Effect of vitamin E on stroke-associated pneumonia.

OBJECTIVE: To study the role of vitamin E in stroke-associated pneumonia. METHODS: We selected 183 patients with stroke-related pneumonia who were divided into different nutrition groups according to the Mini Nutritional Assessment score. Patients were then administered different doses of vitamin E. RESULTS: CD55 and CD47 levels in patients taking vitamin E across different nutrition score groups were better than those in patients who did not use vitamin E. The levels of CD55 and CD47 and the duration of hospitalization were better in the high-dose vitamin E group than in the low-dose vitamin E group. CONCLUSION: Vitamin E may have an auxiliary therapeutic effect in patients with stroke-associated pneumonia.

The effects of Ang-1, IL-8 and TGF-ß1 on the pathogenesis of COPD.

Chronic obstructive pulmonary disease (COPD) is a prevalent smoking-related disease for which no disease­altering therapies currently exist. Airway remodeling is one of the most important mechanisms in the pathogenesis of COPD and is triggered by chronic inflammation mediated by angiopoietin-1 (Ang-1), interleukin-8 (IL-8) and transforming growth factor-ß1 (TGF-ß1). The aim of this study was to investigate the effects of Ang-1, IL-8 and TGF-ß1 on the pathogenesis of COPD. Forty-two COPD patients and 10 healthy adults (group A) were included in this study. We divided the 42 patients into 4 groups (groups B-E) according to the severity of the disease. We investigated the levels of Ang-1, IL-8 and TGF-ß1 and the levels of pulmonary function (PF) in the stable and acute phases of COPD by enzyme-linked immunosorbent assay. We found statistically significant differences in the expression levels of Ang-1, IL-8 and TGF-ß1 between the stable and acute phases in groups B-E. We found statistically significant differences in the expression levels of Ang-1 among all groups in the stable phase. In addition, there were statistically significant differences in the expression levels of TGF-ß1 among all groups. There were statistically significant differences in the expression levels of IL-8 between group A and the other groups in the stable phase. Furthermore, in groups C-E we found higher correlations between Ang-1 and the forced expiratory volume in one second of forced vital capacity (FVC) [FEV1(%)] and FEV1/FVC(%) than between TGF-ß1 and FEV1(%) and FEV1/FVC(%). We conclude that the blood vessel factor is more closely related to the pathogenesis of COPD.

[Reconstruction of rabbit urethra using urethral extracellular matrix].

OBJECTIVE: To evaluate the feasibility of reconstruction of rabbit urethra using urethral extracellular matrix. METHODS: Extracellular matrix was obtained from the urethra of 20 donor New Zealand rabbits. In experimental group, 20 rabbits underwent segmental urethral resection (about 1.0 to 1.5 cm in length) and the defects were replaced by a tube of extracellular matrix. The serum TNFalpha was detected by ELISA to assess the immunity response preoperatively and 12, 24, 48 h postoperatively. The regenerated urethral segments were taken for histologic and pathologic study 10 days, 3 weeks, 6 weeks and 24 weeks after operation. The urodynamics, urethroscopy and urethrography were also performed. RESULTS: The serum TNFalpha in experiment group slightly rised, with no significant difference when compared with that in control group. 10 days after operation, epithelial cell migrated into the extracellular matrix from two ends, and small vessels were also found. 3 weeks later, several layers of urothelium covered the whole surface of the matrix tube. 6 weeks later, the irregularly arranged smooth muscle fibers were fist observed by Van Gieson staining. 24 weeks after operation, the smooth muscle cells increased, the appearance of the regenerated urethra segments were very similar to normal urethral wall components. The urethrography and urodynamic evaluation revealed no difference between the normal and the regenerated urethral tube. CONCLUSIONS: The urethral extracellular matrix might be an ideal replacement material for urethral defect.

Ozone oxidative preconditioning protects the rat kidney from reperfusion injury: the role of nitric oxide.

BACKGROUND: Ischemia/reperfusion (I/R) injury, which is commonly seen in the field of renal surgery or transplantation, is a major cause of acute renal failure. Previous studies have shown that ozone oxidative preconditioning (OzoneOP) attenuated renal I/R injury. The objective of this study was to examine the hypothesis that protective effects of OzoneOP in renal I/R injury were associated with endogenous NO. MATERIALS AND METHODS: In a right-nephrectomized rat mode, anesthetized rats underwent 45 min of renal ischemia. OzoneOP (1 mg/kg) was administered before I/R injury. Rats were killed at 24, 48, and 72 h after I/R injury and blood samples and renal tissues were obtained. RESULTS: OzoneOP prevented the renal dysfunction induced by I/R and increased nitric oxide (NO) release and renal NO synthase (endothelial, eNOS, and inducible, iNOS) expression. In contrast, enhancement of endothelin-1 in the kidney after the reperfusion was markedly suppressed by OzoneOP. CONCLUSIONS: Our findings indicated that the protective effect of OzoneOP was closely related to the NO production following the increase in eNOS and iNOS expression. Ozone treatment may have important clinical implications, particularly in view of the minimizing renal damage before transplantation.

Similarities between ozone oxidative preconditioning and ischemic preconditioning in renal ischemia/reperfusion injury.

