Diosmin is a flavonoid found in a variety of citrus fruits and also an agonist of the aryl hydrocarbon receptor (AhR). Diosmin is known to exhibit anti-inflammatory, antimutagenic, antioxidant, and free radical scavenging as well as blood lipid lowering activities among others. Diosmin-100 and Diosmin-200 significantly attenuated the damage to lung epithelium, alveolar architecture, and reduced inflammatory cell infiltration in the lung tissues of mice. Diosmin significantly attenuated the levels of oxidative stress markers: lactate dehydrogenase and xanthine oxidase[3]. At 5 μM, Diosmin increases the cytotoxicity of 7,12-dimethylbenz(a)anthracene (DMBA), shifting the IC50 of DMBA from an estimated 1.2 μM to 400 nM. Diosmin is not cytotoxic in itself at the concentrations tested. Diosmin causes an increase in CYPIAI activity in MCF-7 cells in a time- and dose-dependent fashion[4]. Diosmin protected the retina from I/R injury, possibly via a mechanism involving the regulation of oxidative parameters[5]. Moreover, diosmin is able to induce caspase-dependent apoptosis specifically in tumor cells and, therefore, could be considered a promising therapeutic compound against glioblastoma[6].
77-67-8 Ethosuximide
Ethosuximide, 2-ethyl-2-methylsuccinimide, has been used extensively for "petit mal" seizures. Commonly observed side effects of ethosuximide are dose dependent and involve the gastrointestinal tract and central nervous system. The spontaneous pacemaker oscillatory activity of thalamocortical circuitry involves low threshold T-type Ca2+ currents in the thalamus, and ethosuximide is presumed to reduce these low threshold T-type Ca2+ currents in thalamic neurons. Ethosuximide also decreases the persistent Na+ and Ca2+ -activated K+ currents in thalamic and layer V cortical pyramidal neurons[7]. Ethosuximide and valproic acid are more effective than lamotrigine in the treatment of childhood absence epilepsy. Ethosuximide is associated with fewer adverse attentional effects[8]. Concentrations of 2 μM or more of Ethosuximide not only are found to be less effective than 1 μM concentration of Ethosuximide, but also induce cell toxicity. The number and percentage of tubulin β-III immunopositive neurons were increased after 6 days treatment with ethosuximide. Ethosuximide may compensate damage caused by seizure attacks and possibly other neuronal loss disorders[9]. Ethosuximide given with drinking water (300 mg/kg/day) over 45 days slightly reduced proneness to audiogenic epilepsy and increased locomotor activity of the animals at the periphery of the open field. A weak anticonvulsant effect of ethosuximide on tonic convulsions with its predominant effect on convulsions with forebrain focus location[10].
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