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.
Acute kidney injury (AKI) is characterized by a sudden and rapid decline of renal function and associated with high morbidity and mortality. AKI can be caused by various factors, and ischemia-reperfusion injury (IRI) is one of the most common causes of AKI. An increasing number of studies found out that exosomes of mesenchymal stem cells (MSCs) could alleviate IRI-AKI by the adjustment of the immune response, the suppression of oxidative stress, the reduction of cell apoptosis, and the promotion of tissue regeneration. This article summarizes the effect and mechanism of MSC-derived exosomes in the treatment of renal ischemia-reperfusion injury, in order to provide useful information for the researches on this field.
Objective To summarize recent research advancement on gene therapy for hepatic ischemia-reperfusion injury (IRI). Methods Relevant references about basic and clinical researches of hepatic IRI were collected and reviewed. Results Recent experimental researches indicated that the expression of several genes and cytokines could protect hepatic cells by suppressing cell apoptosis, decreasing the production of oxyradical, remaining and improving portal venous flow, promoting bilifaction, self immunoloregulation and decreasing inflammatory reaction, so that it could decrease IRI. Conclusion IRI could be decreased by regulating the expressing of target genes or transducing relative genes in vivo, but the path of gene transfer and the selection and optimization of gene carrier still need more basic and clinical researches to prove.
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 review the research progress of Toll-like receptors （TLRs） signaling and its effects in organ transplantation. Methods The structural and functional features of TLRs and their ligands were summarized，the literatures in recent years about the research progress of TLRs signaling in animal experiment and clinical organ transplantation were reviewed. Results TRLs played an important role in the organ transplantation，the activation of TLRs could activate the specific immune system，and contribute to ischemic reperfusion injury，acute and chronic allograft rejections，and induce the immune tolerance. Early treatment intervention could reduce the activation of TRLs through ischemic reperfusion injury in the organ transplantation，and improve the allograft survival. The efficient immunosuppressive drugs which aimed at the related immunosuppressive target in immune and its signal transduction pathway could reduce ischemic reperfusion injury in the organ transplantation and immune rejection. Conclusions TRLs signaling plays an important role in ischemic reperfusion injury，immune rejection，and immune regulation.
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 study the protective effects of pre-storing glycogen on warm ischemia reperfusion injury during partial hepatectomy. Methods Thirty-eight patients were randomly divided into a trial group (n=19) and a control group (n=19). In the trial group, patients were given high concentration glucose intravenously during the 24 hours before the operation. The hepatic lesion was resected after portal triad clamping in the two groups. Liver function of all patients was measured before the operation and the first and fifth days after the operation. Normal hepatic tissue was biopsied to measured hepatic tissue glycogen contents before the operation and the change of superoxide dismutase (SOD) at the point of pre-ischemia, post-ischemia, and reperfusion 2 hour. Bcl-2 mRNA, a well known anti-apoptotic factor, was also detected using quantitative polymerase chain reaction. Results The hepatic tissue glycogen content of the trial group was significantly higher than that of the control group before the operation (Plt;0.01). Liver function of the trial group was significantly better than that of the control group on the first and fifth day after operation (Plt;0.05). There was significant difference in SOD activity between the two groups at the end of hepatic vascular occlusion and at the point of 2-hour reperfusion (Plt;0.05). Furthermore Bcl-2 mRNA expression of the trial group was notably up-regulated at the point of 2-hour reperfusion compared to the control group. Conclusion Pre-store storing glycogen might protect liver ischemia reperfusion injury caused by hepatic vascular occlusion during partial hepatectomy. The potential mechanism might be that pre-storing glycogen enhances Bcl-2 expression.
Perfusion of free flaps from groin of rabbits, after 12 hours of complete ischemia, with superoxide dismutase (SOD), an oxygen free radical scavenger, would significantly increase the survival rate of these flaps from 18.75% to 75% in the control group. Tissue levels of SOD and malonydialdehyde (MDA, an end product of lipoperoxidation) were measured before ischemia, after ischemia but before reperfusion, and 60 minites after reperfusion. In untreated flap, after 12 hours- ischemia, the SOD content of skin decreased significantly as compared with the SOD content before ischemia, and reperfusion further decreased SOD activity, while the concentration of MDA increased after ischemia and further increased after reperfusion. In the treated flaps, the concentration of SOD was not decrease and MADnot increased after reperfusion. There was a negative correlation between the values of SOD and MDA. These findings suggested that free oxygen radicals playedan important role in the free flap ischemia reperfusion injury. SOD could increase the survival of ischemic free-flaps by reducing lipoperoxidation. The results had significant clinical implications with regard to organ preservation and transplantation.
The present study was to investigate the effects of infusing remifentanil-poly-caprolactone (REM-PCL) through the abdominal aorta on spinal cord ischemia reperfusion injury (SCIRI). The model of SCIRI was created by clamping the infrarenal aortic in thirty-six New Zealand white rabbits, which were randomly divided into sham group (group S), control group (group C), and REM-PCL group (group R) with 12 rabbits in each one. The spinal cord microcirculatory blood flow (SCMBF) and blood flow rate (BFR) were monitored before ischemia, 15 min, 30 min, 60 min and 120 min after reperfusion, respectively. Neurologic Function was evaluated before ischemia, 6h, 12h and 24h after reperfusion. The concentration of serum neuron-specific enolase (NSE), interleukin-lβ (IL-lβ) and interleukin-8 (IL-8) were monitored before ischemia, 45 min after ischemia, 30 min, 60 min, 6 h, 12 h and 24 h after reperfusion. The abnormal rate of motor neuron of spinal cord tissues and the level of superoxide dismutase (SOD), reactive oxygen species (ROS), glutathione peroxidase (GSH-PX), malondialdehyde (MDA), total anti-oxidation capacity (T-AOC) and mitochondrial swelling degree (MSD) in neural mitochondria were determined before ischemia, 45 min after clamping, 60 min and 120 min after reperfusion. As a result, the neural mitochondrial SOD, GSH-PX and T-AOC decreased while ROS, MDA, MSD, IL-lβ, IL-8 and NSE distinctly increased after clamping of the abdominal aorta as compared to the value before ischemia in group C (P < 0.01). Neurologic function scores recovered more rapidly in group R than those in group C during reperfusion (P < 0.01). The neural mitochondrial SOD, GSH-PX and T-AOC were distinctly higher while ROS, MDA, MSD, IL-lβ, IL-8 and NSE were distinctly lower in group R than those in group C (P < 0.01). The abnormal rate of motor neuron was significantly higher in group C during reperfusion than that in group R (P < 0.01). It has been shown that the intra-aortic REM-PCL infusion can alleviate SCIRI by inhibiting inflammatory response and improving mitochondrial anti-oxidation capacity.