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.
ABSTRACT
<p><b>OBJECTIVE</b>To perform a meta-analysis of randomized controlled trials (RCTs) assessing the benefit of providing branched chain amino acid (BCAA)-enriched nutrition to improve hepatic function in patients undergoing hepatic operation.</p><p><b>METHODS</b>The electronic databases of PubMed, Springerlink, the Chinese Biomedical Database (CBM), the Cochrane Library, and the China National Knowledge Infrastructure (CNKI) were searched for relevant RCTs using the following search terms: nutritional support, enteral nutrition, parenteral nutrition, hepatic/liver surgery, liver cirrhosis, cancer, hepatectomy, and liver transplantation. The quality of the retrieved RCTs was assessed according to the scale developed by the Cochrane Collaboration. The meta-analysis was conducted using RevMan software, version 5.2.</p><p><b>RESULTS</b>A total of 11 relevant RCTs, representing 510 patients, were included in the meta-analysis. Compared to patients in the control (normal nutrition) group, the patients in the BCAA group experienced an effective improvement in hepatic function, as evidenced by significant decreases in total bilirubin (by 0.07 mumol/L; 95% confidence interval (CI): -0.18 to 0.05, P more than 0.05]. In addition, the BCAA group showed improvements in plasma levels of albumin (weighted mean difference (WMD) = 0.07; 95% CI: 0.06, 0.24, P less than 0.05) and alanine aminotransferase (WMD = +5.61; 95% CI: -8.63 to 19.86, P more than 0.05] but neither of the changes reached the threshold of a statistically significant improvement. The BCAA group did however show significantly lower complication rate after operation (65%, 95% CI: 0.48, 0.87, P less than 0.01] and mean duration of hospital stay (4.61 days; 95% CI: -6.61, -2.61, P less than 0.01].</p><p><b>CONCLUSION</b>BCAA-enriched nutrition improves hepatic function in patients undergoing hepatic operation, thereby helping to reduce the complication risk, duration of hospital stay, and financial burden. BCAA-enriched nutrition is a safe and effective therapy and further clinical application may be beneficial.</p>
Subject(s)
Humans , Amino Acids, Branched-Chain , Therapeutic Uses , Hepatectomy , Methods , Intraoperative Period , Liver , Physiology , General Surgery , Liver Transplantation , Methods , Nutritional Support , Methods , Randomized Controlled Trials as TopicABSTRACT
Objective To study the effect of glutamine (Gln) on the intestinal mucosa inflammatory reaction and permeability after intestine ischemia-reperfusion injury in rats.Methods The rat model of intestinal ischemia-reperfusion injury was established by clamping the mesenteric superior artery and then restoring blood flow.Forty-eight model rats were divided into control group (n =24) and model + Gln group (n =24)according to the stochastic indicator method.Both groups were given enteral nutrition with equal energy and nitrogen [energy 125.4 kJ/ (kg · d) and nitrogen 0.2 g/ (kg · d)].The model +Gln group was fed with enteral nutrition plus 3％ Gln,while the control group was fed with enteral nutrition plus 3％ soybean protein.The experiment lasted 8 days after modeling.The intestinal mucosa and the plasma levels of nuclear factor-κB (NF-κB),tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6),Gln,D-LACtic acid and diamine oxidase (DAO) were observed in rats before and after modeling and on the 3rb and 8rd day of the experiment.Changes in the morphology of intestinal mucosa were observed by electron microscopy.Results After modeling in control and model + Gln group,the level of NF-κB in intestinal mucosa [18 cases (75.0％) and 17 cases (70.8％)] were significantly higher than those before modeling [0 case (0.0％),P =0.013,P =0.019],the level of IL-6 in intestinal mucosa [(313.27±75.28) pg/g and (321.75±76.46) pg/g] were significantly higher than those before modeling [(227.52 ±58.13) pg/g,P =0.023,P =0.043],and the level of TNF-α in intestinal mucosa [(241.28 ±65.29) pg/g and (240.35 ±64.86) pg/g] were significantly higher than those before modeling [(172.45 ±33.76) pg/g,P=0.036,P=0.011].The plasma level