Objective To study the effect of dexamethasone to protect flaps from an ischemia-reperfusion injury and elucidate its mechanism of regulating the death course of the neutrophils.Methods The rats were randomly divided into 3 groups.The vein of the rat was clamped for 8 h after the flap had formed. Group A: the normal flap; Group B: the saline control flap; Group C: the treatment flap with dexamethasone. The survival area of the flaps was measured at 7 days; the apoptotic and necrotic neutrophils,tumor necrosis factor α （TNF-α）, and interleukin 10 （IL-10） concentrations were measured. Results The flap survival areas in Groups A and C were larger than those in Group B. The apoptotic neutrophils in Group B were fewer than those in Groups A and C on the 1st and 3rd days after operation; however, they were more in number in Group B than in groups A andC on the 6th day. The necrotic cells in Group B were more in number than those in Groups A and C. In Group B, the plasma TNF-α concentration reached the maximum level at 1 h,while the IL-10 level reached the lowest 3 h after the reperfusion. In Group C, the TNF-α concentration was lower than that in Group B and decreased dramatically at 6 h. The IL-10 concentration was the lowest at 1 h, and increased rapidly at 3 h. Thus, ischemia reperfusion could injure the flaps, probably through the abnormal action of the neutrophils, such as the disordered secretion of the cytokines and abnormal death course of the neutrophils. Conclusion Dexamethasone can protect the flap from an ischemia-reperfusion injury by its regulation for the neutrophil function.
Objective To observe the protective role of the ectogenesis zinc on the cells in rat flap with ischemia reperfusion injury and study the mechanisms. Methods A right low abdominal island flap was created in Wistar rats. Fortyeight rats were randomly divded into 3 groups (n=16):the control group, the ischemia reperfusion group and adding zinc ischemia reperfusion group.The content of malondialdehyde(MDA) and the activity of myeloperoxidase(MPO) were measured by thiobarbituric acid methods and colorimetry. The location of expression of MT was observed,and the image analysis was performed. The quantity of MT was represented by the integratial optical density. The ultrastructure changes of skin flap with ischemia reperfusion injury and the flap viability were observed. Results In the ischemia reperfusion injury flaps, the content of MDA and MPO show no statistically significant difference among the control group,IR group and the adding-zinc-IR group (P＞0.05). Compared with the control group at 1 h and 24 h of reperfusion, the level of MDA increased 62.2% and 136.4%(P＜0.01) in the IR group, which increased 11.3% and 33.2%(P＜0.01) in the adding-zinc-IR group. The activity of MPO increased 238.4% and 503.4%(P＜0.01)in the IR group when compared with the control group, and increased 17.9%and 24.1%(P＜0.05) when compared with the adding-zinc-IR group. In the ischemia reperfusion injury falps, the content of MT in the control group and the IR group is too minimal to measure. While the content ofMT in the adding-zinc-IR group is 45.30±7.60. At 1 h and 24 h of reperfusiion, the content of MT in the adding-zinc-IR group increased 41.5% and 44.9% (P＜0.01) compared with the IR group, and increased 119.9% and 234.6% (P＜0.01) compared with the control group. The flap viability is 100% in the control group, 19.65%±4.38% in the IR group, and 24.99%±5.12% in the adding-zinc-IR group, which increased 27.2% (P＜0.05) compared with IR group. Conclusion Many kinds of cells in skin flap with ischemiareperfusion injury can be protected by ectogenesis zinc and the flap viability increases significantly.
Objective To study the effect of Kupffer cell on the liver ischemia/reperfusion injury.Methods The literature in recent years on the liver ischemia/reperfusin injury were reviewed.Results The activated kupffer cell can generate and release a variety of soluble toxic mediators, affect the liver microcirculation directly or indirectly. Conclusion Kupffer cell have important effect on liver ischemia/reperfusion injury.
