WHOM will your doctor contact to get this tested for stroke in
humans? No contact then you need to have that doctor fired for
incompetency and dereliction of duty. We need to start clearing out a
lot of dead wood in stroke, probably starting with your stroke hospital
board of directors.
- 1Department of Neurosurgery, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China
- 2Department of Emergency, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China
- 3School of Biomedical Engineering and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China
Traumatic brain injury (TBI) is a major cause of disability and
mortality worldwide, in part resulting from secondary apoptosis of
neurons in peri-contusion areas. Serpina3k, a serine protease inhibitor,
has been shown to inhibit apoptosis in injury models. In this study, we
investigated the anti-apoptotic function of serpina3k
in vivo using a mouse model of TBI, as well as the underlying neuroprotective mechanism
in vitro
using the SH-SY5Y human neuroblastoma cell line. TBI was induced in
adult male C57BL/6 mice using controlled cortical impact. Serpina3k
protein was intravenously administered at a concentration of 0.5 mg/kg
twice daily for up to 14 days. SH-SY5Y cells were subjected to biaxial
stretch injury and then treated with different concentrations of
serpina3k. We found that endogenous serpina3k protein levels were
elevated in peri-contusion areas of the mouse brain following TBI.
Serpina3k-treated mice had fewer apoptotic neurons, lower levels of
oxidative stress, and showed greater recovery of neurological deficits
relative to vehicle-treated mice. Meanwhile, in the SH-SY5Y cell injury
model, serpina3k at an optimal concentration (150 nM) inhibited the
generation of intracellular reactive oxygen species, abrogated changes
of the mitochondrial membrane potential, and reduced the
phospho-extracellular regulated protein kinases (p-ERK)/ERK, phospho-P38
(p-P38)/P38, B cell lymphoma (Bcl)-2-associated X protein/Bcl-2, and
cleaved caspase-3/caspase-3 ratios, thereby reducing the apoptosis rate.
These results demonstrate that serpina3k exerts a neuroprotective
function following TBI and thus has therapeutic potential.
Yao Jing1†, 
Fang Yuan1, 
Hao Chen1, 
Jun Ding1*, 
Hengli Tian1*
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