of IL-6 [(150.32 ± 18.74) ng/L and (148.21 ±20.19) ng/L] were significantly higher than those before modeling [(116.37 ± 14.59) ng/L,P =0.032,P =0.025],the plasma level of TNF-α [(127.62 ± 14.24) ng/Land (123.86 ± 13.75) ng/L] were significantly higher than those before modeling [(85.18 ± 8.84) ng/L,P =0.018,P =0.035],and the plasma level of D-LAC [(0.46 ±0.03) mmol/L and (0.51 ±0.04) mmol/L]were significantly higher than those before modeling [(0.27 ±0.02) mmol/L,P =0.041,P =0.018],and the plasma level ofDAO [(2.76±0.57) U/ml and (2.58 ±0.51) U/ml] were significantly higher than those before modeling [(1.52±0.24) U/ml,P=0.015,P=0.037],while the plasma level of Gln [(0.18 ±0.01) g/L and (0.21 ± 0.01) g/L] were significantly lower than those before modeling [(0.39 ± 0.03) g/L,P =0.026,P =0.031].On the 3rd and 8th days of the experiment in the control group,the level of NF-κB in intestinal mucosa [16 cases (66.7％),15 cases (62.5％)] were significantly higher than those before modeling (P =0.027,P =0.002),the level of TNF-α in intestinal mucosa [(226.23 ±55.35) pg/g and (214.76 ±54.82) pg/g] were significantly higher than those before modeling (P=0.042,P =0.038)],the level of IL-6in intestinal mucosa [(297.56 ± 71.39) pg/g and (291.49 ± 68.46) pg/g] were significantly higher than those before modeling (P =0.031,P =0.012).On the 3rd and 8th days in the control group,the plasma level of IL-6[(147.38 ± 17.25) ng/L and (144.65 ± 15.32) ng/L] were significantly higher than those before modeling (P =0.016,P =0.034),the plasma level of TNF-α [(121.75 ± 13.72) ng/L and (113.83 ± 11.69) ng/L] were significantly higher than those before modeling (P =0.025,P =0.041),the plasma level of D-LAC [(0.41 ±0.03) mmol/L and (0.53 ±0.05) mmol/L)] were significantly higher than those before modeling (P =0.029,P =0.030),the plasma level of DAO [(2.51 ± 0.52) U/ml and (1.76 ± 0.34) U/ml] were significantly higher than those before modeling (P =0.034,P =0.016).The plasma level of Gln [(0.22 ±0.01) g/L and (0.21 ±0.03) g/L] were significantly lower than those before modeling (P =0.042,P =0.035).On the 3rd day of the experiment in the model + Gln group,the levels of NF-κB,TNF-α,and IL-6 in intestinal mucosa [14 cases (58.3％),(213.78 ±43.76) pg/g,(293.72 ±69.86) pg/g] were significantly higher than those before modeling (P =0.038,P =0.026,P =0.013) ; the plasma level of IL-6,TNF-α,D-LAC,and DAO [(135.61 ±14.25) ng/L,(117.35 ±11.29) ng/L,(0.45 ±0.03) mmol/L,and (2.26 ± 0.43) U/ml] were significantly higher than those before modeling (P =0.021,P =0.032,P =0.032,P =0.025).On the 8th day of the experiment in the model + Gln group,the levels of NF-κB,TNF-α,and IL-6 in intestinal mucosa [9 cases (37.5％),(184.53 ± 42.16) pg/g,and (236.83 ±66.52) pg/g] were significantly lower than those after modeling and those in the control group (P =0.024,P=0.027; P=0.026,P=0.039; P=0.013,P=0.028) ; the plasma levels of IL-6,TNF-α,D-LAC,and DAO [(126.35±12.74) ng/L,(92.76±9.42) ng/L,(0.31 ±0.02) mmol/L,and (1.76±0.34) U/ml]were significantly lower than those after modeling and those in the control group (P =0.021,P =0.030; P =0.032,P =0.025 ; P =0.024,P =0.037 ; P =0.022,P =0.036) ; the plasma level of Gln [(0.40 ±0.03) g/L] was significantly higher than those after modeling and in the control group (P =0.028,P =0.032).Under the electron microscope,the structure of villus and recess was damaged after modeling,villi were sparse and short,with a lot of inflammatory cell infiltration in the lamina propria.Lymphangiectasia and edema occured after modeling.On the 8th day,compared with after modeling and the control group,intestinal villi and recess structure were significantly restored in the model + Gln group; compared with the after-modeling status,the recovery of intestinal mucosa villi and recess structure was not obvious,and the inflammatory cell infiltration in the lamina propria persisted in the control group.Conclusion Gln repairs ischemia-reperfusion injury in the intestinal mucosa by regulating intestinal mucosa inflammatory cytokine release,inhibitng inflammatory response,and reducing the permeability of the intestinal mucosa.