Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.23.5 (cathepsin D)
4,130 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Perivascular macrophages are considered as cerebral scavenger cells under physical and pathological conditions. In this study, we tried to examine changes of perivascular macrophages, especially changes of the characteristic lysosomal inclusion bodies that are rich in hydrolytic enzymes, in the process of brain edema induced by cold injury. Wistar male rats aged 4 months were treated with dry ice for 20 minutes through a drilled hole at the parietal bone. At different time points after the cold injury, cerebral cortex was excised and the immunoreaction for cathepsin D, one kind of lysosomal protease, was examined by post-embedding immuno-electron microscopy. The reactions of cathepsin D were located in the inclusion bodies of perivascular macrophages. At 5 and 10 hours after cold injury, the reactions increased dramatically. Then the reactions inclined to decrease, and reached the minimum at 1 week after cold injury. The reactions seemed to recover at 2 weeks after cold injury. The changes of cathepsin D reactions suggest that the function of perivascular macrophages as scavenger cells were activated in the early phase of the process of brain edema, their later declines might be caused by severe pathological conditions.
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PMID:Changes of perivascular macrophages in the process of brain edema induced by cold injury. 1475 53

Previous studies have demonstrated that autophagy induced by caloric restriction (CR) is neuroprotective against cerebral ischemia. However, it has not been determined whether intermittent fasting (IF), a variation of CR, can exert autophagy-related neuroprotection against cerebral ischemia. Therefore, the neuroprotective effect of IF was evaluated over the course of two weeks in a rat model of focal cerebral ischemia, which was induced by middle cerebral artery occlusion and reperfusion (MCAO/R). Specifically, the role of autophagy modulation as a potential underlying mechanism for this phenomenon was investigated. It was demonstrated that IF reduced infarct volume and brain edema, improved neurobehavioral deficits, and rescued neuronal loss after MCAO/R. Furthermore, neuronal apoptosis was decreased by IF in the rat cortex. An increase in the number of autophagosomes (APs) was demonstrated in the cortices of IF-treated rats, using immunofluorescence staining and transmission electron microscopy. Using immunoblots, an IF-induced increase was detected in microtubule-associated protein 1 light chain 3 (LC3)-II, Rab7, and cathepsin D protein levels, which corroborated previous morphological studies. Notably, IF reduced the accumulation of APs and p62, demonstrating that IF attenuated the MCAO/R-induced disturbance of autophagic flux in neurons. The findings of the present study suggest that IF-induced neuroprotection in focal cerebral ischemia is due, at least in part, to the minimization of autophagic flux disturbance and inhibition of apoptosis.
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PMID:Intermittent fasting is neuroprotective in focal cerebral ischemia by minimizing autophagic flux disturbance and inhibiting apoptosis. 2788 10