Cerebral Cell Apoptosis Research Articles

Influence of Grape seed proanthocyanidin extract on deep hypothermia cerebral ischemia-reperfusion in mice

Objective To determine the mechanism of Grape seed proanthocyanidin extract on a model of brain injury induced by deep hypothermic cerebral ischemia/reperfusion (I/R).Methods Sixty four-week-old C57BL6 mice were randomly and equally divided into sham operation group,model group and grape seed proanthocyanidin extract (GSPE) group.The mice were sacrificed 24 h after reperfusion for sampling of brain tissues.The expression of serine/threonine kinase (AKT) protein was detected by using Western blotting,Caspase-3 mRNA was detected by reverse transcription-polymerase chain reaction ( RTPCR) technique,and apoptosis of cerebral cells was examined by using TUNEL staning.Results The expression of p-AKT protein and Caspase-3 mRNA,and apoptotic level in model group and GSPE group were significantly increased as compared with sham operation group ( P ＜ 0.05 ).The expression of p-AKT protein [A ( 1.9 ±0.02) ＞ ( 1.6 t0.01 ),P ＜0.05 ] was increased,and expression of Caspase-3 mRNA and apoptosis were significantly decreased in GSPE group as compared with model group [ ( 0.43 t 0.02 ) ＜(0.86 ±0.03); (40.92 ±3.18)％ ＜ (79.86 ±4.68)％,P＜0.05].Conclusion The results suggest that GSPE has a protective effect against deep hypothermic cerebral I/R injury through AKT-Caspase-3 pathway. Key words: Grape seed proanthocyanidin extract; Cerebral ischemia; Reperfusion; AKT; Caspase-3

Apoptosis in tissues from fatal dengue shock syndrome

Background Apoptosis, or programmed cell death, has been implicated in dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS) pathogenesis. Objectives To determine the in vivo apoptosis contribution to the pathogenesis of fatal DHF/DSS during a Cuban dengue epidemic. Study design We detected apoptosis by the TdT-mediated dUTP Nick-End Labeling (TUNEL) technique and dengue virus (DENV) antigens by an immunohistochemical assay in different tissues from six individuals who died of DHF/DSS during the Santiago de Cuba DENV-2 epidemic in 1997. Results DENV antigens were immunolocalized mainly in hepatocytes. Apoptotic cells were found in five of the six cases studied. Apoptosis was demonstrated in liver, brain, intestinal and lung tissues. Severe brain hypoxia and ischemia in the studied subjects during DHF/DSS probably might induce apoptosis in cerebral cells. Apoptotic microvascular endothelial cells (ECs) in pulmonary and intestinal tissues, a finding only previously reported in vitro, are likely related to vascular plasma leakage manifested by the individuals. Conclusions Apoptosis was demonstrated in cerebral cells, white blood cells, intestinal and pulmonary microvascular ECs from Cuban fatal cases of DHF/DSS. As far as we know, these findings have not been previously reported in DHF/DSS. Our results indicate there is very likely an in vivo contribution of apoptosis to the pathophysiological mechanisms of DHF/DSS.