The Protective Effect Of Atorvastatin On Neurons Induced By Aβ25～35

Background and objectiveAlzheimer’s disease commonly happens in senior people which is characterizedby progressive cognitive impairment and behavioral dysfunctions among the centralnervous system degenerative diseases. In our country, the the focus of scienceresearch and public are on the high mortality rate diseases, such as cardiovasculardiseases and cancer. Correspondingly，Alzheimer ’s disease does not obtain muchattention, and the quantity of Alzheimer’s patients is seriously underestimated. Thereis an urgent need about numerous researches associated with the Alzheimer’s disease.The researches about treatment of Alzheimer’s disease are most important. β amyloidprotein-induced oxidative stress theory occupies a major position in the pathogenesisof Alzheimer’s disease. Research data indicate that statins have a therapeutic effecton Alzheimer’s disease, but some studies hold the opposite view.At present, the exactmechanisms of statins on Alzheimer’s disease are unclear. Statins can lowercholesterol, reduce inflammation reaction, resistant oxidation reaction, stabilizeendothelial cells and adjust immune functions. Statins protective effect on neuronalcells whether via antioxidant is not yet known. The experiment use Aβ25~35toinduce damages on rat cortical neurons and simulate pathological processes ofAlzheimer’s disease in vitro. Different concentrations of atorvastatin arepre-treatmented to neurons to observe changes in neuronal cell morphology, cellviability, MDA content and SOD activity, and in order to explore the possiblemechanisms of statin on Alzheimer’s disease.MethodsThe rat cortical neurons got from newborn SD rats were cultured in vitro for7days. After the identification of cells, neurons were randomly divided into controlgroup, Aβ group,1μmol/L Ato group,5μmol/L Ato group,10μmol/L Ato group,Aβ+1μmol/L Ato group, Aβ+5μmol/L Ato group, Aβ+10μmol/L Ato group. Adenovirus which can express green fluorescent protein (Ad-EGFP) were used totransfect neurons, then neurons morphology were observed by fluorescencemicroscopy. Cell viability of groups were detected by MTS assay.The MDA contentand SOD activity were detected respectively by the thiobarbituric method and WST-1method.ResultsCompared with the control group, cell morphology, viability, MDA content andSOD activity of1μmol/L Ato group,5μmol/L Ato group,10μmol/L Ato groupwere not significantly different (P>0.05). Compared with the control group, in Aβgroup the number of neurons and cell branches reduced, cell viability decreased,MDA content increased and SOD activity decreased, and the differences werestatistically significant (P<0.001). Compared with Aβ group, in Aβ+1μ mol/L Atogroup, Aβ+5μ mol/L Ato group, Aβ+10μ mol/L Ato group, the number ofneurons and cell branches increased, and neural networks still remained; and cellviability increased, MDA content decreased and SOD activity increased, thedifference was statistically significant (P <0.001). In the Aβ+5μmol/L Ato group，the cell viability and SOD activity were highest, the content of MDA was lowest.Compared with the Aβ+1μmol/L Ato group, in Aβ+5μmol/L Ato group, the cellviability and the SOD activity were higher, the content of MDA was lower, thedifferences were statistically significant (P<0.05).Conclusions1．Atorvastatin have no effect on neurons.2．Aβ25~35can induce damages on neurons.3．Atorvastatin have a protective effect on neurons induced by Aβ25~35,and themechanisms may be related to the antioxidant effect of atorvastain.4．The protective effect of atorvastatin on neuronal induced by Aβ25~35is not in aconcentration-dependent manner, and the reason for the phenomenon needs further studies.