scholarly journals Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

2007 ◽  
Vol 54 (5) ◽  
pp. 366-374 ◽  
Author(s):  
Ke-Xuan Liu ◽  
Timo Rinne ◽  
Wei He ◽  
Fang Wang ◽  
Zhengyuan Xia
Keyword(s):  
Intestinal Mucosa ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion

Effect of N-Acetylserotonin on TLR-4 and MyD88 Expression during Intestinal Ischemia-Reperfusion in a Rat Model

2018 ◽  
Vol 29 (02) ◽  
pp. 188-195 ◽  
Author(s):  
Yoav Ben Shahar ◽  
Salim Halabi ◽  
Nir Bitterman ◽  
Tatiana Dorfman ◽  
Yulia Pollak ◽  
...  
Keyword(s):  
Protein Expression ◽  
Intestinal Mucosa ◽  
Intestinal Ischemia ◽  
Structural Changes ◽  
Ischemia Reperfusion ◽  
Mucosal Injury ◽  
Mucosal Damage ◽  
Sprague Dawley ◽  
Gene And Protein Expression ◽  
Intestinal Ischemia Reperfusion

Background Accumulating evidence indicates that changes in intestinal toll-like receptors (TLRs) precede histological injury in a rodent model of necrotizing enterocolitis. N-acetylserotonin (NAS) is a naturally occurring chemical intermediate in the biosynthesis of melatonin. A recent study has shown that treatment with NAS prevents gut mucosal damage and inhibits programmed cell death following intestinal ischemia-reperfusion (IR). The objective of this study was to determine the effects of NAS on TLR-4, myeloid differentiation factor 88 (Myd88), and TNF-α receptor-associated factor 6 (TRAF6) expression in intestinal mucosa following intestinal IR in a rat. Materials and Methods Male Sprague-Dawley rats were randomly assigned to one of the four experimental groups: 1) Sham rats underwent laparotomy; 2) Sham-NAS rats underwent laparotomy and were treated with intraperitoneal (IP) NAS (20 mg/kg); 3) IR rats underwent occlusion of both superior mesenteric artery and portal vein for 20 minutes followed by 48 hours of reperfusion; and 4) IR-NAS rats underwent IR and were treated with IP NAS immediately before abdominal closure. Intestinal structural changes, mucosal TLR-4, MyD88, and TRAF6 mucosal gene, and protein expression were examined using real-time PCR, Western blot, and immunohistochemistry. Results Significant mucosal damage in IR rats was accompanied by a significant upregulation of TLR-4, MyD88, and TRAF6 gene and protein expression in intestinal mucosa compared with control animals. The administration of NAS decreased the intestinal injury score, inhibited cell apoptosis, and significantly reduced the expression of TLR-4, MyD88, and TRAF6. Conclusion Treatment with NAS is associated with downregulation of TLR-4, MyD88, and TRAF6 expression along with a concomitant decrease in intestinal mucosal injury caused by intestinal IR in a rat.

The Effect ofGinkgo bilobaExtract (EGb 761) Pretreatment on Intestinal Epithelial Apoptosis Induced by Intestinal Ischemia/Reperfusion in Rats: Role of Ceramide

2007 ◽  
Vol 35 (05) ◽  
pp. 805-819 ◽  
Author(s):  
Ke-Xuan Liu ◽  
Wei He ◽  
Timo Rinne ◽  
Ying Liu ◽  
Ming-Qi Zhao ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Mrna Expression ◽  
Intestinal Mucosa ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Intestinal Epithelial ◽  
Egb 761 ◽  
Major Mode ◽  
Intestinal Ischemia Reperfusion ◽  
Ceramide Generation

Apoptosis was demonstrated to be a major mode of intestinal epithelial cell death caused by intestinal ischemia/reperfusion ( II / R ). Ceramide has been proposed as a messenger for apoptosis. The present study was aimed to investigate the effect of Ginkgo biloba extract 761 (EGb 761) pretreatment on II / R -induced intestinal mucosal epithelial apoptosis in rats and the mechanism related to ceramide. The rat model of II / R injury was produced by clamping superior mesenteric artery for 60 min followed by reperfusion for 180 min. Twenty four rats were randomly allocated into Sham, II / R and EGb + II / R groups. In EGb + II / R group, EGb 761 (100 mg/kg per day) was administered intragastrically for 7 days before the surgery. Animals in II / R and sham groups were treated with equal volume of normal saline solution. Intestinal mucosal epithelial apoptosis was detected via electron microscopy and TUNEL method. Lipid peroxidation in intestinal mucosa was determined by detecting the malondialdehyde level and the activities of superoxide dismutase and peroxidase glutathione. The ceramide generation and sphingomyelinase (SMase) mRNA expression in intestinal mucosa were determined by high performance, thin layer chromatography, and RT-PCR, respectively. II / R caused intestinal mucosal epithelial apoptosis and over-production of the ceramide accompanied by up-regulation of SMase mRNA expression and increases of lipid peroxidation. EGb 761 pretreatment significantly decreased apoptosis index, and concurrently reduced the ceramide generation accompanied by down-regulation of SMase expression and inhibition of lipid peroxidation. The findings indicate that EGb 761 pretreatment attenuates II / R -induced intestinal epithelial apoptosis, which might be attributable to its antioxidant action of mediating ceramide pathway.

