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Objective
This study aimed to investigate the relationship between the severity of ischemia/reperfusion (I/R) injury and the acute rejection (AR) of allogeneic liver transplants in rats.Methods
The experimental rats were divided in different groups: normal control group (sham group, group I); syngeneic liver transplant control group (similar gene group, group II); and allogeneic liver transplant groups (groups III to VI). The rats were humanely killed at 1, 3, 5, and 7 days after transplantation or sham operation to determine the severity of I/R injury, rejection classification, and hepatocyte apoptosis. Messenger RNA (mRNA) and protein expression levels of Fas, perforin, and granzyme B were assessed in the liver tissues using real-time polymerase chain reaction and immunohistochemistry, respectively.Results
The rejection scores of the transplanted liver tissues gradually increased until these scores were proportional to the severity of I/R injury in groups III, IV, and V. The maximum scores were reached at 7 days after transplantation as the duration of transplantation was extended. The mRNA and protein expression levels of Fas, perforin, and granzyme B were significantly increased at 1, 3, 3, 5, and 7 days after liver reperfusion in groups III, IV, and V compared with those in groups I, II, and VI (P < .05).Conclusion
The occurrence of AR after allogeneic liver transplantation in rats was positively correlated with the severity of I/R injury. Given that I/R injury caused serious damage to the transplanted liver, the occurrence of AR consequently decreased. 相似文献3.
Objective
The aim of this study was to investigate the effect of autologous adipose-derived stem cells (ADSCs) on renal cold ischemia and reperfusion (I/R) injury via intravenous infusion on rats.Methods
A renal cold I/R injury rat model was established. Rats were equally randomized into Sham group, Cold I/R group (cold I/R plus culture medium only), and ADSC-treated group (cold I/R plus immediate intrarenal administration of 2 × 106 autologous ADSCs, followed by intravenous autologous ADSCs 6 hours after reperfusion). All rats were killed 24 hours after the I/R procedure.Results
Serum creatinine levels were significantly reduced in the ADSC-treated group compared with the Cold I/R group (P < .01). The renal tissue in the ADSC-treated group had well conserved renal architecture compared with the Cold I/R group. The mRNA expression of tumor necrosis factor α was significantly lower and Bcl-2 was higher in the ADSC-treated group than in the Cold I/R group (P < .05).Conclusions
Autologous ADSC infusions ameliorated renal damage undergoing cold I/R injury and improved the renal function, partly through inhibiting inflammatory reactions and reducing apoptosis. 相似文献4.
Objective
Reperfusion of the rat kidney has been shown to up-regulate cysteinyl leukotriene-1 receptor, an asthma-associated gene in human bronchioles, and increase expression of leukotriene D4. In this study, we aimed to investigate the efficacy of MK-571, a leukotriene D4 inhibitor, against hypersensitivity induced by kidney ischemia and reperfusion (I/R)–associated acute kidney injury.Methods
Sprague-Dawley male rats were divided into 3 study groups: a sham-operated group, a kidney I/R group, and a group treated with MK-571 before the kidney I/R injury: MK-571 (5 mg/kg) was administered intraperitoneally 15 minutes before ischemia and every 12 hours after reperfusion up to 24 hours. Ischemia was conducted by bilateral occlusion of renal pedicles for 45 minutes, followed by releasing the clamps and closing the abdominal incision. Respiratory function was tested 24 hours after reperfusion, with the use of a 2-chamber whole body plethysmograph for conscious rats. Blood samples, pulmonary bronchoalveolar lavage fluid, and lung tissues were collected at the end of study. In 10 rats, urine was collected at baseline and the end of study.Results
Compared with the sham group, kidney I/R injury markedly increased enhanced pause (Penh) index during methacholine challenge test (P < .05), suggesting airway hypersensitivity; it also increased in inflammatory response and levels of hydroxyl radical production and lipid peroxidation in the lungs. In contrast, in MK-571–treated rats, Penh was muted during methacholine challenge test (P < .05).Conclusions
Kidney I/R injury induces airway hypersensitivity to methacholine challenge test and inflammatory response and oxidative stress in the lungs. Treatment with MK-571, a leukotriene D4 inhibitor, effectively attenuates airway hypersensitivity, pulmonary inflammatory response, and lung and kidney injury. 相似文献5.
