Current Issue : January - March Volume : 2018 Issue Number : 1 Articles : 5 Articles
Diabetic neuropathic pain (DNP), one of the early symptoms of diabetic neuropathy, relates to metabolic disorders induced by high\nblood glucose, neurotrophic vascular ischemia and hypoxia, and autoimmune factors. This study was aimed at exploring the effects\nof long noncoding RNA (lncRNA) BC168687 siRNA on DNP mediated by P2X7 receptor on SGCs inDRGof rats.The mechanical\nwithdrawal threshold (MWT) and thermal withdrawal latency (TWL) of rats, the expression levels of P2X7 mRNA and protein in\nthe DRG, and nitric oxide (NO) in the serum were, respectively, detected in our study. Our experimental results showed that the\nlevel of BC168687mRNA inDNP group wasmarkedly higher than that of control group; theMWTand TWL ofDNP + BC168687\nsi group were significantly increased, and the expression levels of P2X7 in DRG and the concentrations of NO in serum of DNP\n+ BC168687 si group were decreased compared to those of the DNP group. In conclusion, lncRNA BC168687 may participate in\nthe pathogenesis of DNP mediated by P2X7 receptor, which will provide a novel way for the study of the pathogenesis of diabetes\nmellitus complicated with neuropathic pain and its prevention and treatment....
Our aim was to verify the effects of prednisone related to gastrointestinal motility, intestinal histology, and mucosal mast cells\nin rats. Two-month-old male Wistar rats were randomly assigned to control group (vehicle) animals receiving saline 0.9% (...
The aim of this study was to determine if chronic, low-dose administration of a nonspecific cannabinoid receptor agonist could\nprovide cardioprotective effects in a model of type I diabetes mellitus. Diabetes was induced in eight-week-old maleWistar-Kyoto\nrats via a single intravenous dose of streptozotocin (65mg kgâË?â??1). Following the induction of diabetes, Ã?â?9-tetrahydrocannabinol was\nadministered via intraperitoneal injection (0.15mg kgâË?â??1 dayâË?â??1) for an eight-week period until the animals reached sixteen weeks of\nage.Upon completion of the treatment regime, assessments of vascular reactivity and left ventricular function and electrophysiology\nwere made, as were serum markers of oxidative stress and lipid peroxidation. Ã?â?9-Tetrahydrocannabinol administration to diabetic\nanimals significantly reduced blood glucose concentrations and attenuated pathological changes in serum markers of oxidative\nstress and lipid peroxidation. Positive changes to biochemical indices in diabetic animals conferred improvements in myocardial\nand vascular function. This study demonstrates that chronic, low-dose administration of Ã?â?9-tetrahydrocannabinol can elicit\nantihyperglycaemic andantioxidant effects indiabetic animals, leading to improvements in end organ function of the cardiovascular\nsystem. Implications from this study suggest that cannabinoid receptors may be a potential new target for the treatment of diabetesinduced\ncardiovascular disease....
Proanthocyanidins (PCs) have shown inhibition of oxidative damage by improving Nrf-2 expression inmany tissues. However, the\ncytoprotective effects of PCs onH2O2-induced tendon damage have not been verified. The current study was aimed at assessing the\ncytoprotection of PCs on the oxidative cellular toxicity of tendon-derived stem cells (TDSCs) induced by H2O2. The TDSCs were\nisolated frompatellar tendons of Sprague Dawley (SD) rats, and the cells after third passage were used for subsequent experiments.\nThe isolated cells were identified by flow cytometry assay and multidifferentiation potential assay. Cell Counting Kit-8 assay was\nperformed to examine cell viability. Real-Time PCR andWestern Blot were employed to, respectively, assess the mRNA and protein\nexpressions of Nrf-2, GCLM, NQO-1, and HO-1. PCs significantly improved the cell viability of TDSCs. Furthermore, H2O2\nupregulated Nrf-2, GCLM, NQO-1, and HO-1 without significant difference, while the proteins expressions were increased with\nsignificant difference in PCs group and PCs + H2O2 cotreated group. All the findings indicated that PCs could protect against\nthe oxidative damage induced by H2O2 in TDSCs, and the cytoprotective effects might be due to the ability of PCs to activate the\nexpressions of GCLM, HO-1, and NQO-1 via upregulating Nrf-2 signaling pathway....
Background: Atenolol, a hydrophilic beta blocker, has been used as a model drug for studying passive permeability\nof biological membranes such as the bloodââ?¬â??brain barrier (BBB) and the intestinal epithelium. However, the extent of\nS-atenolol (the active enantiomer) distribution in brain has never been evaluated, at equilibrium, to confirm that no\ntransporters are involved in its transport at the BBB.\nMethods: To assess whether S-atenolol, in fact, depicts the characteristics of a low passive permeable drug at the\nBBB, a microdialysis study was performed in rats to monitor the unbound concentrations of S-atenolol in brain extracellular\nfluid (ECF) and plasma during and after intravenous infusion. A pharmacokinetic model was developed, based\non the microdialysis data, to estimate the permeability clearance of S-atenolol into and out of brain. In addition, the\nnonspecific binding of S-atenolol in brain homogenate was evaluated using equilibrium dialysis.\nResults: The steady-state ratio of unbound S-atenolol concentrations in brain ECF to that in plasma (i.e., Kp,uu,brain) was\n3.5% Ã?± 0.4%, a value much less than unity. The unbound volume of distribution in brain (Vu, brain) of S-atenolol was\nalso calculated as 0.69 Ã?± 0.10 mL/g brain, indicating that S-atenolol is evenly distributed within brain parenchyma.\nLastly, equilibrium dialysis showed limited nonspecific binding of S-atenolol in brain homogenate with an unbound\nfraction (fu,brain) of 0.88 Ã?± 0.07.\nConclusions: It is concluded, based on Kp,uu,brain being much smaller than unity, that S-atenolol is actively effluxed\nat the BBB, indicating the need to re-consider S-atenolol as a model drug for passive permeability studies of BBB transport\nor intestinal absorption....
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