Treatment with Astragalus membranaceus Produces Antioxidative Effects and Attenuates Intestinal Mucosa Injury Induced by Intestinal Ischemia-Reperfusion in Rats

2011 ◽  
Vol 39 (05) ◽  
pp. 879-887 ◽  
Author(s):  
Rongfa Chen ◽  
Hua Shao ◽  
Shiqing Lin ◽  
Jin-Jun Zhang ◽  
Kang-Qing Xu
Keyword(s):  
Hemorrhagic Shock ◽  
Reperfusion Injury ◽  
Intestinal Mucosa ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Astragalus Membranaceus ◽  
Limb Weakness ◽  
Antioxidative Effects ◽  
Intestinal Ischemia Reperfusion

Astragalus membranaceus, also known as huang qi, a traditional Chinese medicine, is often used in formulas for deficiency of vital energy characterized by limb weakness, pale face, and dizziness. Previous studies have shown that Astragalus membranaceus could attenuate intestinal ischemia-reperfusion injury induced by hemorrhagic shock in rats; however, the underlying mechanism still remains unclear. Using a hemorrhagic shock rat model to examine the effect of Astragalus membranaceus on intestinal mucosa injury induced by ischemia-reperfusion, we found that treatment (20 g crude drugs/kg, i.v.) produced antioxidative effects in the intestinal mucosa of rats after ischemia-reperfusion (p < 0.05). We also found that Astragalus membranaceus could partly attenuate intestinal mucosa ischemia-reperfusion injury (chiu's score, apoptosis index p < 0.05). These results suggest that Astragalus membranaceus reduces intestinal mucosa injury induced by ischemia-reperfusion in rats, at least in part, through its anti-oxidative effects.

scholarly journals INCREASED TRAFFICKING OF MESENTERIC LYMPH-DERIVED γδ T CELLS INTO INTESTINAL MUCOSA IS ASSOCIATED WITH GUT INJURY AFTER INTESTINAL ISCHEMIA-REPERFUSION IN RATS

Lymphology ◽  
2019 ◽  
Vol 52 (2) ◽  
Author(s):  
J Yang ◽  
Y Shen ◽  
RQ Wu ◽  
H Zhu ◽  
Y Jin ◽  
...  
Keyword(s):  
T Cells ◽  
Intestinal Mucosa ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Γδ T Cells ◽  
Intestinal Injury ◽  
Endotoxin Concentration ◽  
Mesenteric Lymph ◽  
Tnf Α ◽  
Intestinal Ischemia Reperfusion

We sought to investigate the effects of mesenteric lymph-derived γδ T cells trafficking into intestinal mucosa on gut injury after intestinal ischemia-reperfusion (IIR). γδ T cells were separated from mesenteric lymph and then infused into the femoral vein of rats after the γδ T cells were labeled with 51Cr. Migration of γδ T cells in vivo across the intestinal mucosa was determined by γ-counter. Meanwhile, TNF-α activity and endotoxin concentration in mesenteric lymph were detected. The population of γδ T cells of Peyer's patches in the small intestines was analyzed by immunofluorescence double staining methods and flow cytometry. After IIR injury, the mean optical density value (MOD) and population of γδ T cells in Peyer's patches of the gut and migration of 51Cr-γδ T cells across the intestinal mucosa were significantly increased, which had highly positive correlations to degree of intestinal injury, TNF-α levels and endotoxin concentration in mesenteric lymph after reperfusion. The increased population of γδ T cells derived from mesenteric lymph trafficking into the intestinal mucosa might promote the small intestinal injury after IIR.

Role of JNK phosphorylation in intestinal ischemia/reperfusion injury in mice

2010 ◽  
Vol 30 (2) ◽  
pp. 140-143
Author(s):  
De-yi ZHENG ◽  
Jian-ming WNAG ◽  
Yi-tao JIA ◽  
Jin-feng FU ◽  
Kai-yang LU ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intestinal Ischemia Reperfusion
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