Pin-Keng Shih Chih-Mei Cheng Hsien-Pin Li Meei-Feng Huang Chia-Wei Chiu Jian-Xun Chen Nai-Wei Chen Shah-Hwa Chou 《The Journal of surgical research》2013
Background
Lung ischemia-reperfusion (I/R) injury plays an important role in lung transplantation. Less well known is the role of sildenafil in lung I/R injury; therefore, we attempted to determine whether sildenafil could alleviate lung apoptosis and tissue injury in a rat model.Methods
Forty male Sprague-Dawley rats were randomized into four groups: saline + sham, saline + I/R, sildenafil + sham, and sildenafil + I/R groups. Three hours before the operation, each rat received normal saline or sildenafil (10 mg/kg) by lavage. The animals designed to I/R injury were subjected to 2 h of ischemia induced by occlusion of left pulmonary artery, veins, and bronchus, followed by reperfusion for 2 h. The lung tissue was harvested for the analysis of the expression of Bax, Bcl-2, p53, caspase 3, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and wet/dry (W/D) weight ratio.Results
Compared with the saline + sham group, the saline + I/R group had significant increases in Bax, p53, Bax/Bcl-2 ratio, caspase 3, IL-6, TNF-α, and W/D weight ratio but a decrease in Bcl-2 (P < 0.05). Compared with the saline + I/R group, sildenafil + I/R group had significant decreases in Bax, p53, Bax/Bcl-2 ratio, caspase 3, IL-6, TNF-α level, and W/D weight ratio but an increase in Bcl-2 expression (P < 0.05). Compared with the sildenafil + sham group, there were significant increases in p53 and TNF-α expression in the sildenafil + I/R group (P < 0.05).Conclusions
Pretreatment with sildenafil alleviates lung apoptosis and tissue injury in a rat model. 相似文献6.
Mu-qing Yang Yuan-yuan Ma Shao-fu Tao Jing Ding Long-hua Rao Hong Jiang Ji-yu Li 《The Journal of surgical research》2014
Background
Mast cells (MCs) play a role in ischemia–reperfusion (I/R) injury in many organs. However, a recent study found that MCs are not involved in I/R injury in isolated rat livers that were perfused only for 1 h. The purpose of this study is to reevaluate the role of MCs in hepatic I/R injury in rat.Materials and methods
A warm hepatic I/R injury model of 1 h ischemia followed by 24 h of reperfusion was used. MC modulation was induced via cromolyn injection or a method called MC depletion using compound 48/80. The effects of MC modulation were evaluated by toluidine blue staining and assessment of mast cell tryptase in sera. The role of MCs in I/R injury was evaluated by hematoxylin and eosin staining graded by Suzuki criteria, alanine aminotransferase and aspartate aminotransferase levels in sera, and malondialdehyde levels in liver homogenates.Results
First, MC degranulation peaked after 2 h of reperfusion and liver damage peaked after approximately 6 h of reperfusion. Second, a method called MC depletion previously used in the skin with repeated injections of compound 48/80 worked similarly in the hepatic setting. Third, stabilization of MCs with cromolyn or depletion of MCs with compound 48/80 each decreased hepatic I/R injury. The most noticeable effects of cromolyn and compound 48/80 treatment were observed after approximately 6 h of reperfusion.Conclusions
MC degranulation promotes hepatic I/R injury in rats. 相似文献7.
Background
Heme oxygenase-1 (HO-1), an oxidative stress-response gene up-regulated by various physiological and exogenous stimuli, has cytoprotective activities. Ischemic postconditioning (Postcon) can protect an organ from ischemia-reperfusion (I/R) injury. In the present study, we investigated the potential contributions of HO-1 to Postcon-dependent protection against I/R injury in rat liver transplantation models.Materials and methods
Adult male Sprague-Dawley rats were randomly divided into four groups: sham group with laparotomy for liver exposure; I/R group with 24-hour cold ischemia of the donor liver; Postcon group with the same treatment as the I/R group plus ischemic Postcon; and zinc protoporphyrin (ZnPP HO-1 inhibitor) + Postcon group treated the same as the Postcon cohort with donors pretreated using ZnPP 24 hours before the I/R injury. We measured liver tissue and peripheral blood samples collected at 6 hours after reperfusion and serum transaminase levels, histopathology, liver tissue malondialdehyde (MDA) content, superoxide dismutase (SOD) activity and HO-1 expression in the liver.Results
Postcon significantly diminished the elevation of serum transaminases levels after I/R injury when compared with I/R and ZnPP+Postcon groups. Postcon treated rats showed significantly lower MDA production and higher SOD activity. HO-1 was induced in rat livers exposed to Postcon; its levels were obviously overexpressed after 6 hours in Postcon rats. Inhibiting the expression of HO-1, negated the protective effects of Postcon.Conclusions
Induction of HO-1 in the Postcon condition played a protective role against hepatic I/R injury and enhanced the early antioxidative activity. The protective effects of Postcon were significantly associated with greater intrahepatic HO-1 expression. 相似文献8.