【摘要】目的探討丹酚酸(Sal)B 配伍丹皮酚對大鼠心肌缺血再灌注損傷(MIRI)的保護作用。方法大鼠心肌缺血60 min 后再灌注90 min 造成大鼠心肌缺血再灌注損傷模型,測定給藥后心肌組織勻漿、血漿中內皮素(ET)、血清中一氧化氮(NO)和一氧化氮合酶(NOS)的變化,并通過病理組織學檢查,觀察Sal B 配伍丹皮酚5、10、15 mg/kg對大鼠MIRI不同濃度和不同給藥方法的治療作用。結果Sa1 B配伍丹皮酚,中、高劑量組均能減少心肌組織和血漿中ET 的含量,提高NOS 的活性,增加NO的釋放(Plt;005)。結論Sal B減輕大鼠MIRI 可能是通過調節ET/NO 系統的平衡,維持冠脈血管張力,改善心肌能量代謝障礙實現的。
【摘要】 目的 通過建立活體大鼠心肌缺血再灌注模型，模擬人類冠心病，研究聚合血紅蛋白（PolyHb）在心肌缺血再灌注中的保護作用，探究PolyHb在冠心病領域中的保護和治療作用。 方法 將45只Sprague-Dawley（SD）大鼠隨機分成3組:實驗組（15只）、對照組（15只）、假手術組（15只），建立大鼠心肌缺血模型。實驗組建立動物模型后，結扎冠狀動脈35 min，并于結扎后5 min，通過SD大鼠尾靜脈按1 mL/min的速度注射1 mL（100 g/L）的PolyHb溶液。缺血完成后開放灌注120 min。對照組建立動物模型，結扎冠狀動脈35 min，并于結扎后5 min，通過SD大鼠尾靜脈按1 mL/min的速度注射1 mL生理鹽水。缺血完成后開放灌注120 min。假手術組僅建立動物模型，但不結扎冠狀動脈，也不再灌注。比較3組SD大鼠的血流動力學參數左室內壓最大上升和下降速率、心肌酶（血清肌酸激酶、乳酸脫氫酶）及病理學檢查（梗死心肌占總心肌面積的百分比），來衡量PolyHb的作用。 結果 與對照組比較，用PolyHb處理的實驗組可增強再灌注時左室內壓最大上升和下降速率（Plt;0.05），減少血液中血清肌酸激酶和乳酸脫氫酶的含量（Plt;0.05），并明顯減少心肌梗死面積百分比（Plt;0.05）。 結論 在心肌缺血的SD大鼠中，PolyHb可以有效的降低缺血再灌注損傷，從而達到心肌保護作用。【Abstract】 Objective To investigate the protective effect of polymerized hemoglobin (PolyHb) for myocardial ischemia-reperfusion and explore the field of polymerized hemoglobin in the protection and treatment of human coronary heart disease, by simulating human coronary heart disease and establishing myocardial ischemia-reperfusion model in living rats. Methods Forty-five Sprague-Dawley (SD) rats were randomly divided into 3 groups: experimental group (n=15), control group (n=15), and sham operation (SHAM) group (n=15). Rat models of myocardial ischemia-reperfusion were established. For the rats in the experimental group, we ligated their left coronary artery for 35 minutes, and injected 1 mL (100 g/L) PolyHb solution into their body at a speed of 1 mL/min 5 minutes later. After ischemia was completed, reperfusion was performed for 120 minutes. The procedures carried out for the rats in the control group were exactly the same except that the PolyHB solution was replaced by 1 mL saline solution. Ligation of the artery and reperfusion were not performed on the rats in the SHAM group. Hemodynamic parameters (maximal rising and falling rates of left ventricular pressure), enzymes (serum creatine kinase, lactate dehydrogenase) and results of histopathologic examinations (percentage of myocardial infarction area over the total myocardial area) were measured and compared among the three groups to evaluate the function of PolyHb. Results Compared with the control group, the experimental group treated with PolyHb had higher maximum rising and falling rates of left ventricular pressure (Plt;0.05), lower blood levels of creatine kinase and lactate dehydrogenase (Plt;0.05), and lower percentage of myocardial infarction area over the total myocardial area (Plt;0.05). Conclusion Polymerized hemoglobin can effectively reduce the ischemia-reperfusion injury and achieve myocardial protection in SD rats with myocardial ischemia.
