Introduced the "particles" item testing progress and some notes, using Coulter Multisizer, about medical devices and drugs wrapper, with an expectation of some help for the "particles" item tests in the solution in these area.
Equipment Contamination ; prevention & control ; Equipment and Supplies ; Materials Testing ; instrumentation ; methods ; Particle Size ; Quality Control

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