Probiotic Saccharomyces boulardii Alleviates Lung Injury by Reduction of Oxidative Stress and Cytokine Response Induced by Supraceliac Aortic Ischemia-Reperfusion Injury in Rats

Abstract Objectives: Ischemia-reperfusion injury is an important cause of multiple organ failure in cardiovascular surgery. Our aim is to investigate the effect of the probiotic Saccharomyces boulardii on oxidative stress, inflammatory response, and lung injury in an experimental model of aortic clamping. Methods: Twenty-one Wistar rats were randomized into three groups (n=7). Control group animals received saline gavage for a week before undergoing median laparotomy. In other groups, supraceliac aorta was clamped for 45 minutes to induce ischemia followed by reperfusion for 60 minutes. In the ischemia-reperfusion group, saline gavage was given preoperatively for one week. Ischemia-reperfusion+probiotic group rats received probiotic gavage for seven days before aortic clamping. The levels of oxidative stress markers and pro-inflammatory cytokines were determined in both serum and lung tissue samples. Ileum and lung tissues were harvested for histological examination. Results: Ischemia-reperfusion caused severe oxidative damage and inflammation evident by significant increases in malondialdehyde and cytokine levels (tumor necrosis factor alpha and interleukin-1 beta) and decreased glutathione levels in both serum and lung tissues. There was severe histological tissue damage to the lung and ileum in the ischemia-reperfusion group. Probiotic pretreatment before aortic clamping caused significant suppression of increases in serum and lung tissue malondialdehyde and tumor necrosis factor alpha levels. Histological damage scores in tissue samples decreased in the ischemia-reperfusion+probiotic group (P<0,005). Conclusions: Oral supplementation of probiotic S. boulardii before supraceliac aortic ischemia-reperfusion in rats alleviates lung injury by reducing oxidative stress, intestinal cellular damage, and modulation of inflammatory processes.

Probiotic Saccharomyces boulardii Alleviates Lung Injury by Reduction of Oxidative Stress and Cytokine Response Induced by Supraceliac Aortic Ischemia-Reperfusion Injury in Rats.

OBJECTIVES: Ischemia-reperfusion injury is an important cause of multiple organ failure in cardiovascular surgery. Our aim is to investigate the effect of the probiotic Saccharomyces boulardii on oxidative stress, inflammatory response, and lung injury in an experimental model of aortic clamping. METHODS: Twenty-one Wistar rats were randomized into three groups (n=7). Control group animals received saline gavage for a week before undergoing median laparotomy. In other groups, supraceliac aorta was clamped for 45 minutes to induce ischemia followed by reperfusion for 60 minutes. In the ischemiareperfusion group, saline gavage was given preoperatively for one week. Ischemia-reperfusion+probiotic group rats received probiotic gavage for seven days before aortic clamping. The levels of oxidative stress markers and pro-inflammatory cytokines were determined in both serum and lung tissue samples. Ileum and lung tissues were harvested for histological examination. RESULTS: Ischemia-reperfusion caused severe oxidative damage and inflammation evident by significant increases in malondialdehyde and cytokine levels (tumor necrosis factor alpha and interleukin-1 beta) and decreased glutathione levels in both serum and lung tissues. There was severe histological tissue damage to the lung and ileum in the ischemia-reperfusion group. Probiotic pretreatment before aortic clamping caused significant suppression of increases in serum and lung tissue malondialdehyde and tumor necrosis factor alpha levels. Histological damage scores in tissue samples decreased in the ischemia-reperfusion+probiotic group (P<0,005). CONCLUSIONS: Oral supplementation of probiotic S. boulardii before supraceliac aortic ischemia-reperfusion in rats alleviates lung injury by reducing oxidative stress, intestinal cellular damage, and modulation of inflammatory processes.

Effect of Tarantula Cubensis Extract (Theranekron) on Peripheral Nerve Healing in an Experimental Sciatic Nerve Injury Model in Rats.

