- 作者: Li-Man Hung; William Wei; Yi-Jen Hsueh; Wing-Keung Chu; Fu-Chan Wei
- 作者服務機構: Department of Life Science and Plastic and Reconstructive Surgery, College of Medicine, Chang Gung University Chang Gung Memorial Hospital, Taoyuan, Taiwan
- 中文摘要: --
- 英文摘要: Ischemia-reperfusion (I/R) injury is a complex processinvolving the generation and release of inflammatorycytokines, and the accumulation and infiltration of neu-trophils and macrophages, which disturbs the microcir-culatory hemodynamics. Nonetheless, ischemic precon-ditioning (IPC) is known to produce immediate toleranceto subsequent prolonged I/R insults, although its un-derlying mechanism largely remains unknown. Ourstudy investigated the role of the B- -NF- B-TNF- (tu-mor necrosis factor- ) pathway in IPC's ability to amelio-rate I/R-induced microcirculatory disturbances in rat cre-master muscle flaps. Male Sprague-Dawley rats wererandomized (n=8 per group)into 3 groups: a sham-oper-ated control group, an I/R group (4 h of pudic epigastricartery ischemia followed by 2 h of reperfusion), and anIPC+I/R group (3 cycles of 10 min of ischemia followed by10 min reperfusion before I/R). Intravital microscopy wasused to observe leukocyte/endothelial cell interactionsand quantify functional capillaries in cremaster muscles.I/R markedly increased the number of rolling, adhering,and migrating leukocytes. It was also observed that I/Rsignificantly increased TNF- expression in these injuredtissues. On the other hand, IPC prevented I/R-inducedincreases in leukocyte rolling, adhesion, and transmigra-tion. Moreover, TNF- protein production and its mRNAexpression were downregulated in the IPC group. Finally,I/R-induced I B- phosphorylation and NF- B (p65) nu-clear translocation were both suppressed by IPC. Theseresults indicated that IPC attenuated NF- B activationand subsequently reduced TNF- expression, which re-sulted in the amelioration of microcirculatory distur-bances in I/R-injured cremaster muscles.
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- 英文關鍵字: --