Bovine colostrum prevents bacterial translocation in an intestinal ischemia/reperfusion-injured rat model.
This study evaluated whether or not bovine colostrum (BC) is able to treat or prevent intestinal barrier damage, bacterial translocation, and the related systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) in an intestinal ischemia/reperfusion (I/R)-injured rat model. Fifty Sprague-Dawley rats were used. The rats' intestinal I/R injuries were induced by clamping the superior mesenteric artery for 30 minutes. After 3 hours of reperfusion and then twice daily reclamping during the experiment, the experimental group was given BC (4 mL/kg/day) perorally, and the other groups received 0.9% saline and low fat milk (LFM) after intestinal I/R injury. Seventy-two hours later we assessed (1) intestinal damage and intestinal permeability, (2) enteric bacterial count and bacterial translocation, (3) serum albumin, protein, and hepatic enzyme levels, (4) pathologic findings of ileum and lung, (5) activity of oxygen-free radical species, and (6) pro-inflammatory cytokines (tumor necrosis factor-alpha and interleukin-1beta). Intestinal damage, intestinal permeability, and bacterial translocation to other organs were significantly reduced in rats fed with BC after I/R when compared to rats fed LFM/saline after I/R (P < .05). In the evaluation of acute lung injury, neutrophils were found only in the lungs of the saline-fed group after I/R, and the wet/dry ratio of the lung tissue was significantly reduced in the BC-fed group after I/R compared to other I/R groups. A marked difference was found between LFM/saline-fed groups and BC-fed groups regarding malondialdehyde (P < .05) and pro-inflammatory cytokines (P < .01). In conclusion, BC may have beneficial effects in treating and preventing intestinal barrier damage, bacterial translocation and the related SIRS and MODS in the intestinal I/R-injured rat model.
Choi
Han Sung
HS
Department of Emergency Medicine, Kohwang Medical Research Institute, Kyung Hee University, Seoul, Republic of Korea.
Jung
Kyung Hee
KH
Lee
Seung Chul
SC
Yim
Sung Vin
SV
Chung
Joo-Ho
JH
Kim
Youn Wha
YW
Jeon
Woo Kyu
WK
Hong
Hoon Pyo
HP
Ko
Young Gwan
YG
Kim
Chul-Ho
CH
Jang
Ki-Hyo
KH
Kang
Soon Ah
SA
D000818:Animals; D018988:Bacterial Translocation / Q000502:physiology*; D002417:Cattle; D003126:Colostrum; D004195:Disease Models, Animal; D005260:Female; D053583:Interleukin-1beta / Q000378:metabolism; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007422:Intestines / Q000382:microbiology / Q000473:pathology; D015227:Lipid Peroxidation / Q000502:physiology; D008099:Liver / Q000382:microbiology; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009102:Multiple Organ Failure / Q000517:prevention & control*; D009504:Neutrophils / Q000378:metabolism; D010637:Phenolsulfonphthalein / Q000493:pharmacokinetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism / Q000382:microbiology / Q000473:pathology; D018746:Systemic Inflammatory Response Syndrome / Q000517:prevention & control*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D010637:Phenolsulfonphthalein