目的研究依达拉奉影响肝脏缺血再灌注过程中TNF-α的表达情况，探讨依达拉奉对肝脏缺血再灌注损伤的逆转作用。 方法将80只Wistar大鼠编号，根据计算机产生随机数字，前40为一组，后40为一组，分为实验组和对照组2组，建立常温下部分肝缺血再灌注损伤动物模型。 在肝脏缺血再灌注损伤开始前1 h和开始时对实验组大鼠给予依达拉奉注射液10 ml，对照组则给予同等容量的生理盐水。分别于再灌注后0、1、2及4 h测定肝脏脂质过氧化物酶（LPO）和肝脏谷草转氨酶(AST) 浓度； 应用RT-PCR法检测肝组织TNF-α mRNA含量，并测定肝组织和血清中TNF-α水平； 应用TUNEL染色法检测缺血肝组织的细胞凋亡情况。结果再灌注后1、2及4 h，实验组大鼠肝脏LPO及AST浓度均明显低于对照组（Plt;0.001）； 实验组再灌注后1 h时肝组织TNF-α mRNA表达量、肝组织和血清TNF-α含量均明显升高且达峰值，但均明显低于对照组（Plt;0.05）； 再灌注后各时相实验组肝细胞凋亡率明显升高，但均明显低于对照组（Plt;0.05）。 结论依达拉奉能抑制氧化应激反应，从而降低肝缺血再灌注损伤； 并显著减少炎性细胞因子TNF-α的产生，抑制炎性反应的发生，减少肝细胞的凋亡。
Objective To investigate the protective effect of the exosome on the organ damage induced by ische-mia-reperfusion (I/R) so as to provide a new way for the treatment of I/R damage. Methods The literature related to the treatment of I/R damage was reviewed and analyzed. Results The exosome volume is small and it is present in blood, cerebrospinal fluid, and urine, which has the function to cross the blood-brain barrier, and protect the heart, brain and other organs after I/R damage. Conclusion Exosome is a new material for the treatment of I/R organ injury, and it is important to understand the protective effect and possible mechanism.
To investigate the effect of propofol intra-aortic and intravenous infusion on the concentration of propofol for an ischemia-reperfusion spinal cord injury in rabbits. Methods Forty-six healthy adult New Zealand white rabbits were randomly divided into 3 groups: sal ine infusion group (group N, n=10), propofol intra-aortic infusion group (group A, n=16) and propofol intravenous infusion group (group V, n=16). The infrarenal abdominal aorta was occluded for 30 min during which propofol 50 mg/kg was infused continuously intra-aortic or intravenous with a pump in group A and V. In group N, the same volume of normal sal ine was infused in the same way and at the same rate as in group A. Upon reperfusion, propofol concentration of the spinal segments of L4-6 and T6-8 was examined in group A and V. At 48 hoursafter reperfusion, the neurological outcomes were recorded in each group. Results Mean blood pressure in group V from the time of 5 minutes after occlusion decreased more than in group N (P lt; 0.05) and than in group A from the time of 10 minutes after occlusion(P lt; 0.05). The mean blood pressure in group N increased more than in group A from 15 minutes after occlusion (P lt; 0.05). The heart rate increased more in group V from 10 minutes after occlusion than in group N and A (P lt; 0.05) in which no difference was observed. The propofol concentration in L4-6 of group A (26 950.5 ± 30 242.3) ng/g was higher than that in T6-8 of group A (3 587.4 ± 2 479.3) ng/g and both L4-6 (3 045.9 ± 2 252.9) ng/g and T6-8 (3 181.1 ± 1 720.9) ng/g of group V(P lt; 0.05). The paraplegia incidence was lower (30%) and the median of normal neurons was higher (8.4) in group A than in group N (80%, 2.2) and group V(100%, 1.9), (P lt; 0.05). There was no significant difference in group N and V in paraplegia incidenceand the median of normal neurons (P gt; 0.05). Conclusion Intra-aortic infusion shows a better neurological outcome than intravenous infusion and could contribute to higher concentration of propofol in the ischemia spinal cord.
