monodehydroascorbate and Disease-Models--Animal

To study the effects and immunoregulation mechanism of the traditional Mongolian medicine Wuweifengshi capsule on adjuvant arthritis (AA).. Wister rats were divided into several groups: normal group, AA model group, Wuweifengshi capsule groups (with low, moderate, high dose of 0.2, 0.4, 0.8 g x kg(-1) x d(-1) respectively), and Zhonglun-5 group (original dose of 1.68 g x kg(-1) x d(-1)). The edema degree, the level of IL-1beta, TNF-alpha, PGE2, NO and MDA and the activity of SOD in serum were detected. Through cell culture, the effects of the medicine on AA rat's splenic cell's multiplication capacity were studied. The influence of celiac macrophage cell culture fluid of AA rats' on C57BL/6J mice thymic cell multiplication capacity under the medicine was evaluated.. Wuweifengshi capsule showed an inhibiting function on the level of IL-1beta, TNF-alpha, PGE2, NO and increased the activity of SOD in serum, but showed no significant influence on MDA. It also inhibited the AA rat's splenic cell's multiplication capacity and the influence of celiac macrophage cell culture fluid of AA rat's on C57BL/6J mice thymic cell multiplication capacity.. The anti-AA effect of Wuweifengshi capsule is possibly due to its inhibition of relevant cytokines and its adjustment of corresponding enzyme's activity and immunization organ's cell multiplication capacity.

Topics: Animals; Arthritis, Experimental; Capsules; Dehydroascorbic Acid; Dinoprostone; Disease Models, Animal; Edema; Female; Interleukin-1beta; Lymphocytes; Macrophages, Peritoneal; Male; Medicine, Mongolian Traditional; Mice; Nitric Oxide; Rats; Spleen; Superoxide Dismutase; Tumor Necrosis Factor-alpha

Oxidative stress has been implicated in the pathogenesis of many neurodegenerative diseases including Alzheimer's disease (AD). We investigated the effect of a truncated form of the human tau protein in the neurons of transgenic rats. Using electron paramagnetic resonance we observed significantly increased accumulation of ascorbyl free radicals in brains of transgenic animals (up to 1.5-fold increase; P < 0.01). Examination of an in vitro model of cultured rat corticohippocampal neurons revealed that even relatively low level expression of human truncated tau protein (equal to 50% of endogenous tau) induced oxidative stress that resulted in increased depolarization of mitochondria (approximately 1.2-fold above control, P < 0.01) and increases in reactive oxygen species (approximately 1.3-fold above control, P < 0.001). We show that mitochondrial damage-associated oxidative stress is an early event in neurodegeneration. Furthermore, using two common antioxidants (vitamin C and E), we were able significantly eliminate tau-induced elevation of reactive oxygen species. Interestingly, vitamin C was found to be selective in the scavenging activity, suggesting that expression of truncated tau protein preferentially leads to increases in aqueous phase oxidants and free radicals such as hydrogen peroxide and hydroxyl and superoxide radicals. Our results suggest that antioxidant strategies designed to treat AD should focus on elimination of aqueous phase oxidants and free radicals.

Topics: Animals; Antioxidants; Ascorbic Acid; Brain; Cells, Cultured; Cerebral Cortex; Dehydroascorbic Acid; Disease Models, Animal; Electron Spin Resonance Spectroscopy; Free Radicals; Hippocampus; Humans; Mitochondria; Neurons; Oxidative Stress; Rats; Rats, Transgenic; Reactive Oxygen Species; tau Proteins; Tauopathies; Vitamin E

The purpose of this study is to assess the effect of beta1-selective blocker on coronary vasospasm.. Balloon epicardial coronary artery endothelial denudation was performed at the left anterior descending coronary artery every 2 weeks for a total of 4 times in pigs. Changes in denuded site diameter and left anterior descending coronary artery blood flow caused by acetylcholine or serotonin were assessed before each endothelial denudation and at week 8 in untreated pigs (ED group) and in those treated with metoprolol (Meto group) or propranolol (Pro group).. In the ED group, decreased blood flow response to acetylcholine enhanced from -20+/-10% before the first ED to -100% (i.e. zero flow) at week 8 without denuded site narrowing, suggesting microvascular spasm, and serotonin-induced left anterior descending coronary artery diameter reduction at week 8 was -92+/-15%. In the Pro group, blood flow reduction by acetylcholine and left anterior descending coronary artery diameter reduction by serotonin did not change compared with those of the ED group. In the Meto group however, blood flow reduction by acetylcholine (week 8, -70+/-16%) and left anterior descending coronary artery diameter reduction by serotonin (week 8, -64+/-15%) were blunted (P<0.01) compared with those of ED and Pro groups.. The beta1-selective blocker metoprolol was effective to prevent coronary vasospasm.

Topics: Acetylcholine; Adrenergic beta-1 Receptor Antagonists; Adrenergic beta-Antagonists; Animals; Cholinergic Agents; Coronary Angiography; Coronary Vasospasm; Coronary Vessels; Dehydroascorbic Acid; Disease Models, Animal; Laser-Doppler Flowmetry; Metoprolol; Nitric Oxide; Propranolol; Serotonin; Serotonin Agents; Swine

We investigated the influence of deep hypothermia (4 degrees C) during ischemia-reperfusion in the isolated rat heart model.. Isolated, perfused rat hearts underwent either 30 minutes of normothermic ischemia (control group) or 30 minutes of hypothermic ischemia (hypothermia-treated group), followed by 30 minutes of reperfusion in both groups. We recorded functional parameters and used electron spin resonance (ESR) spectroscopy to detect ascorbyl radicals, as markers of free-radical production, in samples of coronary effluents.. Functional parameters were stable in the 2 groups during pre-ischemic and ischemic periods. During reperfusion, coronary flow, left diastolic ventricular pressure, left ventricular developed pressure, and heart rate more rapidly recovered to values close to those obtained during the pre-ischemic period in the hypothermia-treated group than in the control group. Moreover, the post-ischemic contracture observed in the control group did not appear in the hypothermia-treated group. Finally, ESR analysis showed that the post-ischemic release of ascorbyl radicals decreased in the hypothermia-treated group.. These results demonstrate that the protective effect of hypothermia against functional injury caused by ischemia-reperfusion may decrease the free-radical burst at reperfusion.

Topics: Animals; Coronary Circulation; Dehydroascorbic Acid; Disease Models, Animal; Electron Spin Resonance Spectroscopy; Hypothermia, Induced; Myocardial Ischemia; Rats; Rats, Wistar; Recovery of Function; Reperfusion Injury; Ventricular Pressure