1. 60 ± 0. 39 ) U/g, respectively,and chronic inflammation was observed histologically. Conclusions:Both DSS and TNBS can induce experimental colitis model in rats. The course of TNBS-induced colitis model presents a transformation of acute to chronic inflammation,and may be more suitable for treatment-related studies of UC.
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BACKGROUND:Dendritic cel s can regulate the immunological reaction in the intestinal tract, this functional deficit may induce inflammatory bowel disease. Tol-like receptor-4/nuclear factor-κB pathway is highly involved in this reaction. OBJECTIVE:To establish experimental colitis model in rats, to observe effects of resina draconis on dendritic cel s and Tol-like receptor-4/nuclear factor-κB expression in rats with experimental colitis, and to explore its action mechanism. METHODS:A total of 44 male Sprague-Dawley rats were randomly assigned to four groups (n=11):blank control group, model group, resina draconis group, 5-aminosalicylic acid treatment group. With the exception of blank control group, 2,4,6-trinitrobenzenesulfonic acid-induced ulcerative colitis models were established in the model group, resina draconis group and 5-aminosalicylic acid treatment group. After the models were successful y established, the rats in the resina draconis and 5-aminosalicylic acid treatment groups were intragastrical y treated with resina draconis [(0.75 g(kg·d)] and 5-aminosalicylic acid [100 mg(kg·d)] respectively for 10 days. RESULTS AND CONCLUSION:Disease activity index, macroscopic colonic damage score and histopathological score were significantly decreased in the resina draconis group compared with the model group (P<0.05). Symptoms and tissue damages were obviously lessened in the 5-aminosalicylic acid treatment and resina draconis groups compared with the model group. Expression rates of CD80 and CD86, as wel as expression levels of Tol-like receptor-4 and nuclear factor-κB were significantly higher in the model group compared with the blank control group, resina draconis group and 5-aminosalicylic acid treatment group (P<0.05, P<0.01). Tol-like receptor-4 and nuclear factor-κB expression was significantly lower in the resina draconis group than that in the 5-aminosalicylic acid treatment group. Experimental findings indicate that, resina draconis can partial y relieve experimental colitis symptoms in rats and effectively inhibit the activation of dendritic cel s in the mesenteric lymph node. Resina draconis can relieve enteric inflammatory reaction by suppressing the expression of Tol-like receptor-4 and nuclear factor-κB in rats.
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Objective: To investigate the electrophysiology characteristics of dorsal root ganglion (DRG) neurons in rats with 2, 4, 6-trinitrobenzenesulfonic acid (TNBS)-induced colitis, so as to provide reference for a better understanding of inflammatory bowel disease(IBD). Methods: SD rats(male, 160-200 g)were randomly divided into two groups. Experimental colitis was induced in colitis group (n=5) by intracolonic administration of TNBS (40 mg/kg diluted in 70% ethanol), and control rats (n = 5) received normal saline in the same manner. Rats were sacrificed on the eighth day (acute inflammation phase) after administration of TNBS or normal saline, and the DRG neurons were obtained to investigate its electrophysiology characteristics by the whole-cell patch clamping. Results: The body weight of rats in the experimental group was significantly decreased. H-E staining showed severe damage of the intestinal mucosa glands and inflammatory cell infiltration, indiating successful model creation. The action potential threshold of DRG neurons was significantly decreased in rats with TNBS-induced colitis (P<0. 05). Conclusion: The excitability of DRG neurons is increased in rat model of TNBS-induced colitis.
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Crohn’s disease and Ulcerative colitis were chronic inflammatory disorders of the bowel categorized as inflammatory bowel diseases. Trinitrobenzene sulfonic acid (TNBS)-induced colitis was one of the most common methods for studying inflammatory bowel disease in animal models. Several factors may, however, affect its reproducibility, rate of animal mortality, and macroscopic and histopathological outcomes.The current study was undertaken with the objective to validate the main contributing factors to this method and compare the effects of different reference drugs upon better amelioration of trinitrobenzenesulfonic acid (TNBS) induced colitis. With the above objectives, ulcerative colitis was induced by intrarectal administration of TNBS in male Wistar rats at a dose rate of 20 mg in 0.5 mL of ethanol per animal for all groups except the negative control group, which received 0.5 mL of normal saline. Different reference drugs like dexamethasone (1 mg/kg, intraperitoneally (i.p.) and 2 mg/kg, orally (p.o.)), hydrocortisone acetate (20 mg/kg, i.p.; 20 mg/kg, enema) and sulfasalazine 500mg/kg ,p.o.were administered daily once from Day 3 to 9 except the negative and positive controls which received normal saline at the rate of 10 mL/kg body weight. All the animals were sacrificed on Day 10; the colons were excised and the colon morphology and net weight of the colon segment were graded and measured, respectively. The intestinal damage had improved significantly in the experiment groups that received different reference drugs which is comparable with sulfasalazine treated group. The experimental observations, gross pathology of intestinal lesions and statistical analysis reveals no significant difference among the different reference drugs treated groups.