AIM: To investigate the effects of systemic application of Theranekron on peripheral nerve healing after compression type peripheral nerve injury. MATERIAL AND METHODS: Twenty-one female Wistar albino rats were randomly divided into 3 groups (n=7): Control (C), injury (I), and Theranekron (T). The right sciatic nerves of rats in the I and T groups were compressed via an aneurysm clip for 5 minutes and 0.3 ml Theranekron D6 was applied via subcutaneous administration once a week in the T group for a total period of four weeks. Nerve conduction velocity and proximal and distal latency of the rats were measured at the end of day 30. The right sciatic nerves of the rats were then removed and myelin damage grading, axon counting, fibrosis assessment, caspase-3, and NF-kB immunochemical staining were performed. The data were analysed statistically and a p value of less than 0.05 was considered to be significant. RESULTS: Axonal degeneration, vacuolization and myelin destruction were found to be markedly greater in group T. Fibrosis and caspase-3 immunoreactivity were less intense in group T. There was a statistically significant difference in the electrophysiological results of groups I and T. However, there were no statistically significant differences in axon number and NF-kB immunochemical evaluation of groups I and T. CONCLUSION: The findings of this study show that Theranekron decreases axonal and myelin damage after sciatic nerve injury and that this neuroprotective effect of Theranekron can be attributed to its anti-inflammatory effect on pro-inflammatory cytokine levels.

Effect of Curcumin on the Formation of Epidural Fibrosis in an Experimental Laminectomy Model in Rats.

AIM: To clarify the effects of topical application of curcumin on the prevention of epidural fibrosis. MATERIAL AND METHODS: Twenty-one rats were randomly divided into three equal groups (control, spongostan, local curcumin) and a laminectomy procedure was performed between T11 and L1 in all rats. Subsequently, spongostan soaked with curcumin (100 mg/kg) was applied topically. After four weeks, the vertebral column from T9 to L3, which included the paraspinal muscles and epidural scar tissue, was removed as a single piece and the epidural fibrosis and arachnoidal scarring were graded and histopathological analysis carried out accordingly. Kruskal-Wallis and Pearson Chi-Square tests were used for statistical analysis. A p-value of less than 0.05 was considered to be significant. RESULTS: The grading of epidural fibrosis was far lower in the experimental group with curcumin compared to the control and spongostan groups, but the difference was not statistically significant. CONCLUSION: The findings of this study show that local curcumin decreases the formation of epidural fibrosis and this effect of curcumin is thought to be mediated by reducing the functions of inflammatory cells such as macrophages, neutrophils and fibroblasts, and the anti-inflammatory and antioxidant effects.

Effect of Etanercept on the Formation of Epidural Fibrosis in an Experimental Model.

AIM: To investigate the effects of local and systemic administration of etanercept on the formation of epidural fibrosis. MATERIAL AND METHODS: Twenty-eight rats were randomly divided into four equal groups (Control, SpongostanTM, Local etanercept and Systemic etanercept) and laminectomy was performed between T11 and L1 in all rats. SpongostanTM was soaked with saline (0.1 mg/kg), local etanercept (300 ?g/kg) was applied with SpongostanTM and systemic etanercept (300 ?g/kg/week) was applied subcutaneously. Four weeks later, the vertebral column from T9 to L3, including the paraspinal muscles and epidural scar tissue, was removed en bloc, and epidural fibrosis and arachnoidal involvement were graded and evaluated histopathologically. RESULTS: The grading of epidural fibrosis was statistically significantly lower in systemic and local administration of etanercept groups compared to the control group (p < 0.005), but systemic etanercept administration was more effective. CONCLUSION: Systemic administration of etanercept can be effective in reducing epidural fibrosis in rats after laminectomy.

Boric acid reduces axonal and myelin damage in experimental sciatic nerve injury.

The aim of this study was to investigate the effects of boric acid in experimental acute sciatic nerve injury. Twenty-eight adult male rats were randomly divided into four equal groups (n = 7): control (C), boric acid (BA), sciatic nerve injury (I), and sciatic nerve injury + boric acid treatment (BAI). Sciatic nerve injury was generated using a Yasargil aneurysm clip in the groups I and BAI. Boric acid was given four times at 100 mg/kg to rats in the groups BA and BAI after injury (by gavage at 0, 24, 48 and 72 hours) but no injury was made in the group BA. In vivo electrophysiological tests were performed at the end of the day 4 and sciatic nerve tissue samples were taken for histopathological examination. The amplitude of compound action potential, the nerve conduction velocity and the number of axons were significantly lower and the myelin structure was found to be broken in group I compared with those in groups C and BA. However, the amplitude of the compound action potential, the nerve conduction velocity and the number of axons were significantly greater in group BAI than in group I. Moreover, myelin injury was significantly milder and the intensity of nuclear factor kappa B immunostaining was significantly weaker in group BAI than in group I. The results of this study show that administration of boric acid at 100 mg/kg after sciatic nerve injury in rats markedly reduces myelin and axonal injury and improves the electrophysiological function of injured sciatic nerve possibly through alleviating oxidative stress reactions.

