The platelet-to-lymphocyte ratio could represent pro-thrombotic inflammatory state in acute ischemic stroke patients because having a high-PLR values increased the poor prognosis, the rate of insufficient recanalization, and the size of infarcted area.
AIm: Current stroke therapies include lipid-lowering drugs, which reduce inflammation and serve to stabilize the atherosclerotic plaque to demonstrate better outcome and neuroprotection. Peroxisome proliferator activated receptors (PPAR) α regulates lipid homeostasis and is a target of fibrates, which have a neuroprotective function by various mechanisms. In this study, we aimed to evaluate the role of the PPARα agonist, fenofibrate, in the modulation of cleaved caspase-3 immunoreactivity and at the final infarct volume in an experimental ischemia/reperfusion rat model by induced transient proximal middle cerebral artery occlusion. mATERIAl and mEThODS: A total of 65 male Sprague Dawley rats were allocated into 4 groups; sham (n =5), experiment 1 (n=20), experiment 2 (n=20), experiment 3 (n=20). All experiment groups were divided to 3 subgroups in order to evaluate the final infarct volume at 24 th hour (n=5) and the immunoreactivity of cleaved caspase -3 at different time periods [at first hour (n=5), at 6 th hour (n=5), at 24 th hour (n=5)] after transient middle cerebral artery occlusion (MCAo). At the study, the experiment groups (Experiment 1 and Experiment 2) were received the fenofibrate-diet during 14 days before ischemia procedure. All animals were sacrificed at 24 th hours after MCAo. Infarction volumes were calculated from 2,3,5,triphenyltetrozolium chloride (TTC)-stained brain sections.
RESUlTS:We found that fenofibrate-therapy reduced significantly more body weight than the other experiment groups (p<0.05). At the time intervals, a decrease of immunoreactivity of cleaved caspase-3 was significantly observed with fenofibrate therapy after MCAo (p<0.05). Chronic fenofibrate treatment before cerebral ischemia significantly reduced the infarction size after MCAo compared with the other groups (respectively; p = 0.011 and p< 0.000).
CONClUSION:Fenofibrate treatment has neuroprotective effects on middle cerebral artery infarcts.
Boron is a naturally occurring trace element found in organic and inorganic complexes. Boron-containing compounds are required for living organisms for diverse metabolic functions, including nitrogen fixation in microorganisms, cell wall stability in plants, and bone and carbohydrate metabolism in animals. The number of studies about the effect of boron in biological model systems is very limited; so far, there has been no study on the correlation between boron and amyloid-beta toxicity. Here, we investigated the possible effects of 2 boron-containing compounds—sodium borate decahydrate and boric acid—against amyloid-beta toxicity. In our in vitro amyloid-beta toxicity model, we showed that these 2 compounds increase the survival of the SH-SY5Y cells. Furthermore, boron in these 2 forms increases the expression of Sirt1, which has protective functions against cellular stress. The compounds also change the expressions of GSK-3α/β; by doing so, boron may contribute to the stimulation of intracellular prosurvival pathways. This is the first experimental study indicating the prosurvival effect of boron in an amyloid-beta toxicity model.
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