V.S. Augusto A.J. Rodrigues G.S. Reis A.P.C. Silveira O. de Castro e Silva Jr. E.D. Mente A.A. Jordão Jr. P.R.B. Evora 《Transplantation proceedings》2014
Introduction
Liver transplant recipients are at an increased oxidative stress risk due to pre-existing hepatic impairment, ischemia-reperfusion injury, immunosuppression, and functional graft rejection. This study compared the oxidative status of healthy control subjects, patients with liver cirrhosis on the list for transplantation, and subjects already transplanted for at least 12 months.Patients and Methods
Sixty adult male patients, aged between 27 and 67 years, were subdivided into 3 groups: a control group (15 healthy volunteers), a cirrhosis group (15 volunteers), and a transplant group (30 volunteers). Oxidative stress was evaluated by activity of reduced glutathione, malondialdehyde, and vitamin E.Results
There was a significant difference (P < .01) in the plasma concentration of reduced glutathione in the 3 groups, with the lowest values observed in the transplanted group. The malondialdehyde values differed significantly (P < .01) among the 3 groups, with the transplanted group again having the lowest concentrations. The lowest concentrations of vitamin E were observed in patients with cirrhosis compared with control subjects, and there was a significant correlation (P < .05) among the 3 groups. No correlations were found between reduced glutathione and vitamin E or between vitamin E and malondialdehyde. However, there were strong correlations between plasma malondialdehyde and reduced glutathione in the 3 groups: control group, r = 0.9972 and P < .0001; cirrhotic group, r = 0.9765 and P < .0001; and transplanted group, r = 0.8981 and P < .0001.Conclusions
In the late postoperative stage of liver transplantation, oxidative stress persists but in attenuated form. 相似文献9.
Objective
Lung ischemia and reperfusion (I/R) injury is one of the major causes of postoperative pulmonary dysfunction after cardiopulmonary surgery and thoracic organ transplantation. Recent studies suggest that lung I/R injury may be associated with defects in pulmonary mitochondrial function, in addition to damage from reactive oxygen species. In this study, we examined effects of one lung I/R injury on the other lung, and the protective efficacy of resveratrol on mitochondrial biogenesis in lungs.Methods
Studies were performed in male Sprague-Dawley rats in 3 groups: sham-operated, lung I/R injury, and treated with resveratrol before lung I/R injury (20 mg/kg/d, orally). Lung ischemia was established by occluding the lung left hilum for 60 minutes, followed by releasing the occlusion and closing the chest. Four days after ischemia, we assessed the lung water content and protein concentration in lung lavage of the nonischemic lung; lung inflammation and pulmonary oxidative stress were assessed by leukocyte counts and tissue content of malondialdehyde (MDA), respectively. The level of mitochondrial biogenesis was determined according to PGC1-α mRNA expression.Results
The left lung I/R injury significantly suppressed right lung PGC1-α mRNA expression, increasing pulmonary oxidative stress, lung water content, and lavage leukocyte count and protein concentration (P < .05). Resveratrol treatment attenuated lung injury as well as increasing PGC1-α mRNA expression.Conclusions
Resveratrol treatment protects lung against I/R injury through improving mitochondrial biogenesis and reducing oxidative stress and leukocyte infiltration. 相似文献10.