BACKGROUND: Many studies indicate that the production of reactive oxygen species (ROS) after renal ischemia/reperfusion (I/R) may initiate the cascade of cellular injury. It has been demonstrated that ozone oxidative preconditioning (OzoneOP) may prevent the damage induced by ROS and attenuate renal I/R injury. On the basis of those results, we postulated that OzoneOP was similar to the ischemic preconditioning (IP). The aim of our present work was to assess whether the combination of OzoneOP and IP provided synergistic protection. METHODS: Seven groups of rats were classified as follows: 1) sham-operated control; 2) I/R; 3) OzoneOP+I/R; 4) IP+I/R; 5) OzoneOP+IP+I/R; 6) O2+I/R; 7) sham-operated control+OzoneOP. Rats were sacrificed at 24 h after I/R injury. Serum and tissue were taken to determine urea nitrogen (BUN), creatinine (Cr), nitric oxide (NO), histological examination, and NO synthase (endothelial, eNOS and inducible, iNOS) expression. Malondialdehyde (MDA) content, glutathione (GSH) content, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activity were determined in renal tissue. RESULTS: Renal dysfunction, histological damage, and renal oxidative stress were significantly improved by OzoneOP or IP alone. OzoneOP+IP could not further relieve severe renal damage. Either IP or OzoneOP treatment alone increased NO release and NO synthase (endothelial, eNOS and inducible, iNOS) expression. The combination of OzoneOP and IP could not further enhance NO levels and NOS expression. CONCLUSIONS: These findings indicate that both of the preconditioning settings shared similar mechanisms of protection in the parameters measured. However, OzoneOP combined with IP had no synergistic effect. IP and OzoneOP appeared to share a common mediator: NO. These findings suggested the potential role of OzoneOP against renal failure during surgery or transplantation.

Ozone oxidative preconditioning inhibits inflammation and apoptosis in a rat model of renal ischemia/reperfusion injury.

Ischemia/reperfusion injury, which is commonly seen in the field of renal surgery or transplantation, is a major cause of acute renal failure. Previous studies showed that ozone oxidative preconditioning (OzoneOP) attenuated renal ischemia/reperfusion injury. The objective of this study was to examine the role of the OzoneOP in modulating inflammation and apoptosis after renal ischemia/reperfusion injury. Rats were subjected to 45 min of renal ischemia, with or without treatment with OzoneOP (1 mg/kg). Renal function, inflammation and apoptosis were compared at 24 h after renal injury. OzoneOP improved the renal dysfunction and reduced inflammation and apoptosis after ischemia/reperfusion injury. In conclusion, OzoneOP has potent anti-apoptotic and anti-inflammatory properties. These findings may have major implications in the treatment of human ischemic acute renal failure.

Ischemic postconditioning inhibits apoptosis after renal ischemia/reperfusion injury in rat.

Ischemic postconditioning is a phenomenon that intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from ischemia/reperfusion (I/R) injury. In the present study, we investigated whether the protective effect of ischemic postconditioning was associated with modulation of apoptosis after renal I/R injury. Rats were subjected to 45 min of renal ischemia, both with and without treatment with ischemic postconditioning. Serum urea nitrogen and creatinine levels, phosphorylation of Akt and ERK1/2 and apoptosis were compared after renal injury. Our data showed that ischemic postconditioning attenuated the renal dysfunction and cell apoptosis induced by I/R and increased phosphorylation of Akt and ERK1/2. The results indicated that ischemic postconditioning decreased apoptosis and improved renal function. This protective effect may be related with the levels of Akt and ERK1/2 activation. These findings may have major implications in the treatment of renal transplantation.

Attenuation of reperfusion injury by renal ischemic postconditioning: the role of NO.

Ischemic postconditioning (Postcond) is defined as rapid intermittent interruptions of blood flow in the early phase of reperfusion and mechanically alters the hydrodynamics of reperfusion. Although Postcond has been demonstrated to attenuate ischemia/reperfusion (I/R) injury in the heart and brain, its roles to renal I/R injury remain to be defined. In the present study, we examined the role of Postcond in I/R injury in a right-nephrectomized rat model. Postcond prevents the renal dysfunction and cell apoptosis induced by I/R and increases nitric oxide (NO) release and renal NO synthase (endothelial, eNOS and inducible, iNOS) expression. In contrast, enhancement of endothelin-1 (ET-1) in the kidney after the reperfusion was markedly suppressed by Postcond. These findings indicate that Postcond can inhibit renal I/R injury. The protective effect of Postcond is closely related to the NO production following the increase in eNOS and iNOS expression and the suppressive effect of ET-1 overproduction.

[Extracellular matrix for the replacement of ureteral defect].

This is an experiment on rabbits to evaluate the possibility of ureteral replacement by extracellular matrix. We adopted a biochemical method for preparing a new tissue engineering material named Extracellular Matrix (ECM), and the ECMs were used as homologous grafts to replace the defect in the ureters. Light microscopy, scanning electron microscopy, immunohistochemical technique and intravenous urography were used. The routine blood and biochemical laboratory tests were made before and after operation, and the measured values of pressure in the ureter of experiment and control groups were compared. The ureteral ECM was found in the experiment to promote the regeneration of all ureteral wall components. There were no significant differentces between the regenerative tissue and the normal tissue in morphology and function 16 weeks after replacement. The homologous ECM might be an ideal replacement material for ureteral defect.