OBJECTIVETo investigate the protective effects of selenium on rat hippocampal neurons against ischemia-reperfusion (IR) injury.

METHODSThirty-two rats were randomly divided into sham-operated group, IR group and selenium-treated group, and in the latter two groups, cerebral IR injury was induced by middle cerebral artery occlusion; Na2SeO3 treatment was administer in selenium-treated group. At 14 days after reperfusion, the brain tissues were harvested from the rats and hippocampal neuron injuries were observed by TUNEL and Methylene Blue staining. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and nerve growth factor (NGF) in the hippocampal tissues were measured by ELISA.

RESULTSCompared with IR group, the rats in selenium-treated group showed no significant increase in the expression of m-NGF (P>0.05), but pro-NGF expression was significantly increased (P<0.05) in the hippocampal tissue. Na2SeO3 treatment significantly inhibited the expressions of TNF-α and IL-1β and decreased the apoptosis of hippocampal neurons following cerebral IR injury (P<0.05).

CONCLUSIONSelenium produces antiapoptotic effect to protect the hippocampal neurons following cerebral IR injury possibly not by increasing the level of m-NGF but by decreasing the expressions of the inflammatory factors.

Animals ; Apoptosis ; Brain Ischemia ; metabolism ; pathology ; Hippocampus ; cytology ; metabolism ; pathology ; Interleukin-1beta ; metabolism ; Male ; Nerve Growth Factor ; metabolism ; Neurons ; drug effects ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; pathology ; Sodium Selenite ; pharmacology ; Tumor Necrosis Factor-alpha ; metabolism

Objective To evaluate the differences among five representative and useful Doppler parameters in the diagnosis of the three common types of renal artery stenosis (RAS). Methods Five Doppler parameters including renal peak systolic velocity (RPSV), renal-aortic ratio (RAR), renal-interlobar ratio (RIR),acceleration time (AT),and resistant index (RI) were measured in 221 patients before renal arteriography. Differences between the groups of patients with various clinical causes of RAS were analyzed by Chi-Squared test. One-way ANOVA or t test were used to compare the means between different groups.The optimal cutoff value was determined with the maximum sum of sensitivity and specificity. Results Of the 442 renal arteries (main and accessory renal arteries) demonstrated at arteriography,214 were normal or stenosed less than 50 %, 204 stenoses 50% - 99 %, and 24 occlusions. RIR, RAR and RI were significantly different between the atherosclerotic and non-atherosclerotic RAS groups (P ＜0.05), while RPSV and AT were not. The optimal cutoff values of RAR,RIR and RI for detecting RAS between the atherosclerotic and non-atherosclerotic groups were much different (2.5 versus 1.9, 5. 1 versus 6.5, 0.57 versus 0.50,respectively) ,but those of RPSV and AT were similar or the same (170 cm/s versus 200 cm/s,51 ms versus 51 ms,respectively). Conclusions In the case of RAS (diameter reduction≥50%),it is advised to establish separate cutoff values of RAR, RIR and RI according to atherosclerotic and non-atherosclerotic RAS, but the same cutoff value of RPSV and AT can be applied. RIR is a good Doppler parameter in the diagnosis of RAS,especially atherosclerotic and fibromuscular dysplasia RAS.

Coronary heart disease (CHD) is a kind of cardiovascular diseases originated from atherosclerosis (AS), and chronic inflammation is one of the pathological characteristics. The peripheral blood leukocytes, especially mononuclear cells, play an important role in the AS processes. Recently, in a series of Epigenome-Wide Association Studies (EWAS), multiple DNA differential methylation sites in peripheral blood cells were found to be statistically associated with CHD, which suggested that these DNA differential methylation sites might serve as new risk factors for CHD. The recognition of the variant of DNA methylation as a common epigenetic nucleic acid modification in the occurrence and development of CHD, is ongoing. DNA methylation has the potential to become warning biomarkers, which might provide new ideas and evidences for mechanistic studies of CHD.