Evidence suggests that gut microbiota dysbiosis plays a critical role in the initiation and promotion of inflammatory bowel disease (IBD). Kefir is a fermented dairy product including yeast and bacterial species. We aimed to investigate the effect of kefir on trinitrobenzene sulfonic acid (TNBS)‐induced colitis in rats using two different doses. Fifty‐four Wistar rats were divided into six groups. For 14 days, the normal control and colitis control groups were given tap water, kefir10 control, kefir10 colitis, and kefir30 control, and the kefir30 colitis groups were given phosphate‐buffered saline containing 10% or 30% kefir, respectively, instead of tap water. Colitis was induced by intracolonically administrating TNBS in the colitis control, kefir10 colitis, and kefir30 colitis groups. On the 14th day, the rats were sacrificed. The weights and lengths of the colons were measured and macroscopically evaluated, and the distal 10 cm segments were subjected to a histopathological examination. The incidence of bloody stool and diarrhea in the kefir10 colitis group was found to be less than the colitis control and kefir30 colitis groups. The colonic weight/length ratio in the kefir10 colitis group was lower than that in the colitis control and kefir30 colitis groups. We detected that the 10% kefir treatment reduced TNBS‐induced macroscopic colonic damage, while it was exacerbated by the 30% kefir treatment. No significant difference was observed between the colitis groups in terms of microscopic colonic damage scoring. These results indicate that kefir, with a careful dose selection, may be a useful agent in the treatment of IBD.

Kefir reduces the clinical DAI and histologic colitis scores in a DSS-induced colitis model, possibly via reduction of MPO, TNF-α, and iNOS levels.

Doxorubicin (DOX) is a chemotherapeutic agent, and is widely used in cancer treatment. The most common side effect of DOX was indicated on cardiovascular system by experimental studies. There are some studies suggesting oxidative stress-induced toxic changes on liver related to DOX administration. The aim of the present study was to evaluate whether antioxidant N-acetylcysteine (NAC) relieves oxidative stress in DOX- induced liver injury in rat. Twenty-four male rats were equally divided into three groups. First group was used as a control. Second group received single dose of DOX. NAC for 10 days was given to constituting the third group after giving one dose of DOX. After 10 days of the experiment, liver tissues were taken from all animals. Lipid peroxidation (LP) levels were higher in the DOX group than in control whereas LP levels were lower in the DOX+NAC group than in control. Vitamin C and vitamin E levels were lower in the DOX group than in control whereas vitamin C and vitamin E levels were higher in the DOX+NAC group than in the DOX group. Reduced glutathione levels were higher in the DOX+NAC group than in control and DOX group. Glutathione peroxidase, vitamin A and β-carotene values were not changed in the three groups by DOX and NAC administrations. In histopathological evaluation of DOX group, there were mononuclear cell infiltrations, vacuolar degeneration, hepatocytes with basophilic nucleus and sinusoidal dilatations. The findings were totally recovered by NAC administration. In conclusion, N-acetylcysteine induced modulator effects on the doxorubicin-induced hepatoxicity by inhibiting free radical production and supporting the antioxidant vitamin levels.

BACKGROUND: Receptor-binding cancer antigen expressed on SiSo cells (RCAS1) is a novel tumour marker that has been described in various kinds of cancer. The majority of observations include immunohistochemical studies; however, there are not enough data about the utility of this antigen as a serum tumour marker and its tumour specificity. AIM: To measure the serum levels of RCAS1 in patients with gastrointestinal (GI) tract cancers and compare them with other GI tract tumour markers. PATIENTS AND METHODS: Sera collected from patients with GI cancers (14 esophagus, 32 gastric and 36 colon) and from healthy volunteers (30 individuals) were analyzed for RCAS1 and compared with carcinoembryonic antigen (CEA) and cancer antigen 19-9. The relationship between serum RCAS1, tumour stage and tumour grade was also evaluated. RESULTS: Mean serum RCAS1 level was higher in patients with GI tract cancers compared with the control group (P=0.001). Among GI tract cancers, RCAS1 had lowest and highest sensitivity for esophagus and colon cancer diagnosis, respectively. Serum RCAS1 had a higher sensitivity for malignancy, except in the colon, and lower specificity in all groups compared with CEA. In comparison with cancer antigen 19-9, serum RCAS1 was more sensitive but less specific for all GI cancer groups. Mean serum RCAS1 levels were not statistically significant among histopathological tumour types (P>0.05). Although serum RCAS1 levels were significantly higher in cases with lymph node involvement compared with lymph node-negative cases (P=0.009), there was no difference between cases with and without serosal involvement, vascular invasion and distant metastasis; no correlation was found between tumour size and RCAS1 levels. CONCLUSIONS: RCAS1 may be used and combined with CEA as a tumour marker in GI tract cancers.

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