Background
Hepatic ischemic-reperfusion injury (HIRI) is a major cause of morbidity and mortality following liver surgery. Octreotide (Oct) has been reported to improve hepatocellular energy metabolism in a rat HIRI model. This study was designed to evaluate whether Oct could protect the liver of rabbits against ischemic-reperfusion (I/R) injury.Methods
Twenty-four adult New Zealand rabbits were randomly divided into a sham operated group (Control), an ischemia/reperfusion group (I/R), and an ischemia/reperfusion + Oct pretreatment group (I/R + Oct). The hemodynamic (mean arterial pressure [MAP] and heart rate [HR]) changes, liver enzymes (alanine aminotransferase [ALT], aspartate aminotransferase [AST], and lactate dehydrogenase [LDH]) release, inflammatory cytokines (tumor necrosis factor [TNF]α and interleukin [IL]-1β) levels, and endotoxin (ETX) levels were measured during I/R.Results
Compared with the Control group, the MAP decreased and HR increased in I/R and I/R + Oct groups at ischemia 15 minutes (P < .05) but were less in the I/R + Oct group relative to the I/R group (P < .05). ALT, AST, LDH, IL-1β, and ETX levels were increased in the I/R and I/R + Oct groups at ischemia 30 minutes (P < .05), however, the increase was lower in the I/R + Oct group relative to the I/R group (P < .05). Bcl-2 expression in the I/R + Oct group was higher compared with other groups (P < .05) and Bax expression in the I/R group was reduced compared with other groups (P < .05). Hepatocellular damage in the I/R + Oct group appeared to be less than in the I/R group by microscopy.Conclusions
Oct pretreatment attenuated hemodynamic changes and decreased liver enzyme changes induced by HIRI in a rabbit model. The protection mechanisms of Oct may be related to reduced ETX levels, down-regulation of the inflammatory cytokines TNFα and IL-1β, and inhibition of hepatocellular apoptosis, as well as the modulation of the mitochondrion-mediated Bcl-2/Bax apoptosis pathway. Based on our study it appears that Oct may be useful in decreasing liver injury after liver surgery and/or transplantation and may serve as a promising agent against HIRI. 相似文献11.
Yaomei Cui MD Hao Zhang Muhuo Ji Min JiaHuixian Chen MD Jianjun Yang Manlin Duan 《The Journal of surgical research》2014
Background
Hydrogen, a popular antioxidant gas, can selectively reduce cytotoxic oxygen radicals and has been found to protect against ischemia–reperfusion (I/R) injury of multiple organs. Acute neuronal death during I/R has been attributed to loss of mitochondrial permeability transition coupled with mitochondrial dysfunction. This study was designed to investigate the potential therapeutic effect of hydrogen-rich saline on neuronal mitochondrial injury from global cerebral I/R in rats.Materials and methods
We used a four-vessel occlusion model of global cerebral ischemia and reperfusion, with Sprague–Dawley rats. The rats were divided randomly into six groups (n = 90): sham (group S), I/R (group I/R), normal saline (group NS), atractyloside (group A), hydrogen-rich saline (group H), and hydrogen-rich saline + atractyloside (group HA). In groups H and HA, intraperitoneal hydrogen-rich saline (5 mL/kg) was injected immediately after reperfusion, whereas the equal volume of NS was injected in the other four groups. In groups A and HA, atractyloside (15 μL) was intracerebroventricularly injected 10 min before reperfusion, whereas groups NS and H received equal NS. The mitochondrial permeability transition pore opening and mitochondrial membrane potential were measured by spectrophotometry. Cytochrome c protein expression in the mitochondria and cytoplasm was detected by western blot. The hippocampus mitochondria ultrastructure was examined with transmission electron microscope. The histologic damage in hippocampus was assessed by hematoxylin and eosin staining.Results
Hydrogen-rich saline treatment significantly improved the amount of surviving cells (P < 0.05). Furthermore, hydrogen-rich saline not only reduced tissue damage, the degree of mitochondrial swelling, and the loss of mitochondrial membrane potential but also preserved the mitochondrial cytochrome c content (P < 0.05).Conclusions
Our study showed that hydrogen-rich saline was able to attenuate neuronal I/R injury, probably by protecting mitochondrial function in rats. 相似文献12.
