Protective Effect of Kefir Grain Against Dextran Sodium Sulfate-Induced Colitis in Rats.
- Author:
Young Eun KO
1
;
Mi Kyoung KIM
;
Han Young CHO
;
In Young LEE
;
Sun Yung LY
Author Information
1. Department of Food and Nutrition, Chungnam National University, Daejeon 305-764, Korea. sunly@cnu.ac.kr
- Publication Type:Original Article
- Keywords:
kefir;
DSS-induced colitis;
thiobarbituric acid reactive substances;
DNA fragmentation
- MeSH:
Animals;
Edible Grain;
Colitis;
Colitis, Ulcerative;
Colon;
Cultured Milk Products;
Dextrans;
Diarrhea;
DNA;
DNA Damage;
DNA Fragmentation;
Drinking;
Eating;
Edema;
Feces;
Inflammation;
Lipid Peroxidation;
Lymphocytes;
Mass Screening;
Mucous Membrane;
Peroxidase;
Probiotics;
Rats;
Sodium;
Sulfates;
Thiobarbiturates;
Thiobarbituric Acid Reactive Substances
- From:The Korean Journal of Nutrition
2008;41(5):391-401
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Probiotics have emerged as a potential treatment modality for numerous gastrointestinal disorders, including IBD. However, few probiotics have undergone appropriate preclinical screening in vivo. Kefir is considered a probiotic, benefiting the host through its effects in the intestinal tract. Despite numerous studies examining the action of probiotics on the host organism, few have analyzed the effects on intestinal environment. We assessed the protective effect of kefir for three weeks before inducing colitis with 2% dextran sodium sulfate for five days. The DSS loads were similar in all DSS treatment group. The results of the experiment are as follows. Food intake and FER of experimental groups were not significantly different each other, but water consumption tended to be higher in all DSS treatment groups as compared with the normal control. And visual inspection of feces revealed mild diarrhea in rat given 2% DSS. The anti-inflammatory activity of kefir was determined by myeloperoxidase activity during the DSS treatment, and there was no significant difference in any group. The levels of thiobarbituric acid reactive substances (TBARS) as a colonic lipid peroxidation were significantly lower in the kefir intake groups than in rats treated with 2% DSS alone. The DNA % in tail and tail moment values as a DNA damage level of the blood lymphocytes in kefir intake groups tended to be lower than 2% DSS treatment alone, especially tail lengths were significantly diminished. According to the colonic histopathological assay, there were a severe inflammation of lamina propria and submucosa and mild edema in mucosa and sub mucosa in DSS alone treated group. We found a slight regenerative change in kefir treatment groups. In our experiments, this means that ulcerative colitis related to oxidative injury might be prevented by kefir as a probiotic. Further studies of the potential benefits of kefir as a probiotic in inflammatory condition are encouraged.
