Abstract
Caspase-3 is a key enzyme to execute apoptosis and may be cause internucleosomal DNA fragmentation in ischemic neurons. However, whether caspase-3 inhibitor can directly inhibit caspase-3–dependent deoxyribonuclease activity and prevent neuronal apoptosis following cerebral ischemic is unknown. In this study, we detected the caspase-3 and CAD protein, as well as the frequencies of neuronal apoptosis in both model control group (DMSO injection) and treatment group (Ac-DEVD-CHO injection) after focal cerebral ischemia-reperfusion in rats. Our data showed that caspase-3 and CAD protein were detectable, and apoptotic-like neuronal death occurred following cerebral ischemic in both groups. However, these results obtained were inhibited by Ac-DEVD-CHO in treatment group as compared with model control group. Taken together, these data further support that the pathway of caspase-3–dependent CAD activity and neuronal apoptosis is an important mechanism in ischemic neuronal injury, and Ac-DEVD-CHO has the neuroprotective effect to a certain degree. Key words: Caspase-3, caspase-activated deoxyribonuclease, Ac-DEVD-CHO, apoptosis, cerebral ischemia.
Highlights
These data further support that the pathway of caspase-3–dependent Caspase-activated deoxyribonuclease (CAD) activity and neuronal apoptosis is an important mechanism in ischemic neuronal injury, and Ac-DEVD-CHO has the neuroprotective effect to a certain degree
Neuronal injury can be caused by many mechanisms after cerebral ischemia, in which neuronal apoptosis mediated by caspases family is an important one (Martin and Green, 1995; Alnemri, 1997; Salvesen and Dixit, 1997; Nunez et al, 1998; Porter and Janicke, 1999; Le et al, 2002)
Cellular edema was relieved at the early stage compared to the model control group; no obvious difference in apoptosis was found at the late stage
Summary
Neuronal injury can be caused by many mechanisms after cerebral ischemia, in which neuronal apoptosis mediated by caspases family is an important one (Martin and Green, 1995; Alnemri, 1997; Salvesen and Dixit, 1997; Nunez et al, 1998; Porter and Janicke, 1999; Le et al, 2002). Caspase-activated deoxyribonuclease (CAD), which is named DNA fragmentation factor (DFF40), participates in the apoptotic cascades as an important effector of caspase-3 (Liu et al, 1997; Inohara et al, 1999; Cao et al, 2001). Previous studies have suggested that caspase-3 dependent CAD activity play an essential role during neuronal apoptosis after ischemia in the brain (Chen et al, 1998; Tsukada et al, 2001; Luo et al, 2002; Abas et al, 2010; Yan et al, 2010). Antiapoptotic mechanisms through caspase inhibition may play neuroprotective role in the brain after focal ischemic injury
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
