Rol antioxidante de la L-carnitina en un modelo experimental de estrés oxidativo inducido por consumo elevado de fructosa / Antioxidant role of L-carnitine in an experimental model of oxidative stress induced by increased fructose consumption

RESUMEN Objetivos: Evaluar el rol de la L-carnitina (LC) sobre el estrés oxidativo inducido por fructosa en ratas Holtzman. Materiales y métodos: Se realizó un estudio experimental durante 56 días, con cuatro grupos: control, control+LC, fructosa y fructosa+LC. Los grupos con fructosa recibieron el tratamiento durante los 56 días, y los grupos con LC lo recibieron en los últimos 28 días. La fructosa se dio a libre demanda y la LC se administró por vía oral a una dosis de 500 g/kg/24 h. En el hígado se midió la lipoperoxidación (MDA), la actividad de superóxido dismutasa, las proteínas mitocondriales y posmitocondriales, y la LC libre. En el plasma se midió la glicemia, el índice de modelo homeostático para evaluar la resistencia a la insulina (HOMA-IR) e insulina. En el páncreas se midió la insulina y se realizó la histología. Resultados: El tratamiento con LC en el hígado mostró disminución (p < 0,05) de MDA frente al grupo control (21,73 ± 5,36 nmol/g tejido vs. 64,46 ± 7,87 nmol/g tejido). Las proteínas mitocondriales y posmitocondriales aumentaron (p < 0,05) frente al grupo control. La insulina pancreática también aumentó frente al control (341,8 ± 42,3 μUI/ml vs. 70,1 ± 9,6 μUI/ml, p<0,05). El rol de LC frente al estrés oxidativo inducido por fructosa no mostró disminución de MDA, pero produjo disminución (p < 0,05) en la actividad de SOD Cu/Zn (9,39 ± 1,5 USOD/mg proteína vs. 13,52 ± 1,5 USOD/mg proteína). En el plasma, se observó que la LC mejora el valor de la HOMA-IR. Histológicamente, la presencia de LC aumentó el número y tamaño de islotes de Langerhans. Conclusiones: La LC favorece los cambios del metabolismo oxidativo y ante el consumo de fructosa contribuye con la homeostasis glicémica.

ABSTRACT Objectives: To evaluate the role of L-carnitine (LC) on fructose-induced oxidative stress in Holtzman rats. Materials and methods: An experimental study was carried out during 56 days, in patients assigned to 4 groups: control, control+LC, fructose and fructose+LC. Patients in the fructose group received treatment during 56 days, and those in the LC groups were treated during the last 28 days. Fructose was given on demand and LC was administered orally at a dose of 500 g/kg/24 h. Lipid peroxidation (MDA), superoxide dismutase activity, free LC and mitochondrial and post-mitochondrial proteins were measured in liver tissue. Glycemia, insulin and the homeostasis model assessment of insulin resistance (HOMA-IR) were measured in blood plasma. We measured insulin concentration and studied the histology of pancreatic tissue. Results: LC treatment showed a decrease (p < 0.05) of MDA when compared to the control group (21.73 ± 5.36 nmol/g tissue vs. 64.46 ± 7.87 nmol/g tissue). Mitochondrial and post-mitochondrial proteins increased (p < 0.05) in comparison to the control group; pancreatic insulin also increased when compared to the control (341.8 ± 42.3 μUI/ml vs. 70.1 ± 9.6 μUI/ml, p<0.05). The role of LC against fructose-induced oxidative stress did not show any decrease of MDA, but decreased (p < 0.05) SOD Cu/Zn activity (9.39 ± 1.5 USOD/mg protein vs. 13.52 ± 1.5 USOD/mg protein). We observed that LC improves HOMA-IR in blood plasma. Histological analysis of the pancreas showed that the presence of LC increased the number and size of the islets of Langerhans. Conclusions: LC favors changes in the oxidative metabolism and it also contributes to glycemic homeostasis when fructose is consumed.

Effect of Ginkgo Biloba Extract on Intestinal Function after Spinal Cord Injury in Rats / 中国康复理论与实践

@#Objective To observe the effect of Ginkgo biloba extract (EGb) on intestinal function after spinal cord injury (SCI) in rats. Methods 36 Sprague-Dawley rats were randomly divided into group A (n=12), group B (n=12) and group C (n=12). SCI model was established with Allen's mode (10 g×25 mm) at T10. 30 minutes later, group A was intraperitoneally injected with methylprednisolone 30 mg/kg every 24 hours; group B was injected with Shuxuening injection (EGb) 1.75 mg/kg every 24 hours; group C were injected with equal volume of saline. The slow wave of intestinal smooth muscle was measured, the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in serum were determined 1 day, 3 days and 7 days after modeling, while intestinal tissue was tested with HE staining. Results The amplitude and frequency of the myoelectric slow wave increased in the groups A and B 3 and 7 days after modeling compared with those in the group C (P<0.05); meanwhile, the activity of SOD increased and content of MDA decreased in the groups A and B (P<0.05). The HE scores decreased in the groups A and B compared with those in the group C (P<0.05), which presented that the inflammatory exudation was mild, the hemorrhagic spot was few and the area was limited. The intestinal villous of the group C was blunt with large infiltration of inflammatory cells and inflammatory exudate on the mucosal surface. Conclusion EGb can improve the recovery of intestinal function in rats spinal cord injury through antioxidant.