Objective To investigate the effect of mesenteric lymphatic duct liagtion and glutamine enteral nutrition on intestine and distant organs in intestinal ischemia/reperfusion injury. Methods Forty male SD rats undergoing gastrostomy were randomly assigned into 5 groups (n=8): sham operation group, normal enteral nutrition group, normal enteral nutrition+lymphatic duct ligation group, glutamine group and glutamine+lymphatic duct ligation group. Sham operation group only received laparotomy after 7 days of full diet, the other four groups were subjected to 60 min of intestinal ischemia after 7 days of enteral nutrition, and the two lymphatic duct ligation groups were plus mesenteric lymphatic duct ligation. The original nutrition continued 3 days after reperfusion. Intestinal permeability was detected on day 1 before reperfusion, day 1 and 3 after reperfusion. Intestinal morphology was observed, endotoxin, D-lactate and diamine oxidase levels in serum, and apoptotic index in lung tissue were detected on day 3 after reperfusion. Results The intestinal permeability in each group was significantly increased on day 1 after reperfusion (Plt;0.05), and which in normal enteral nutrition+lymphatic duct ligation group and glutamine+lymphatic duct ligation group were significantly decreased on day 3 after reperfusion (Plt;0.05). The mucosal thickness and villus height of ileum and mucosal thickness of jejunium in glutamine+lymphatic duct ligation group were significantly higher than those in other groups (Plt;0.05), and villus height of ileum in glutamine group was higher than that in normal enteral nutrition group (Plt;0.05); those morphology indexes in normal enteral nutrition+lymphatic duct ligation group were higher than those in normal enteral nutrition group, but there was no statistical signification (Pgt;0.05). Apoptosis index of lung tissue in lymphatic duct ligation groups was significant lower than that in no-ligation groups (Plt;0.05). Levels of endotoxin, D-lactate, and diamine oxidase in lymphatic duct ligation groups had downward trends compared with no-ligation groups, but there was no statistical signification (Pgt;0.05). Conclusions Intestinal ischemia/reperfusion injury of rats can cause intestinal permeability increase, bacterial endotoxin translocation and systemic inflammatory response. Mesenteric lymphatic duct ligation and glutamine enteral nutrition intervention can weak lung tissue damage, increase thickness of intestinal mucosa, maintain intestinal barrier function, reduce endotoxin translocation and attenuate systemic inflammatory response. Enteral nutrition with glutamine was better than normal enteral nutrition.
Objective To summarize the function of Kupffer cell for the ischemia reperfusion injury after liver’s transplatation. Methods The literatures which about the function of Kupffer cell for the ischemia reperfusion injury after liver’s transplatation were reviewed. Results Kupffer cells are the resident macrophages of the liver, which can be activated to generate a range of inflammatory mediators, including cytokines, reactive oxygen intermediates, chemokines, and other factors to startup the ischemia reperfusion injury （IRI）, and to cause the liver graft dysfunction. On the other hand, Kupffer cells can protect the ischemia reperfusion injury by release NO and HO-1. The CO, which is the byproduct of heme degradation by the heme oxygenases （HO-1），has the same function for IRI. Conclusions The Kupffer cells have bidirectional function for the ischemia reperfusion injury of liver’s transpatation. Thus, how to decrease the harmful factors and up-regulate the beneficial substances by Kupffer cells will be the key points in preventing IRI after liver transplantation in future.
Effective neuroprotective strategies are still lacking for cerebral ischemia-reperfusion injury secondary to ischemic stroke and cardiac arrest-cardiopulmonary resuscitation. Growing evidence suggests that adiponectin (APN) and its receptors exert pivotal protective effects in these pathological processes. This article summarizes the underlying mechanisms and translational potential of the APN signaling pathway. Exogenous interventions, including recombinant APN, APN peptides, and gene transfection, exert neuroprotective effects through multiple mechanisms such as anti-inflammatory and antioxidant actions, attenuation of excitotoxicity, and inhibition of apoptosis. Endogenous regulatory strategies, such as exercise preconditioning and pharmacological interventions, can upregulate APN and its receptor expression to mitigate injury. In addition, members of the APN homologous CTRP family exhibit synergistic neuroprotective potential. Integrating evidence from basic and clinical studies, targeting the APN pathway provides a promising therapeutic strategy for cerebral ischemia–reperfusion injury.
