ABSTRACT
Peroxisome proliferators-activated receptor γ (PPARγ) belongs to a nuclear receptor superfamily. Many studies have shown that PPARγ can help to improve the outcome of cerebrovascular disease. PPARγ can reduce inflammatory response, oxidative stress as wel as enhance the hematoma removal abilities of microglia and macrophages, and it plays an important protective role in intracerebral hemorrhage.
ABSTRACT
objective To examine nuclear transIocation of peroxisome proliferator-activated receptor γ(PPARγ)in rats following focal cerebral ischemia/reperfusion(I/R),and to explore the significance of altered PPARγ,nuclear translocation in ischemic brain injury.Methods Healthy adult male SD rats underwent 60-min cerebral artery occlusion followed by reperfusion of 4,8,or 24 h,respectively.The cytoplasmic-to-nuclear shuttling of PPARγ was characterized by Western blot,immunohistochemical and immunofluoreseence staining.The effects of PPARγ agonist rosiglitazone (Ros) and antagonist GW9662 on I/R-induced PPARγ nuclear translocation were also examined in the present study. Furthermore,TTC staining war adopted to determine the change in cerebral infarction volume. Results (1)Western blot analysis revealed an increase of PPARγ in the nucleus and a simultaneous reduction in the cytosol following ischemia and reperfusion for 4 h(tcytosol=9.03,tmuclear=27.19,P=0.00).Prolonged the reperfusion further enhanced this I/R induced PPARγ translocation in a time-dependent manner.Using immunohistochemistry and immunofluorescence,nuclear PPAR γ positive staining increased from 48.3%in the sham control to 80.3% following ischemia and reperfusion for 24 h.(2)Western blot analysis revealed that PPARγ agonist Ros further increased I/R-induced nuclear enrichment of PPARγ,whereas PPARγ antagonist GW9662inhibited I/R-stimulated change in PPARγ.(3)When compared to the L/R group using TTC staining,Ros treatment significantly decreased the infarction volume by 48.40%(15.46±4.94 versus 29.96±3.39,t=5.93.P=0.00),whereas GW9662 increased by 58.95%(47.62±4.93 versus 29.96±3.39,t=7.23,P=0.00).Conclusions Cerebral I/R injury induces PPARγ translocation from the cytosol to the nucleus.This change may represent an intrinsic neuroprotective response against brain I/R injury.
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OBJECTIVE@#To study the inhibitory effect of resveratrol on growth of human laryngeal cancer cell line, Hep-2.@*METHOD@#Count cell number under microscope, MTT assay was used to determine the cell growth inhibitory rate. Soft agar colony forming experiment was performed to observe the proliferation ability, before or after resveratrol treatment.@*RESULT@#Resveratrol was able to depress cell growth and inhibit cell proliferation.@*CONCLUSION@#Resveratrol strongly inhibit Hep-2 cell proliferation in a time- and dose-dependent manner.
Subject(s)
Humans , Cell Cycle , Cell Line, Tumor , Cell Proliferation , Dose-Response Relationship, Drug , Resveratrol , Stilbenes , PharmacologyABSTRACT
Objective Investigate MR resonance diffusion tensor im-aging (DTI) characteristics of non-pyramid tracts in the patients with amyotrophic lateral sclerosis(ALS). Methods 21 patients with ALS were served as case group.20 healthy volunteers were served as healthy controls. All subjects underwent a DTI sequence, chose region of interest (ROI) to measure fractional anisotropy (FA) and mean diffusivity (MD).Results In case group, FA decreased on the splenium of corpus callosum (0.73?0.087)(u=-2.004,P