J.K. Hwang J.M. Kim Y.K. Kim S.D. Kim S.C. Park J.I. Kim H.W. Nam J. Kim I.S. Moon 《Transplantation proceedings》2013
Background
Heat shock proteins (HSP) play an important role in protecting cells against stress.Methods
Using a rat model, we tested the hypothesis that pretreatment with glutamine (Gln) and ischemia preconditioning (IPC) increase the expression of HSP resulting in attenuation of renal ischemia/reperfusion (I/R) injury. Sprague-Dawley rats were randomized into 4 groups [group I, Gln injection (+), IPC (+); group II, Gln injection (+), IPC (−); group III, saline injection (+), IPC (+); group IV, saline injection (+), IPC (−)]. Renal HSP70 expression was determined by Western blotting and kidney function was assessed by blood urea nitrogen and serum creatinine. Renal cross-sections were microscopically examined for tubular necrosis, exfoliation of tubular epithelial cells, cast formation, and monocyte infiltration.Results
Gln pretreatment increased intrarenal HSP expression (P = .031). In group I, tubulointerstitial abnormalities were clearly slighter compared with the other groups (P < .001).Conclusion
Our experiments suggest that (1) a single dose of Gln could induce HSP expression and (2) IPC could relieve renal I/R injury. In addition, IPC combined with Gln pretreatment had a synergic protective effect against renal I/R injury. 相似文献13.
Background
Orthotopic liver transplantation (OLT) is being used for studying cold ischemia reperfusion (I/R)-induced injury in experimental animals, but the technique is complicated and it does not accurately reflect the pathophysiology. Here, we report a novel model, termed “in situ liver cold ischemia (ISLCI)”, in Wistar rats.Methods
ISLCI was achieved in rats by establishing a portal-jugular shunt and a cannula shunt in inferior vena cava, and the liver was continuously perfused with lactate Ringer's solution at a speed of 150 mL/h through the portal vein for 60 min. Portal venous pressure, serum levels of total bilirubin, alkaline phosphatase, alanine aminotransferase and γ-glutamyl transpeptidase (GGT), and hepatic histopathology were examined, and compared with rats undergoing OLT, in which the donor liver was subjected to a 60 min cold ischemia.Results
Livers from ISLCI and OLT rats showed histopathologic changes characteristic of I/R-induced injury when examined on days 1 and 7, with complete recovery 14 d after reperfusion. Compared with OLT rats, ISLCI rats had significantly lower levels of portal venous pressure 1 and 10 min after porta hepatis clamping. They suffered a milder degree of I/R-induced hepatic injury, reflected by significantly lower levels of GGT, alanine aminotransferase, and alkaline phosphatase on day 1, and a significant lower level of GGT and a lower histopathologic score on day 7 after reperfusion.Conclusions
Our preliminary results indicate that the ISLCI model is reliable and technically easier, and is superior to OLT for studying cold I/R injury. 相似文献14.
Tuba Avci Dilek Erer Aysegul Kucuk Yasin Oztürk Murat Tosun Gursel L. Oktar Mustafa Arslan Erkan Iriz Mustafa Kavutcu Tolga Tatar 《The Journal of surgical research》2014
Purpose
The aim of this study was to investigate the effects of iloprost (IL) on ischemia-reperfusion injury in a rodent model.Materials and methods
Twenty-four Wistar Albino rats were randomized into four groups (n = 6). Laparotomy was performed in all groups under general anesthesia. Only laparotomy was applied in group S (Sham). Ischemia-reperfusion group (group I/R) underwent ischemia and reperfusion performed by clamping and declamping of the infrarenal abdominal aorta for 120 min. The iloprost group (group IL) received intravenous infusion of IL 0.5 ng/kg/min, without I/R. Group I/R + IL received intravenous infusion of IL 0.5 ng/kg/min immediately after 2 h period of ischemia. At the end of the reperfusion period, all rats were killed under anesthesia and skeletal muscle samples of lower extremity were harvested for biochemical and histopathologic analyses.Results
Tissue levels of endothelial nitric oxide were significantly higher in I/R groups than those in groups S and IL. The heat shock protein 60 levels were higher in group I/R than the other groups. But the heat shock protein 60 levels in group I/R + IL were found to be similar with the groups S and IL. Malondialdehyde levels were significantly higher in group I/R. On the other hand, in group I/R + IL, malondialdehyde levels were higher than those in groups S and IL but lower than those in group I/R. Superoxide dismutase (SOD) enzyme activities were found to be significantly lower in group I/R than the other groups. Also in group I/R/I, the SOD enzyme activities were higher than those in group I/R. But, in group I/R + IL, SOD levels were found to be higher than those in group I/R but lower than those in groups S and IL.Conclusions
These results indicate that IL has protective effects on I/R injury in skeletal muscle in a rodent model. 相似文献15.
