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Page 44
Volume 3
Journal of Neurology and Clinical Neuroscience
Neurosurgery 2019 & Neuroimmunology 2019
May 22-23, 2019
Neurosurgery and Neurological Surgeons
Neuroscience and Neuroimmunology
May 22-23, 2019 London, UK
6
th
Annual Meeting on
9
th
Global Summit on
&
J Neurol Clin Neurosci, Volume 3
Notes:
Resveratrol attenuates endoplasmic reticulum stress (ERS) induced cell death and
results in functional improvement after traumatic brain injury
Mark Nyanzu
Wenzhou Medical University, China
T
raumatic brain injury (TBI) is often caused by accidents that damage the brain. TBI can induce endoplasmic reticulum stress
and lead to neuronal and glial cell death. Persistent overwhelming stimuli trigger ER stress to initiate apoptosis, autophagy,
and cell death. Caspase-12 and CHOP signaling pathways are important players of ER stress, which is also modulated by ROS
production, calcium disturbance, and inflammatory factors. In this study, we investigated the mechanism of cell death during the
damage caused by TBI in vivo and in vitro, as well as the protective effect of resveratrol (RV), which is a polyphenol antioxidant
found in red wine and has been shown to play a neuroprotective role. Here we report that Endoplasmic reticulum stress was
activated in mice brains exposed to TBI. In the in vitro TBI model, apoptotic and neuroinflammatory cytokines were induced
through the activation of BV2 microglial cell by LPS. LPS triggered activation of microglia, detected by an increase of TNF-α, and
IL-1β, detected by qPCR. Treatment of RSV reduced neuroinflammation by inhibited LPS-induced TNF-α, IL-1β production in
a concentration-dependent manner.
We investigated the effect of the administration of resveratrol (RSV) post-traumatic brain injury (TBI) on reducing ERS markers.
TBI was induced by cortical contusion injury in mice. RSV (40 mg/kg in dimethyl sulfoxide) was administered intraperitonially
at 5 min after TBI, followed by a daily dose for 3days. The expressions of GRP78, caspase-12, chop and caspase-3 were evaluated
by Western blot. Neurological function was further evaluated to investigate the development of TBI. We found that post-TBI
treatment with RSV could markedly inhibit the expressions of GRP78, CHOP and CASPASE-12. However, RSV treatment failed
to reduce caspase-3 although neurological deficits at 72 h after TBI improved. These results indicated that RSV treatment could
alleviate EBI after TBI, at least in part, via inhibition of ERS signaling pathway.
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