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Objective To investigate the protective effects and mechanism of Faecalibacterium prausnitzii (Fp) and its products in 2,4,6-trinitrobenzene sulfonic acid (TNBS) induced colitis rats.Methods A total of 40 Sprague-Dawley rats were divided into healthy control group,colitis model group,Fp supernatant group,Fp bacteria group and Bifidobacterium longum (B.longum) group.The rats of the later four groups were enemaed with TNBS to establish the model.At five days before and one day after modeling,the rats were gavaged with phosphate buffer saline (PBS),the supernatant of Fp,live Fp bacteria and live B.longum respectively.Rats were executed at 48 hour after modeling.The colon tissues were taken for pathology examination.The content of short-chain fatty acids (SCFA) in fecal was tested by gas chromatography.The plasma level of interleukin-10 (IL- 10),interleukin-12 ( IL-12),interleukin-17 (IL-17) and interleukin-23 (IL-23) were detected by enzyme-linked immunosorbnent assay (ELISA) and the expression of IL-17 in intestinal mucosal tissues was measured by immunohistochemistry.The data were analyzed by one way ANOVA.Results Compared with the healthy control group,the rats of colitis group suffered serious weight loss and their intestinal pathology score increased [(193.57±14) g vs (170.25±19.18) g,(1.00±0.99) vs (3.34±0.38),t=2.83 and 7.55,all P value＜0.05].The Fp supernatant group showed protective effects in terms of weight and intestinal pathology score [(187.00± 14.67) g,(2.50±0.44),t=2.1 and 2.9,all P＜0.05].Compared with healthy control group,the plasma and colon tissue IL-17 concentration of colitis model group increased (16.61 pg/ml±2.45 pg/ml vs 20.47 pg/ml± 1.45 pg/ml,0.83±0.98 vs 5.14±0.90) (all P＜0.05).Compared with the colitis model group,the plasma and colon tissue IL-17 concentration of Fp supernatant group decreased ( 17.54 pg/ml± 1.51 pg/ml and 2.86±0.69).Conclusion Fp can regulate immune response and suppress rat colonic inflammation,which may be related with the expression of IL-17.
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Objective To screen the difference of gene expression in dorsal root ganglia (DRG)of inflammatory visceral hypersensitivity rats and to explore the role of voltage gated calcium channel (VGCC) in inflammatory visceral hypersensitivity. Methods Total 180 male Sprague-Dawley rats were in this study,the weight varied from 200 gram to 300 gram. 2,4,6-trinitrobenzenesulfonic acid (TNBS) model group was maken by 2. 0% TNBS slowly injection,the dosage was 100mg per kilogram. The normal control group was only injected with same volume of 0. 9% sodium chloride solution. After the model had been maken for four days,gene expression profiles of L6-S2 DRGs were tested by rat cDNA microarray chips. And the result was verified by RT-PCR and Western blot. The changes of intracellular Ca2+ and the voltage gated calcium currents were recorded by patch-clamp.The special Ca2+ channel blockers were given by intrathecal injection,and then the changes of visceral sensitivity were observed. The visceral sensitivity was measured by abdominal withdrawal reflex (AWR). Results There were significant changes of 172 genes expression in L6-S2 DRGs of TNBS model rats,which included Ca2+ channel,membrane receptor and intracellular second messenger. Of those,L-type Ca2+ channel (Cav1. 2) and R-type Ca2+ channel (Cav2. 3) were significantly up-regulated. The results of gene microarray chips were further confirmed by RT-PCR and Western blot.The intracellular Ca2+ testing indicated that there was no statistical significant of resting intracellular Ca2+ in colonic special sensory neuron between TNBS group and normal control group (P＞0. 05);while the evoked transients [Ca2+] significantly increased compared with normal control group (P＜0. 05). The whole cell patch clamp recording showed that the L-type and R-type calcium current were significantly increased in colonic primary sensory neurons of TNBS group compared with normal control group (P＜0. 05). The inflammatory visceral hypersensitivity was significantly reduced by intrathecal injection of nimodipine and SNX-482 (P＜0. 05). Conclusion The up-regulation of Cav1. 2and Cav2. 3 play an important role in inflammatory visceral hyperalgesia,which may be the possible potential therapeutic targets for visceral inflammatory hyperalgesia.