Murat Yildar Hasan Aksit Oguzhan Korkut Musa O. Ozyigit Bahar Sunay Kamil Seyrek 《The Journal of surgical research》2014
Background
To investigate the protective effect of 2-aminoethyl diphenylborinate (2-APB) against ischemia–reperfusion (I/R) injury in the rat kidney by an experimental study.Materials and methods
Thirty male Sprague-Dawley rats were randomly divided into the following three groups: (1) sham group, (2) I/R group, and (3) I/R + 2-APB group. Renal I/R injury was induced by clamping the left renal pedicle for 45 min after right nephrectomy, followed by 3 h of reperfusion. The therapeutic agent 2-APB was administered intravenously at a dose of 2 mg/kg 10 min before renal ischemia. Glutathione, superoxide dismutase, total antioxidant capacity, malondialdehyde, tumor necrosis factor α, interleukin 6, aspartate aminotransferase, alanine aminotransferase, and creatinine levels were measured from blood samples, and the rats were sacrificed subsequently. Tissue samples were scored histopathologically. Visualization of apoptotic cells was performed using the terminal deoxynucleotidyl transferase dUTP nick end labeling staining method.Results
2-APB significantly reduced serum malondialdehyde, tumor necrosis factor α, interleukin 6, aspartate aminotransferase, alanine aminotransferase, and creatinine levels in the I/R injury group. However, glutathione, superoxide dismutase, and total antioxidant capacity levels increased significantly. Histopathologic scores were significantly better and the rate of apoptosis was lower in the 2-APB group.Conclusions
2-APB reduces oxidative stress and damage caused by renal I/R injury. The results of this study demonstrate that 2-APB can be used as an effective agent against I/R injury in the kidney. 相似文献16.
Yun-peng Wang Gang Li Lu-lin Ma Yi Zheng Shu-dong Zhang Hong-xian Zhang Min Qiu Xin Ma 《The Journal of surgical research》2014
Background
Renal ischemia–reperfusion (I/R) injury is a major cause of acute kidney failure by mechanisms that involve oxidative stress, inflammation, and apoptosis. Penehyclidine hydrochloride (PHC), a selective anticholinergic agent, possesses anti-inflammatory, antioxidative stress, and antiapoptotic effects. Therefore, we investigated the ability of PHC to ameliorate renal I/R injury in Sprague–Dawley rats.Materials and methods
Rats were randomly assigned to three groups (35 rats per group): sham operated, saline-treated I/R, and PHC-treated I/R. After removing the right kidney, renal I/R injury was induced by clamping the left renal artery for 45 min followed by reperfusion. The rats were administered PHC (0.45 mg/kg, intravenously) or saline 30 min before renal ischemia. The blood and kidneys were harvested at 1, 3, 6, 12, or 24 h after reperfusion. Renal function and histologic changes were assessed. Markers of oxidative stress, inflammation, and apoptosis in the kidneys were also measured.Results
PHC treatment significantly attenuated renal dysfunction and histologic damage caused by I/R injury. The treatment also decreased malondialdehyde level and attenuated the reduction in superoxide dismutase activity in the kidney. Moreover, the levels of activated p38 mitogen-activated protein kinase, nuclear factor kappa B, and caspase 3 were lower in the PHC-treated animals.Conclusions
PHC protected rat kidneys from I/R injury by attenuating oxidative stress, inflammatory response, and apoptosis. Thus, PHC may represent a novel practical strategy for the treatment of renal I/R injury. 相似文献17.
Background
Ischemia-reperfusion (I/R) injury is one of the risk factors for delayed graft function, acute rejection episodes, and impaired long-term allograft survival after kidney transplantation. This antigen-independent inflammatory process produces tissue damage. Isogeneic transplantation in a rat model is a useful method for study of nonimmunologic risk factors for kidney damage.Objective
To study the effect of sirolimus on I/R injury using only 1 dose of the drug in the donor.Materials and Methods
Eighteen rats were allocated to 3 groups of 6 rats each: sham group, control group, and rapamycin group.Results
Improved renal function and systemic inflammatory response were observed in the rapamycin group compared with the control group (Δurea, Δcreatinine, and ΔC3, all P < .01). The number of apoptotic nuclei in the renal medulla in the control group was higher than in the rapamycin group (P < .01). Tubular damage was less severe in the rapamycin group compared with the control group (P < .01). Complement 3 and tumor necrosis factor-α expression in the kidney samples were significantly decreased when rapamycin was given to the donor rats (P > .01). Bcl-2 protein was upregulated in the rapamycin group compared with the control group (P < .01).Conclusion
Administration of rapamycin in donors attenuates the I/R injury process after kidney transplantation in a rat model. 相似文献18.
