Eeperimental Study Of Oxiditave Tissue Damage In Rast With Colitis Induced By Trinitro-benzene-sulfonic Acid

Background: In colitis ,iron therapy may be given to treat anemia ,but it may also be detrimiental based on the prvious studies using a rat model with colitis where iron sunpplentation incressed disease activity and oxidative stress. This effect was partially reduced by an antioxidant.Objective:The aim of this study was to further evaluate, in rats with trinitro-benzene-sulfonic acid (TNBS) induced colitis, the effect of ferrous sulfate on neutrophlilic infiltration,cytokines, malondialdeh - yde,superoxide dismutase and nuclear factor kappa-B-associated inflammation.Methods:Totally 60 male SD rats were equally randomized into 6 groups, and UC was induced by intrarectal andmiistration of TNBS(125mg/kg in 50% ethanol).Twelve hours later ,the colitis rats were given three doses of oral iron ferrous fulfate and sodium chloride was used as the standard drug for comparison.The body weight change , reactal bleeding ,colon length,histological, ,the level of malondialdehyd(eMDA),superoxide dismutas(eSOD),myeloperoxidase (MPO), nuclear factor-kappa B(NF-ΚB)and tumor necrosis factor-alpha(TNF-α) in colon tissue and blood were measured to evaluate effect of oral ferrous sulfate supplementation on colonic inflammation in colitis rat . Result: Oral ferrous fulfate supplementation significantly increased the body weight loss and occurrence of diarrhea and rectal bleeding .And in the TNBS+iron group showed a significant MDA ,MPO, NF-ΚB and TNF-αactivity in colon mucosa compared to Sodium Chloride, TNBS or iron.Iron supplementation significantly increased the level of MDA in colitis rat blood and decreased the level of SOD in colon tissue and blood.Conclusin: Oral ferrous fulfate supplementation enhanced the disease activity in the ulcreattive colitis rat model induced by trinitrobenzene sulfonic acid,and this is associated with oxidative stress ,neutrophilic infiltration, increased cytokines and activation of NF-ΚB and TNF-α. Objective:To study the protective mechanism of Salvia miltiorrhiza Bge injecta on 2,4,6-trinitrobenzene sulfonic acid induced ulcerative colitis(UC) in rats.Methods:Totally 40 male SD rats were equally randomized into 4 groups, and UC was induced by intrarectal andmiistration of TNBS(125mg/kg in 50% ethanol).Twelve hours later the rats were given Salvia miltiorrhiza Bge injecta (10g/kg body weight) and sulfasalazine was used as the standard drug for comparison.The protective mechanism of Salvia miltiorrhiza Bge was assessed through the following parameters:body weight loss,diarrhea and bloody stool,macrosopic score,histological changes, expression of nuclear factor-κB(NF-κB) and tumor necrosis factor-а(TNF-а) in colon tissue, myeloperoxidase(MPO) activity in colon tissue, hemocuprein(SOD) activity and the level of malonaldehyde in blood serum and colon tissue.Result: Salvia miltiorrhiza Bge injecta treatment significantly inhibited the body weight loss and occurrence of diarrhea and rectal bleeding in the rats.The MPO acitivity in colon tissue in colon tissue ,expression of NF-κB and TNF-аin colon tissue in colon tissue and level of MDA in blood serum and colon tissue was decreasd and SOD activity in blood serum and colon tissue was increased in treatment rat models.Conclusin: Salvia miltiorrhiza Bge injecta has protective effects on the ulcreattive colitis rat model induced by trinitrobenzene sulfonic acid.The mechanism possibly contributes to their antioxidant function and anti-inflammatory activity.