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Objective To investigate the effect of Astragalus polysaccharides (APS) on 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats and on dendritic cells (DCs) in mesenteric lymph nodes.Methods Forty-four male Sprague-Dawley rats were randomly divided into four groups (n = 11) using simple random sampling: normal control group, TNBS group, APS group, and 5-aminosalicylic acid (5-ASA) group.Experimental colitis was induced in rats by TNBS enema in the last three groups.Rats in APS and 5-ASA groups were treated by gavage with APS (0.75 g ? kg-1 ? d-1) and 5-ASA (100 mg ? kg-1 ? d-1) on the 10 consecutive days following TNBS administration.The rats were then sacrificed and the colonic inflammatory scores of rats were measured, including the scores of disease activity index ( DAI) , macroscopic lesions, and histological damages,as well as the activity of myeloperoxidase (MPO).The expressions of major histocompatibility complex class Ⅱ(MHC Ⅱ ) and costimulatory molecule CD86 on DCs were determined by flow cytometry.Results Compared with the TNBS group, APS group had significantly decreased scores of DAI ( P = 0.007 ) , macroscopic lesions (P =0.017), and histological damages (P = 0.016).Moreover, its level of the activity of MPO dropped but without statistical significance (P =0.183).TNBS group had significantly higher expressions of MHC Ⅱand CD86 molecules on DCs than the normal control group (P = 0.005, P = 0.008), APS group (P = 0.023, P = 0.018), and 5-ASA group (P = 0.017, P=0.013).Conclusion APS may attenuate TNBS-induced colitis in rats and downregulate the activation of DCs in mesenteric lymph nodes.
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@#Objective To investigate the effects of Astragalus polysaccarides (APS) on 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats. Methods Forty male Sprague-Dawley rats were randomly divided into five groups (n = 8 ): control group, TNBS group, low-dose APS group, high-dose APS group, and prednisone group. Experimental colitis was induced in rats by enema administration of TNBS. Rats in APS and sions and histological damages were determined, and the activity of myeloperoxidase (MPO) was measured in the excised colonic tissues. Cytokine levels including interleukin (IL)-4 and IL-10 were determined by enzyme-linked immunosorbent assay. Results Both macroscopic lesions and histological colonic damages induced by TNBS were reduced by low-dose APS treatment. These were accompanied by significantly attenuated colonic MPO activity (P = 0. 03) and the increase of IL-4 and IL-10 levels. The macroscopic lesions and MPO activities of high-dose APS group were higher than TNBS group, histological damage and level of IL-4 were lower, and level of IL-10 was higher, but all without statistical significance. Levels of IL-4 and IL-10 were lower than those of TNBS group, but there was no significant difference between prednisone group and TNBS group. Levels of IL-4 and IL-10 were significantly lower in prednisone group than in control group ( P = 0. 049, P = 0. 001 ). Conclusions Different doses of APS have different effects on TNBS-induced colitis. Lower dose of APS has the therapeutic potential inexperimental colitis, while higher dose of APS may aggravate the disease.
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Objective: To study the influence of glucosidorum tripterygii tororum (GTT) and Mesalazine on the expression of IL-23, IL-17 and IL-12 in the colonic tissues of mice with rinitrobenzene sulphonic acid (TNBS)-induced acute colitis, and to study the possible mechanism. Methods: The C57BL/6 mice were divided into 4 groups, namely, a control group, a model group, a Mesalazine group and a GTT group. Colitis was induced by TNBS in the last 3 groups. The mice in the model group received no additional treatment; those in the GTT group received GTT daily by oral gavage 4 days before exposure to TNBS till the end of the experiment, and those in the Mesalazine group received Mesalazine enema solution daily 4 days before exposure till the end of the experiment. All the mice were sacrificed at 48 h after enema with TNBS. The macroscopic and histological scores of colon damage and myeloperoxidase (MPO) activity in colonic tissue were evaluated in every group. IL-23p19 and IL-17 contents in colonic tissues were measured by ELISA; the expression of IL-23p19, IL-17 and IL-12p35 mRNA in colonic tissues were examined by real-time fluorescent quantitative reverse transcriptase polymerase chain reaction (RT-FQ-PCR) with SYBR Green I. Results: Compared with the model group, GTT group and Mesalazine group had significantly lower macroscopic and histological scores and MPO activity (P<0.05). Expression of IL-23p19, IL-17 and IL-12p35 mRNA in the colonic tissues of the model group was significantly higher than that of the other 3 groups(P<0. 05); the expression of IL-23p19, IL-17 protein was significant higher in the model group than that in the other 3 groups (P<0. 05), with no significant difference found between the later 3 groups. Conclusion: GTT, like Mesalazine, can effectively inhibit inflammation in mice with TNBS-induced acute colitis through non-selectively inhibiting the expression of IL-23p19, IL-17 and IL-12p35.
