Abstract

Objective To investigate the role of mitochondrial permeability transition pore (mPTP)in ischemic post-conditioning for counteracting small intestinal ischemia-reperfusion(I/ R)injury in rabbits. Methods Forty New Zealand rabbits were randomly divided into sham-operated group(Sham group), I/R group,ischemic post-conditioning group(IPO group), mPTP inhibitor cyclosporine A group(Cs A group), and IPO+ mPTP agonist atraotydin group(IPO+ Atr group).Parts of small intestine tissues were collected from each group of rabbits after intervention for hematoxylin-eosin(HE) staining. Malondialdehyde(MDA) activity in small intestine tissue was measured by the relevant kit.The mitochondria were isolated and mPTP opening was detected by relevant kits.Intestinal mucosal injury was observed by Chiu's grade 6 scoring method.The apoptosis of intestinal epithelial cells was examined by Td T-mediated d UTP nick end labeling(TUNEL) assay. Results As compared with Sham group, mPTP opening in I/R group was significantly increased(3. 53±0. 36 vs. 1. 37±0. 16, P< 0. 05); MDA activity was significantly increased[(0. 98±0. 14) nmol/mg vs. (0. 34±0. 03) nmol/mg, P< 0. 05]; intestinal mucosa score was significantly increased(4. 66± 0. 41 vs.0. 92±0. 58, P< 0. 05); apoptosis index of intestinal cells was significantly increased [(60. 34±6. 02)% vs.(4. 65±1. 68)%, P< 0. 05].As compared with I/R group, mPTP openings in IPO group and Cs A group were significantly decreased(2. 32±0. 23 and 2. 62±0. 18 vs.3. 53± 0. 36, P< 0. 05); MDA activity was significantly decreased[(0. 55±0. 04) and(0. 62±0. 06) nmol/mg vs.(0. 98±0. 14) nmol/mg, P< 0. 05]; intestinal mucosa score was significantly decreased(3. 25±0. 27 and 3. 52±0. 55 vs.4. 66±0. 41, P< 0. 05); apoptosis of intestinal cells was significantly decreased[(28. 33±3. 20)% and(20. 49±4. 10)% vs.(60. 34±6. 02)%, P< 0. 05]. As compared with IPO group, mPTP openings in IPo+ Atr group were significantly increased(2. 32 ±0. 23 vs.1. 05±0. 16, P< 0. 05); MDA activity was significantly increased[(1. 08±0. 18) vs. (0. 55±0. 04) nmol/mg, P< 0. 05]; intestinal mucosa score was significantly increased(4. 57± 0. 32 vs.3. 25±0. 27, P< 0. 05); apoptosis index of intestinal cells was significantly increased [(40. 35±2. 18)% vs.(28. 33±3. 20)%,P< 0. 05]. Conclusion The mechanism of ischemic post-conditioning for counteracting intestinal ischemia-reperfusion injury in rabbits may be associated with the inhibition of mitochondrial permeability transition pore opening. Key words: Mitochondrial permeability transition pore; Ischemic post-conditioning; Intestine ischemia; Reperfusion injury

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