Current Issue : July - September Volume : 2019 Issue Number : 3 Articles : 5 Articles
A MIL series metal-organic framework (MOF), MIL-100(Fe), was successfully synthesized\nat the nanoscale and fully characterized by TEM, TGA, XRD, FTIR, DLS, and BET. A toxicological\nassessment was performed using two different cell lines: human normal liver cells (HL-7702) and\nhepatocellular carcinoma (HepG2). In vitro cytotoxicity of MIL-100(Fe) was evaluated by the MTT\nassay, LDH releasing rate assay, DAPI staining, and annexin V/PI double staining assay. The safe\ndose of MIL-100(Fe) was 80micro g/mL. It exhibited good biocompatibility, low cytotoxicity, and high\ncell survival rate (HL-7702 cellsâ?? viability >85.97%, HepG2 cellsâ?? viability >91.20%). Therefore,\nMIL-100(Fe) has a potential application as a drug carrier....
Parkinsonâ??s disease (PD), a multifactorial movement disorder that involves progressive\ndegeneration of the nigrostriatal system affecting the movement ability of the patient. Oxidative\nstress and neuroinflammation both are shown to be involved in the etiopathogenesis of PD.\nThe aim of this study was to evaluate the therapeutic potential of thymol, a dietary monoterpene\nphenol in rotenone (ROT)-induced neurodegeneration in rats that precisely mimics PD in humans.\nMale Wistar rats were injected ROT at a dose of 2.5 mg/kg body weight for 4 weeks, to induce\nPD. Thymol was co-administered for 4 weeks at a dose of 50 mg/kg body weight, 30 min prior to\nROT injection. The markers of dopaminergic neurodegeneration, oxidative stress and inflammation\nwere estimated using biochemical assays, enzyme-linked immunosorbent assay, western blotting and\nimmunocytochemistry. ROT challenge increased the oxidative stress markers, inflammatory enzymes\nand cytokines as well as caused significant damage to nigrostriatal dopaminergic system of the brain.\nThymol treatment in ROT challenged rats appears to significantly attenuate dopaminergic neuronal\nloss, oxidative stress and inflammation. The present study showed protective effects of thymol\nin ROT-induced neurotoxicity and neurodegeneration mediated by preservation of endogenous\nantioxidant defense networks and attenuation of inflammatory mediators including cytokines\nand enzymes....
According to a previous study, YGDEY from tilapia fish skin gelatin hydrolysates has\nstrong free radical scavenging activity. In the present study, the protective effect of YGDEY against\noxidative stress induced by ethanol in HepG2 cells was investigated. First, cells were incubated\nwith YGDEY (10, 20, 50, and 100 micron) to assess cytotoxicity, and there was no significant change in\ncell viability. Next, it was established that YGDEY decreased the production of reactive oxygen\nspecies (ROS)..........................
Arsenic trioxide (ATO) has been verified as a breakthrough with respect to the management\nof acute promyelocytic leukemia (APL) in recent decades but associated with some serious adverse\nphenomena, particularly cardiac functional abnormalities. Salvianolic acid A (Sal A) is a major\neffective component in treating ATO-induced cardiotoxicity. Therefore, the objective of our study\nwas to assess whether Sal A had protective effects by the regulation of calcium homeostasis and\nendoplasmic reticulum (ER) stress. For the in vivo study, BALB/c mice were treated with ATO\nand/or Sal A via daily tail vein injections for two weeks. For the in vitro study, we detected the effects\nof ATO and/or Sal A in real time using adult rat ventricular myocytes (ARVMs) and an IonOptix\nMyoCam system Our results showed that Sal A pretreatment alleviated cardiac dysfunction and\nCa2+ overload induced by ATO in vivo and vitro. Moreover, Sal A increased sarcoplasmic reticulum\n(SR) Ca2+-ATPase (SERCA) activity and expression, alleviated [Ca2+]ER depletion, and decreased\nER stress-related protein expression. Sal A protects the heart from ATO-induced injury and its\nadministration correlates with the modulation of SERCA, the recovery of Ca2+ homeostasis, and the\ndown-regulation of ER stress-mediated apoptosis...
Purpose: Investigating the triple effect of doxorubicin, 5-fluorouracil, propranolol\non MCF-7 (ER+, WTp53) breast cancer cell line with MTT test and\nsurvival analysis. Materials/Methods: In order to determine effective dosages\nof a combination of doxorubicin, 5-fluorouracil, propranolol on the MCF-7\ncell line by using MTT and survival analysis technique. Result: IC50 values\nacquired by MTT tests are 0.01 mg/ml for doxorubicin, 6 mg/ml for\n5-fluorouracil, 30 mg/ml for propranolol and 0.2/1/30 mg/ml (with previous\nrespect) if all three agents are combined. It is found that the use of doxorubicin,\n5-fluorouracil, and propranolol in combination is much effective than\ntheir single application. Discussion: Moderate concentrations of doxorubicin,\n5-fluorouracil, and propranolol, if they are applied individually, showed\nhigh toxicity. When we used these drugs in combination; toxic effects lessened\nwith respect to monotherapy. In the MCF-7 cell line, doxorubicin (IC50:0.01microM)\n increases cell death rates significantly and propranolol (IC50: 3 microM)\nhas minimum effects in monotherapy in contrast to others. Propranolol is\nonly superior to itself in combination therapy (IC50: 4 microM). However\n5-fluorouracil (IC50: 30 microM) showed antagonistic effects with respect to other\ndrugs. Additionally, having applied the three drugs in combination on the\nMCF-7 cell line for the first time in literature, it is highly possible to assess the\napplication of doxorubicin, 5-fluorouracil and propranolol combination as a\nnovel therapy option....
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