Structural and biochemical characterization of the Clostridium perfringens autolysin catalytic domain.

Bacterial autolysins can partially hydrolyze cell wall peptidoglycans into small sections to regulate cell separation/division and the growth phase. Clostridium perfringens autolysin (Acp) has an N-terminal cell wall-binding domain and a C-terminal catalytic domain with glucosaminidase activity that belongs to the glycoside hydrolase 73 family. Here, we determined the X-ray structure of the Acp catalytic domain (AcpCD) at 1.

3,5,6,7,8,3',4'-Heptamethoxyflavone, a citrus flavonoid, on protection against memory impairment and neuronal cell death in a global cerebral ischemia mouse model.

The present study evaluated the effects of treatment with the citrus flavonoid, 3,5,6,7,8,3',4'-heptamethoxyflavone (HMF) on protection against memory impairment and neuronal death in a global cerebral ischemia mouse model. The results showed that HMF, administrated for three days immediately after ischemic surgery, protected against ischemia-induced memory dysfunction, rescued neuronal cell death in the CA1 cell layer, increased the production of BDNF, stimulated the autophosphorylation of CaMK II and suppressed microglial activation in the hippocampus. These results suggest that HMF has a neuroprotective effect after brain ischemia by inducing BDNF production and anti-inflammatory effects.

Oenothein B suppresses lipopolysaccharide (LPS)-induced inflammation in the mouse brain.

Oenothein B has been recently evaluated for its ability to affect inflammatory responses in peripheral tissues. In this study, we examined its effect on the damage to the central nervous system due to systemic inflammation. For this purpose, ICR mice were injected with an intraperitoneal (i.

Anti-inflammatory and neuroprotective effects of auraptene, a citrus coumarin, following cerebral global ischemia in mice.

Cerebral ischemia causes delayed neuronal cell death in the hippocampus resulting in sequential cognitive impairments. Hyper-activated inflammation following ischemia is one of the etiologies for delayed neuronal cell death. In the present study, using a transient global ischemia mouse model, we showed that auraptene (AUR), a citrus coumarin, effectively inhibited microglia activation, cyclooxygenase-2 expression by astrocytes, and neuronal cell death in the hippocampus following ischemic insults.