Apelin-13 as a novel target for intervention in secondary injury after traumatic brain injury.

The adipocytokine, apelin-13, is an abundantly expressed peptide in the nervous system. Apelin-13 protects the brain against ischemia/reperfusion injury and attenuates traumatic brain injury by suppressing autophagy. However, secondary apelin-13 effects on traumatic brain injury-induced neural cell death and blood-brain barrier integrity are still not clear. Here, we found that apelin-13 significantly decreases cerebral water content, mitigates blood-brain barrier destruction, reduces aquaporin-4 expression, diminishes caspase-3 and Bax expression in the cerebral cortex and hippocampus, and reduces apoptosis. These results show that apelin-13 attenuates secondary injury after traumatic brain injury and exerts a neuroprotective effect.

[The relationship between the degradation of actin and the postmortem interval in rats].

OBJECTIVE: To observe the degradation of actin in cardiac muscle, brain and skeletal muscle of rats after death and to find an objective parameter interval (PMI) estimation. METHODS: Twenty eight clear Sprague Dawley rats put into an artificial climate incubator (set at 20 degrees C) for 0, 24, 48, 72, The actin contents in the above tissues were quantitated by Western-blot Pro Plus 5.0 image analysis system, and were then statistically analyzed RESULTS: Actin content in all these tissues decreased gradually with prolonged differences between the groups was statistically significant (P < 0.05), with fastest, then the lung, the spleen, the liver, the kidney, the cardiac muscle order. There was a strong correlation between actin degradation and determination (R2) exceeded 0.75 in all these tissues. CONCLUSION: degradation, the actin contents in cardiac muscle, liver, spleen, lung, kindey, rats decreased gradually with prolonged PMI, which may potentially be PMI estimation.