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Objective To evaluate the effect of live combined bifidobacterium, lactobacillus and enterococcus capsules for colitis in rats induced by trinitrobenzenesulfonic acid (TNBS), so as to explore a new therapy for inflammatory bowel diseases (IBD). Methods 50 female adult Sprague-Dawley rats were randomly divided into 5 groups i. e. normal control group(G1) ,untreated TNBS-induced colitis(G2) ,TNBS-induced colitis treated with live combined bifidobacterium, lactobacillus and enterococcus (G3), TNBS-induced colitis treated with olsalazine (G4) and TNBS-induced colitis treated with both live combined bifidobacterium, lactobacillus and enterococcus and olsalazine at the same dose and duration (G5). Each group received its respective treatment. Serum levels of C-reactive protein (CRP), TNFα and IL-10 were measured with ELISA, colonic myeloperoxidase (MPO) activity was determined with spectrophotometric method, histopathologic picture of the colon of each rat was studied with microscope and colonic mucosa damage index(CMDI) was recorded. Results Serum CRP,TNFα,IL-10,CMDI and colonic MPO in G1 were significantly lower than those in G2 (P < 0. 001) with normal colonic architecture. G2 exhibited the most severe colonic inflammation and the highest levels of CRP,TNFα, IL-10, CMDI and colonic MPO with stastical significance. Treatment groups G3, G4 and G5 showed more obvious colonic inflammatory remission and lower levels of serum CRP,TNFα , IL-10 and colonic MPO, G5 being most notable when compared to G2 with stastical significance. In G2, serum levels of CRP, TNFα, IL-10 and colonic MPO activity each correlated positively with CMDI (P < 0. 001). Conclusions Live combined bifidobacterium, lactobacillus and enterococcus can effectively ameliorate colitis in rats induced by TNBS; the underlying mechanism may possibly be associated with the serum levels of cytokines.
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TNF-alpha is a major cytokine involved in inflammatory bowel disease (IBD). In this study, water extract of Grifola frondosa (GFW) was evaluated for its protective effects against colon inflammation through the modulation of TNF-alpha action. In coculture of HT-29 human colon cancer cells with U937 human monocytic cells, TNF-alpha-induced monocyte adhesion to HT-29 cells was significantly suppressed by GFW (10, 50, 100 microg/ml). The reduced adhesion by GFW correlated with the suppressed expression of MCP-1 and IL-8, the major IBD-associated chemokines. In addition, treatment with GFW significantly suppressed TNF-alpha-induced reactive oxygen species production and NF-kappaB transcriptional activity in HT-29 cells. In differentiated U937 monocytic cells, LPS-induced TNF-alpha production, which is known to be mediated through NF-kappaB activation, was significantly suppressed by GFW. In an in vivo rat model of IBD, oral administration of GFW for 5 days (1 g/kg per day) significantly inhibited the trinitrobenzene sulfonic acid (TNBS)-induced weight loss, colon ulceration, myeloperoxidase activity, and TNF-alpha expression in the colon tissue. Moreover, the effect of GFW was similar to that of intra-peritoneal injection of 5-aminosalicylic acid (5-ASA), an active metabolite of sulfasalazine, commonly used drug for the treatment of IBD. The results suggest that GFW ameliorates colon inflammation by suppressing production of TNF-alpha as well as its signaling through NF-kappaB leading to the expression of inflammatory chemokines, MCP-1 and IL-8. Taken together, the results strongly suggest GFW is a valuable medicinal food for IBD treatment, and thus may be used as an alternative medicine for IBD.