Effect of Grape Seed Proanthocyanidin Extract on Ultrastructure Injury in Hippocampous and Cognition Impairment in Rats of Obstructive Sleep Apnea Hypoxia / 中国康复理论与实践

@#Objective To investigate the effect of grape seed proanthocyanidin extract (GSPE) on ultrastructure injury in hippocampous and cognition impairment in rat model of obstructive sleep apnea hypoxia. Methods 80 male Sprague-Dawley rats were randomly divided into control group, model group, high and low dose GSPE groups. The control group was exposed in air, while the model group was suffered from intermittent hypoxia conditions (50 ml/L, 8 h everyday, for 2 or 6 weeks), and the GSPE groups accepted GSPE 200 mg/kg or 100 mg/kg 2 weeks respectively before hypoxia. Pathology in hippocampal region was observed under electromicroscope. Malondialdehyde (MDA) contents and superoxide dismutase (SOD) activity were detected with colorimetry, and apoptotic cells were measured with TUNEL. The cognition function of rats was assessed with the Morris water maze (MWM). Results The ultrastructure in hippocampous was significantly injured,with the increase of MDA and decrease of SOD (P<0.001) in the model group. The apoptotic cells increased (P<0.001). The escaping latency prolonged (P<0.001) and the frequency of crossing the platform decreased (P<0.001) in MWM test in the model group. Compared with the model group, the GSPE groups decreased in MDA content, increased in SOD level, decreased in apoptotic cells and ultrastructure damages, shortened the escaping latency, and increased the frequency of crossing the platform (P<0.001), especially in the high dose group (P<0.05). Conclusion GSPE can relieve the damage of ultrastructure and improve cognition function after obstructive sleep apnea hypoxia in rats.

Effect of Aprotinin Preconditioning on Nitric Oxide, Nitric Oxide Synthase and Oxyradical During Spinal Cord Ischemia-reperfusion Injury in Rabbits / 中国康复理论与实践

@# Objective To observe the effect of aprotinin preconditioning on nitric oxide (NO), nitric oxide synthase (NOS) and oxyradical during spinal cord ischemia-reperfusion injury in rabbits.Methods 21 rabbits were randomly divided into the aprotinin treatment group (8 rabbits), control group (8 rabbits) and sham operative group (5 rabbits). The infrarenal segment in abdominal aorta was clamped for 60 min to construct the model of lumbosacral spinal cord ischemia in rabbits. Reperfusion was followed and kept on for 24 h until the blood flow regained normal. In the treatment group, aprotinin was given at 3×107 IU/kg as a short time intravenous injection for 10 min before ischemia, and then was drilled with micro pump by 1×107 IU/kg/h. Normal saline was used in the control group, the ischemia-reperfusion duration between aprotinin treatment group and control group remained same. The sham operative group was only exposured abdominal aorta and not clamped. The rabbits were killed before ischemia and 8 h, 24 h after ischemia-reperfusion, lumbar segment was harvested to detect content of NO, malondialdehyde (MDA), induced nitric oxide synthase (iNOS) and superoxide dismutase (SOD) of spinal cord.Results 8 h after spinal cord ischemia-reperfusion, compared with the control group, the content of NO, MDA and the activity of iNOS were less, and the activity of SOD was more in the aprotinin treatment group ( P<0.05).Conclusion Aprotinin pretreatment can reduce the content of NO, MDA and descend the activity of NOS. Moreover aprotinin pretreatment can ascend the activity of SOD and improve apoptosis of nerve cell.

Clinical evaluation of the change of SOD and MDA in the unstable angina pectoris cases after percutaneous coronary intervention / 介入放射学杂志

Objective To evaluate the changes and significances of malondialdehyde(MDA)and Superoxide dismutase(SOD)in unstable angina pectoris(UAP)patient after percutaneous coronary intervention(PCI). Methods MDA and SOD were tested in 25 UAP patients before and 1h,24h,72h after PCI.20 UAP patients who were performed on coronary angiography(CAG) and 20 normal individuals entered this study as contrasts.All the UAP patients were followed up for 3 months。 Results Level of MDA in UAP cases significantly increased compared with the normal individuals, P