To investigate the effect of intracellular glycogen on liver ischemia-reperfusion and its mechanism, histomorphological and enzymological changes, histic ATP contents, the activity of Ca2+-ATPase on cytoplasmic membrane and intracellular free Ca2+concentration were observed during the ischemia-reperfusion of three groups of rabbit livers with different glycogen content. We found that the more vigorous energy metabolism, the higher activity of Ca2+-ATPase, the lower concentration of intracellular free Ca2+ and the slighter injury of histic structure and function appeared in the liver with the more abundant glycogen. The results suggest that intracellular abundant glycogen may reduce liver ischemiareperfusion injury.
【摘要】 目的 研究双侧迷走神经切断对肺缺血再灌注引起的氧化应激反应的影响。 方法 将24只健康雄性新西兰大白兔随机分为:假手术组（S组）、缺血再灌注组（IR组）、双侧迷走神经切断合并缺血再灌注组（NIR组）。缺血前和再灌注末抽取动脉血进行血气分析，观察动脉血氧分压PaO2及肺泡动脉氧分压差（A-aDO2）的变化。再灌注末取肺组织检测肺的湿干重比值（W/D）和氧化应激指标，包括丙二醛（MDA）、超氧化物歧化酶（SOD）及过氧化氢酶（CAT）。 结果 与S组比较，缺血再灌注明显降低了PaO2，增加了A-aDO2和W/D值，增加了肺组织MDA含量并降低了SOD、CAT活性；双侧迷走神经切断进一步降低了SOD活性。 结论 切断实验兔的双侧迷走神经，降低了肺组织抗氧化酶-超氧化物歧化酶的活性，提示迷走神经在降低肺缺血再灌注引起的氧化应激反应中发挥了重要的调节作用。【Abstract】 Objective To evaluate the effect of bilateral vagal nerves transection on lung ischemia-reperfusion induced oxidative stress. Methods A total of 24 New Zealand male rabbits were randomly divided into 3 groups: sham group (S group), ischemia-reperfusion group (IR group), and bilateral vagal nerves transection with ischemia-reperfusion group (NIR group). Before ischemia and at the end of reperfusion, arterial blood samples were collected for blood gas analysis. Arterial partial pressure of oxygen (PaO2) and alveolo-arterial oxygen tension difference (A-aDO2) were detected. At the end of reperfusion, lung tissues were obtained to measure wet/dry weight ratio (W/D). Evaluation of oxidative stress indicators, including content of lung malondialdehyde (MDA), superoxide dismutase enzyme (SOD) and catalase (CAT) activities was also performed. Results Compared with the S group, lung ischemia-reperfusion significantly decreased the PaO2, elevated A-aDO2 and lung W/D weight ratio. At the same time, MDA level in the lung tissue was elevated and SOD and CAT activities were decreased. After bilateral vagal nerves transection, SOD activity was further decreased. Conclusion Transection of bilateral vagal nerves reduced the activity of antioxidant enzyme, especially superoxide dismutase in lung tissue, suggesting that the integrity of the vagal nerves plays an important regulatory role in ischemia-reperfusion mediated oxidative stress in the lung.
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.
OBJECTIVE: To study the hemorheology of island flap after ischemia-reperfusion injury and modulation of dexamethasone. METHODS: Sixty Wister rats were made ischemia-reperfusion injury model, and divided into two groups randomly(Group I: intraperitoneal injection of normal saline 2 ml/kg as control group; Group II: intraperitoneal injection of dexamethasone 5 mg/kg as experimental group). Flap survived areas were measured and neutrophil necrosis numbers in flaps were counted. Erythrocytes and neutrophil hemorheology were observed. RESULTS: Area survived flap in group II was larger than that in group I. Neutrophil necrosis numbers were less in group II than in group I (P lt; 0.05). Whole blood hyposhear viscosity, erythrocyte aggregation, Casson yield stress and nerutrophil adhesion ability were higher in group I than in group II (P lt; 0.05); and the neutrophil deformability was lower in group I than in group II. CONCLUSION: Flap inchemia-reperfusion can increase erythrocyte aggregation index and neutrophil adhesion ability. Dexamethasone can improve these and decrease neutrophil necrosis numbers, so as to prevent flap from ischemia-reperfusion injury.