Background
Dexmedetomidine (DEX) has been shown to decrease ischemia–reperfusion (I/R) injury in kidney and brain tissues. In this study, the effects of DEX were evaluated in skeletal muscle during I/R injury.Materials and methods
Animals were divided into four groups: sham-operated (sham group), saline + I/R, DEX + I/R, and α-tocopherol + I/R groups. Hind limb ischemia was induced by clamping the common femoral artery and vein. After 4 h of ischemia, the clamp was removed and the animals underwent 2 h of reperfusion. Animals in the drug treatment group received DEX or α-tocopherol by intraperitoneal injection 1 h before reperfusion. We measured plasma concentrations of interleukin 1β and tumor necrosis factor α levels using an enzyme-linked immunosorbent assay. The right gastrocnemius muscle was harvested and immediately stored at −80°C for the assessment of superoxide dismutase (SOD) and catalase (CAT) activities as well as glutathione (GSH), malondialdehyde (MDA), and protein oxidation (PO) levels. DEX (25 μg/kg) and normal saline (10 mL/kg) were administered by intraperitoneal injection 1 h before reperfusion.Results
Plasma tumor necrosis factor α or interleukin 1β levels increased significantly in the I/R group (P < 0.01 compared with sham group) and decreased significantly in the DEX group (P < 0.01 compared with I/R group). Muscle tissues of the I/R group had significantly decreased SOD, GSH, and CAT activities and increased levels of MDA and PO content compared with the sham group. The activity of antioxidant enzymes in the DEX + I/R group was greatly elevated compared with that in the I/R group (SOD, 1.068 ± 0.120 versus 0.576 ± 0.072 U/mg protein; GSH, 2.436 ± 0.144 versus 1.128 ± 0.132 μmol/g; and CAT, 69.240 ± 6.456 versus 31.884 ± 6.312 U/mg protein; P < 0.01), whereas the levels of MDA and PO content were clearly reduced (23.268 ± 3.708 versus 53.604 ± 5.972 nmol/g protein and 1.908 ± 0.192 versus 5.208 ± 0.612 nmol/mg protein, respectively; P < 0.01). Moreover, DEX exhibited more potent antioxidant activity than vitamin E in the skeletal muscle I/R.Conclusions
We found that DEX exhibits protective effects against skeletal muscle I/R injury. These results underscore the necessity of human studies with DEX to determine if it is beneficial for preventing skeletal muscle I/R injury. 相似文献19.
Background
Liver injury caused by ischemia-reperfusion (I/R) processes is a complication of hepatic resection surgery and transplantation, particularly using grafts from marginal donors. Despite improvements in organ preservation and advances in surgical techniques, I/R injury remains a significant clinical problem. In this study, we investigated whether aprotinin provided protection against the adverse effects of I/R injury in liver tissue.Methods
Forty rats were randomized into four groups (n = 10): group I: (control group) I/R + no medication; group II: sham-operated group + no medication or I/R; group III: I/R + aprotinin; group IV: I/R + α-tocopherol. Malondialdehyde (MDA) was measured in the liver tissue and superoxide dismutase (SOD), catalase (CAT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), as well as lactate dehydrogenase (LDH) in rat serum.Results
Administration of aprotinin and α-tocopherol before I/R resulted in significant reductions of MDA levels compared to the I/R alone group (group I; P = .01 and P < .01, respectively). Administration of aprotinin or α-tocopherol prior to I/R resulted in significant increases in SOD and CAT levels compared with the I/R group (P < .05 each). Compared to the I/R group, significant decreases in plasma AST, ALT, and LDH levels were observed both in the aprotinin and in the α-tocopherol group (P < .05). Histological evaluation revealed the injury grade to be relatively lower among groups III and IV compared to group I.Discussion
In conclusion, rat hepatic structures in aprotinin and α-tocopherol administered groups were well protected. Therefore, aprotinin may provide protection against the adverse effects of I/R injury in liver transplantation. 相似文献20.