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Animals , Humans , Rats , Cell Adhesion/drug effects , Cell Extracts/administration & dosage , Chemokine CCL2/biosynthesis , Coculture Techniques , Colon/drug effects , Grifola , HT29 Cells , Inflammatory Bowel Diseases/chemically induced , Interleukin-8/biosynthesis , Intestinal Mucosa/drug effects , Monocytes/drug effects , NF-kappa B/genetics , Peroxidase/metabolism , Rats, Sprague-Dawley , Reactive Oxygen Species/metabolism , Stomach Ulcer , Transcription, Genetic/drug effects , Trinitrobenzenesulfonic Acid/administration & dosage , Tumor Necrosis Factor-alpha/biosynthesis , U937 Cells , Weight LossABSTRACT
Objective To study the relationship between coagulation abnormal and inflammatory in the TNBS induced rats colitis model as well as the therapeutic effect of heparin on this model Methods Forty SD-rats were separated into 4 groups randomly, including normal control group, colitis group, heparin group and SASP group. PT, APTT and the activity of antithrombin (AT)were chosen as indexs of coagulation. The level of damage ancl inflammatory state of the colitis rats were assessed by macroscopical score, histological score and the level of TNFα in each group. Results Compared with normal control group, TNBS induced colitis group has a shorter PT [(14.83±0.45)s vs(16.68±1.08 )s, P < 0.05] and APTT[(12.49±1.30)s vs(29.06±1.60) s, P<0.05] and a lower activity level of AT [(111.33± 8.50)% vs(122.13±3.52)%,P<0.05]. In heparin group, PT, APTT were prolonged [PT: (17.83± 0.78)s vs (14.83±0.45)s,P<0.05, APTT:(53.34±9.49)s vs (12.49±1.30)s,P<0.05] and AT activity was higher than colitis group [(131.67±6.92)% vs (111.33±8.50) %, P < 0.05]. SASP group has a similar data in PT, APTT compared with colitis group and no statistical significance(P>0.05). The activity of AT in SASP group is higher than in colitis group [(122. 33±5.82)% vs (111.33±8.50)%,P <0.05]. The heparin therapy group showed lower macroscopical score(2.50±0.55 vs 4.75±1.16, P< 0.05), histological scores(3.83±0.41 vs 7.75±1.04, P<0.05) and the level of TNFα[(84.75± 18.03) ng/L vs (149.93±23.52)ng/L, P < 0.05] compared with the colitis group. Conclusion Coagulation was abnormality in the rat colitis model induced by TNBS; heparin therapy is effective in the colitis model It seemed that the abnormality of coagulation plays an important role in the pathogenesis of the rat colitis model.
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Objective To develop a model of inflammatory bowel disease in rats induced by 2,4,6-trinitrobenzenesulfonic acid(TNBS).Methods Fifty Wistar rats were randomly divided into three groups:model,mock model and normal group.2% TNBS,50% ethanol and physiological saline were administered per-rectum to each of the three groups,respectively.Feces,psychosis and appetite were observed,body weight and food eaten were recorded daily.Rats were killed after 3,6 and 14 d,and the colons were isolated and histological findings were examined.Results On the first day,rats in the model group had loose and bloody stools,and the symptoms lasted for about 8 days.Body weight and food eaten were markedly decreased for 7-10 days.Obvious pathological changes in the colon were observed on third day and heavier on sixth day,characterized by mucosal necrosis and transmutable inflammation.In the mock model group,the rats had loose stools on first day,and recovered on second day.Light pathological changes were found on third day.In the normal group,no pathological changes were found in colon.Conclusion Rats treated with TNBS showed obvious characters of inflammatory bowel disease,which could be used as a model in study on etiopathogenesis and evaluation effects of medicines.
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OBJECTIVE: Researching the appropriate methods to separation,purification and detection the mixture of PEG modifier SC-mPEG with BHB.METHODS: Adopting cation-exchange chromatography and organic solvent precipitation to separate the mixture,then detecting it by SDS-PAGE and TNBS methods.RESULTS: Modifer and non-modifer product were separation by cation-exchange chromatography.The average modification rates of two peak product from cation-exchange chromatography are 52.95% and 14.19% detected by TNBS methods.CONCLUSIONS: Cation-exchange chromatography methods could be to separate and purify the SC-mPEG-BHB,TNBS methods coule be to detect the average modification rate of the SC-mPEG-BHB.
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Objective:To study the preventive and therapeutic effects of Acalypha decoction on 2,4,6-trinitrobenzene sulfonic acid induced ulcerative colitis(UC) in rats.Methods: Totally 70 male SD rats were equally randomized into 7 groups, and UC was induced by intrarectal administration of TNBS (125 mg/kg in 50% ethanol). Six hours later the rats were given 3 different doses of Acapha decoction (2.5, 6.5, 9.5 g crude drug/kg body weight) daily for 10 d.Some rats were pretreated with Acalypha decoction (6.5 g crude drug/kg body weight) 3 d before the colitis was induced. Sulfasalazine was used as the standard drug for comparison. The efficacy of Acalypha decoction was assessed through the following parameters: bodyweight loss, diarrhea and bloody stool, macroscopic score,histological changes,and MPO activity in colon tissue. Results: Acalypha decoction treatment(9.5 g/kg, 6.5 g/kg) and prevention administration (6.5 g/kg) significantly inhibited the bodyweight loss and occurrence of diarrhea and rectal bleeding in the rats(P