ObjectiveTo investigate the effect of power-assisted intravascular shunt in replantation of amputated limbs of rabbits. MethodsEighty rabbits weighing 1.8-2.5 kg (male or female) were selected to establ ish the model of circular amputation at the hind groin, only femoral arteries and veins were completely preserved. After the femoral artery was clamped in 60 rabbits, the rabbits underwent power-assisted intravascular shunt with high-flow rate (group A, n=20), powerassisted intravascular shunt with low-flow rate (group B, n=20), and no power-assisted intravascular shunt (group C, n=20) to reconstruct blood supply; the femoral artery was not clamped in another 20 rabbits of sham group (group D). Before and after intravascular shunt (1, 3, 6, and 12 hours), the malondialdehyde (MDA), lactate dehydrogenase (LDH), and creatine kinase (CK) of the serum were determined. The myeloperoxidase (MPO), MDA, and wet to dry weight ratio (W/D ratio) of the gastrocnemius muscle were measured, and the thrombogenesis and survival rate of limb were observed. ResultsBefore intravascular shunt, MDA, LDH, and CK of the serum and MPO, MDA, and W/D ratio of the muscle showed no significant difference among 4 groups (P>0.05). At each time point after intravascular shunt, no significant difference was found in all indexes between groups A and D (P>0.05); the indexes of groups B and C were significantly higher than those of groups A and D (P<0.05); the values were the highest in group C (P<0.05), and reached the peak at 12 hours. All limbs of group A survived with low thrombosis rate, and less limbs could survive with high thrombosis rate in group C. ConclusionThe power-assisted intravascular shunt with high-flow rate can effective ensure the blood supply of the amputated limbs of rabbits with lower limb injury and higher survival rate of amputated limbs after replantation.
Objective To investigate the effects of adenosine 2A receptor (A2AR) activation on oxidative stress in small-forsize liver transplantation. Methods A rat orthotopic liver transplantation model was performed using 40% graft, 18 recipients were given intravenously saline (control group), CGS21680 (A2AR agonist, CGS21680 group) or ZM241385 (A2AR antagonist, CGS21680+ZM241385 group) randomly. Aspartate aminotransferase (AST), enzymatic antioxidants 〔superoxide dismutase (SOD); catalase (CAT); glutathione peroxidase (GSH-Px)〕, non-enzymatic antioxidants 〔ascorbic acid (AA); glutathione (GSH); α-tocopherol (TOC)〕 and lipid oxidant metabolites malondialdehyde (MDA) were measured and analyzed at 6 h after reperfusion. Results Compared with the control group and CGS21680+ZM241385 group, A2AR activation increased the activities of SOD and GSHPx (Plt;0.05), reduced the productions of AST and MDA (Plt;0.05), increased the levels of AA, GSH and TOC (Plt;0.05) in CGS21680 group. But there was no significant change in CAT activity (Pgt;0.05) among 3 groups. Conclusions A2AR activation improves the antioxidant enzyme activities, promotes the production of antioxidants, and slowes down the increase in MDA level, depresses of the increase in AST activity. A2AR activation suppresses oxidative damage and increases the antioxidant capacity which in turn minimizes their harmful effects of ischemia-reperfusion in small-for-size liver transplantation.
Objective To summarize the mechanism and research progress of Kruppel-like factor 2 (KLF2) in various liver diseases and related drug development, providing theoretical basis for further mechanism exploration and clinical application. Method The literatures on the mechanism of KLF2 in liver diseases at home and abroad were collected and summarized. Results KLF2 was widely distributed and had various functions in human body, mainly regulating the growth, differentiation and function of endothelial cells, inhibiting pro-inflammatory and pro-thrombotic gene expression, and participating in important physiological processes such as liver inflammation, oxidative stress and thrombosis, and affecting the occurrence and development of various liver diseases. The regulation of KLF2 expression by statins had been widely used in the treatment of liver diseases. Conclusion KLF2 regulates the expression of related molecules through a variety of pathways and affects the functions of various cells in the liver, which is the focus of research on improving liver injury.