The Effects of Rifampin, Povidone-Iodine and Hydrogen Peroxide on the Formation of Epidural Fibrosis in the Experimental Epidural Fibrosis Model.

The aim of the study was to determine the effect of direct application of rifampin, povidone-iodine, and hydrogen peroxide on the formation of epidural fibrosis in rats. Forty-eight adult male Wistar albino rats were equally and randomly divided into four groups (laminectomy, topical rifampin, topical povidone-iodine, and topical hydrogen peroxide). Laminectomy was performed at the T12 level in all rats. Four weeks later, the extent of epidural fibrosis was assessed both macroscopically and histopathologically. ANOVA test was used for the evaluation of dural thickness. Kruskal-Wallis test was used for the pathology and macroscopic evaluation. Chi-square test was used for evaluation of the arachnoid involvement. p value <0.05 was accepted as statistically significant. Our data revealed that topical application of both povidone-iodine and hydrogen peroxide were effective in reducing epidural fibrosis formation. The results of our study provide the experimental evidence of the preventive effects of topical application of povidone-iodine and hydrogen peroxide over epidural fibrosis.

Primary intraosseous hydatid cyst of femur.

INTRODUCTION: Echinococcosis is a parasitic and zoonotic disease of animals and humans. The cause is Echinococcus granulosus and occasionally, Echinococcus multilocularis. Hydatid cysts are mostly seen in the liver and lungs, although almost all organs and systemscan be involvement. Hydatid cysts seen with bone involvement comprise approximately 3% of all hydatid cysts. Even if a long period of survey is possible, it is still difficult to eradicate the disease and effect a cure. CASE PRESENTATION: In this study, an evaluation was made of a patient referred at Yozgat State Hospital Orthopedics and Traumatology Polyclinic with complaints of pain in her left thigh close to the knee. After examinations of plain radiographs, computerized tomography, magnetic resonance images, and blood parameters, a diagnosis was made of left femoral intramedullary hydatid cyst from excised intraoperative material. Throughout a 6-month follow-up period, there was no recurrence and functional results were good. CONCLUSIONS: Based on this report (of a patient presented with an intramedullary cyst in the long bones), the primary bone hydatid cyst disease should be kept in mind and be investigated in the differential diagnosis.

Effects of cilostazol on oxidative stress, systemic cytokine release, and spinal cord injury in a rat model of transient aortic occlusion.

BACKGROUND: Cilostazol is a phosphodiesterase inhibitor that has anti-inflammatory potential in addition to vasodilator and antiplatelet effects. The aim of this study was to determine the influence of cilostazol on biochemical markers of oxidative damage, proinflammatory cytokine release, and spinal cord injury after transient aortic occlusion in rats. METHODS: Animals were randomized into 3 groups. Sham group rats were subjected to laparotomy without aortic occlusion. Control group rats were pretreated with intraperitoneal dimethyl sulfoxide, and cilostazol group rats received intraperitoneal cilostazol (20 mg/kg/day) for 3 days before the induction of ischemia. Ischemia was induced by clamping of the infrarenal aorta, and 48 hours after reperfusion, Tarlov grades were assessed and spinal cord conduction velocities (SCCVs) were measured using epidural electrical stimulation. Erythrocyte superoxide dismutase (SOD) and catalase activities and plasma malondialdehyde, serum tumor necrosis factor-α, interleukin-1ß, and interleukin-6 levels were analyzed. Spinal cord histopathology was examined to determine neuronal damage and tissue inflammation. RESULTS: Aortic occlusion caused significant increases in SOD, catalase activities, and malondialdehyde and cytokine levels accompanied by spinal cord injury. Cilostazol significantly reduced malondialdehyde levels but did not significantly alter the activations of antioxidant enzymes, levels of proinflammatory cytokines, or histologic severity of inflammation. The differences regarding the results of Tarlov grading, SCCVs, and neuronal viability between the ischemic and cilostazol pretreated groups were statistically nonsignificant. CONCLUSION: The present experimental study indicated that cilostazol pretreatment used in this study before aortic occlusion decreased lipid peroxidation, which may be related to the reduction of reactive oxygen species. Cilostazol did not significantly suppress systemic cytokine release and prevent spinal cord inflammation and injury; however, it did show some benefit. Additional investigations might be needed to determine the critical dose of cilostazol for clarifying the protective role of this drug in spinal cord ischemia/reperfusion injury.