ABSTRACT
Present study aimed to investigate the eff ect of curcumin-pretreatment on intestinal I/R injury and on intestinal mucosa barrier. Thirty Wistar rats were randomly divided into: sham, I/R, and curcumin groups (n=10). Animals in curcumin group were pretreated with curcumin by gastric gavage (200 mg/kg) for 2 days before I/R. Small intestine tissues were prepared for Haematoxylin & Eosin (H&E) staining. Serum diamine oxidase (DAO) and tumor necrosis factor (TNF)-alpha levels were measured. Expression of intestinal TNF-alpha and tight junction protein (ZO-1) proteins was detected by Western blot and/or immunohistochemistry. Serum DAO level and serum and intestinal TNF-alpha leves were signifi cantly increased after I/R, and the values were markedly reduced by curcumin pretreatment although still higher than that of sham group (p<0.05 or p<0.001). H&E staining showed the significant injury to intestinal mucosa following I/R, and curcumin pretreatment signifi cantly improved the histological structure of intestinal mucosa. I/R insult also induced significantly down-regulated expression of ZO-1, and the eff ect was dramatically attenuated by curcumin-pretreatment. Curcumin may protect the intestine from I/R injury through restoration of the epithelial structure, promotion of the recovery of intestinal permeability, as well as enhancement of ZO-1 protein expression, and this eff ect may be partly attributed to the TNF-alpha related pathway.
Subject(s)
Animals , Amine Oxidase (Copper-Containing) , Blotting, Western , Curcumin , Eosine Yellowish-(YS) , Immunohistochemistry , Intestinal Mucosa , Intestine, Small , Intestines , Permeability , Rats, Wistar , Reperfusion Injury , Tight Junctions , Tumor Necrosis Factor-alpha , Zonula Occludens-1 ProteinABSTRACT
Objective To observe the adjuvant therapy efficacy of Saccharomyces boulardii sachets in liver cirrhosis patients with spontaneous bacterial peritonitis(SBP).Methods 72 liver cirrhosis patients with SBP were randomly divided into the observation group and control group.The patients in the control group (30 cases) were giv-en routine medical treatment such as anti-infection,correction of hypoproteinemia,liver protection,and diuresis,etc. At the base of the control group,the patients in the observation group (32 cases) were orally given Saccharomyces boulardii ( Baili Pharmaceutical Factory,French) 0.5g for one time,two times daily for 10 days.The changes of serum interleukin-6(IL-6),pmcalcitonin (PCT) and hypersensitive c-reactive protein (hs-CRP) levels in the two groups were observed and compared before and after treatment, and curative effect and safety were also observed. Results Before treatment,the serum IL-6,PCT and hs-CRP levels in the two groups had no obviously statistical difference(all P>0.05),but after treatment,the serum IL-6,PCT and hs-CRP levels of the observation group were much lower than those of the control group[(60.50 ±19.10) pg/mL vs (98.32 ±17.20) pg/mL,(1.80 ± 0.34)μg/L vs (6.38 ±3.56)μg/L,(6.20 ±4.15) mg/L vs (20.28 ±8.30) mg/L,t=8.147,7.246,8.529,all P0.05).Conclusion Saccharomyces boulardii can significantly reduce serum IL-6,PCT and hs-CRP levels of liver cirrhosis patients with SBP,and reduce inflamma-tion reaction to control development of SBP.
ABSTRACT
Objective To study the role of IL-18 in the pathogenesis and treatment of ulcerative colitis (UC). Method An enzyme-linked immunosorbent assay (ELISA) was utilized to detect the serum IL-18 level of 58 UC patients. Results The serum IL-18 level in acute period of UC patients was significantly higher than that in control ones(P < 0.05 ). There was no significant difference between remisson period of UC and control ones (P> 0.05). The serum IL-18 level was closely related with the degree of UC (P < 0.05),the mean concentration of serum IL-18 was significantly higher in patients with severe ulcerative colitis [ (392.78 ± 50.17)pg/ml]than in patients with mild colitis ulcerative [ (138.92 ± 23.41 )pg/ml]and in control ones. Serum IL-18 in active ulcerative colitis were positively related to clinical disease severity and activity or laboratory parameters,including CAI,serum CRP,erythrocyte sedimentation rates,or total leukocyte counts (r = 0.775,0.705,0.662,0.625,P < 0.01 ). The level of IL-18 was declined after treatment with corticoids(P< 0.05). Conclusions IL-18 might play an important role in the pathogenesis of UC. The measurement of IL-18 is helpful to estimate the disease activity of UC and it may be considered as laboratory and activity criteria for UC.