Ming Sun
Capital Medical University
5 Papers
26 Citations
Ming Sun is an academic researcher from Capital Medical University. The author has contributed to research in topics: Calpain & Apoptosis. The author has an hindex of 3, co-authored 5 publications.
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Papers
Protective actions of PJ34, a poly(ADP-ribose)polymerase inhibitor, on the blood–brain barrier after traumatic brain injury in mice
TL;DR: Treatment with PJ34 markedly attenuated the permeability of the BBB and decreased the brain edema at 6 h and 24 h after CCI, suggesting the protective effects of PJ34 on BBB integrity and cell death during acute TBI.
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Citicoline protects brain against closed head injury in rats through suppressing oxidative stress and calpain over-activation.
TL;DR: Protection of citicoline against white matter and grey matter damage due to CHI through suppressing oxidative stress and calpain over-activation is demonstrated, providing additional support to the application of citIColine for the treatment of traumatic brain injury.
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Taurine attenuates hippocampal and corpus callosum damage, and enhances neurological recovery after closed head injury in rats
TL;DR: It was found that taurine lessened the corpus callosum damage, attenuated the neuronal cell death in hippocampal CA1 and CA3 subfields and improved the neurological functions 7 days after CHI, and it is suggested that down-regulating calpain activation could be one of the protective mechanisms of t aurine against CHI.
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Antiapoptotic and Anti-Inflammatory Effects of CPCGI in Rats with Traumatic Brain Injury
TL;DR: CPCGI can reduce brain injury due to trauma by suppressing both mitochondrial apoptotic signaling and PARP/NF-κB inflammatory signaling, and decreased the immunoreactivities of neutrophils, GFAP and Iba-1 in the region of CCI-induced contusion.
CPCGI Reduces Gray and White Matter Injury by Upregulating Nrf2 Signaling and Suppressing Calpain Overactivation in a Rat Model of Controlled Cortical Impact.
TL;DR: Data confirm the neuroprotective effect of CPCGI against gray and white matter damage due to CCI and suggest that activating Nrf2 signaling and alleviating oxidative stress-mediated calpain activation could be one mechanism by which CPCGI protects against brain trauma.