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Chinese Journal of Clinical Nutrition ; (6): 43-48, 2014.
Article in Chinese | WPRIM | ID: wpr-443099

ABSTRACT

Objective To investigate the effect of bifidobacterial adhesin (BA) on nuclear factor of κB (NF-κB) and cytokines of intestinal mucosa of stressed rats.Methods Forty-eight rats were divided into stress group (n =24) and BA group (n =24) using the stochastic indicator method.After the stressed rat models were established withfettering as the stress condition,the experiment lasted 8 days.Both groups were given enteral nutrition (EN) with heat 125.4 kJ/(kg · d) and nitrogen 0.2 g/(kg · d).The BA group was fed with EN plus 5 mg/ (kg · d) bifidobacterial adhesin,and the stress group was fed with EN plus equivalent volume of normal saline [5 mg/ (kg · d)].The levels of NF-κB,interleukin-10 (IL-10),tumor necrosis factor (TNF-α),and interferon-γ (IFN-γ) were measured in both groups before modeling,after modeling,on the 3rd intervention day,and on the 8th intervention day.The changes in the morphology of intestinal mucosal were observed by transmission electron microscopy.Results (1) Expression of NF-κB:The positive expression rate of NF-κB in the intestinal mucosa was 0,79.2%,63.5%,and 66.7% in the control group and 0,68.4%,55.7%,and 45.8% in the BA group before modeling,after modeling,on the 3rd intervention day,and on the 8th intervention day.The expressions of NF-κB in both groups significantly increased after the modeling (both P =0.000).Even on the 3rd and 8th intervention days,the positive expression rates of NF-κB in the intestinal mucosa were still significantly higher than the pre-modeling level (both P =0.000).Compared with the levels after modeling and in the control group,the expression of NF-κB in the intestinal mucosa in the BA group on the 8th intervention day was significantly down-regulated (P =0.015,P =0.021).(2) Quantitative expressions of TNF-α and IFN-γ:Compared with the pre-modeling levels,the intestinal mncosa levels of TNF-α [stressed group:(154.63 ± 17.52) pg/g,(198.72 ±26.59) pg/g; BA group:(154.63 ±17.52) pg/g,(201.45 ±28.16) pg/g],IFN-γ [stressed group:(39.47 ±5.76) pg/g,(55.32 ±5.93) pg/g; BA group:(39.47 ± 5.76),(60.75 ± 7.68) pg/g] and the plasma levels of TNF-α [stressed group:(17.35±2.62) pg/g,(30.56±4.85) ng/L; BA group:(83.31 ±9.78) pg/g,(114.82±13.78) ng/L] and IFN-γ [stressed group:(17.35 ±2.62) pg/g,(28.73 ±4.17) ng/L; BA group:(17.35 ± 2.62) pg/g,(30.56 ± 4.85) ng/L] significantl increased (all P < 0.05).On the 3rd and 8th intervention day,the intestinal mucosa levels of IFN-γ [(58.16 ± 7.38) pg/g,(56.37 ± 7.29) pg/g] and TNF-α [(215.76 ±31.54) pg/g and (211.83 ±33.61) pg/g] and plasma levels of IFN-γ [(29.35 ±4.76) ng/L,(30.25±3.67) ng/L] andTNF-α [(125.71 ±17.38) ng/L,(141.26±19.65) ng/L] in the stressed group were significantly higher than the pre-modeling levels (all P < 0.05).On the 3rd and 8th intervention day,the intestinal mucosa levels of IFN-γ [(165.43 ± 24.58) pg/g,(171.57 ± 26.87) pg/g]and IFN-γ [(42.35 ±4.92) pg/g,(40.58 ±4.65) pg/g] and the plasma levels of TNF-α [(103.96 ±13.68) ng/L,(94.53±12.66) ng/L] and IFN-γ [(20.78±2.84) ng/L,(19.65±2.45) ng/L] in the BA group were significantly lower than the post-modeling levels (all P < 0.05),whereas those of IL (intestinal mucosa:(62.82 ±8.34) pg/g,(75.16 ±9.65) pg/g; plasma:(43.32 ±5.28) ng/L,(55.64 ±6.87) ng/L] were significantly higher than the post-modeling levels (all P < 0.05).Compared with the stressed group,the intestinal mucosa levels of TNF-α and IFN-γand plasma levels of IFN-γ and TNF-α significantly decreased while the IL-10 level significantly increased (all P <0.05) in the BA group.(3) Histomorphology showed that,compared that the ileal mucosal villi and crypt structure were recovered in the BA group on the 8th intervention day.Compared with the post-modeling conditions,the ileal mucosal villi and crypt structure were damaged in the stressed group,showing edema of the lamina propria,in which inflammatory cell infiltration was observed.Conclusions BA is helpful for the repair of the intestinal mucosa injury after stress by regulating the release of inflammatory mediators and cytokines of intestinal mucosa.

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