Propofol Protects Regulatory T Cells, Suppresses Neurotoxic Astrogliosis, and Potentiates Neurological Recovery After Ischemic Stroke

Network-based drug repurposing for potential stroke therapy

“…For instance, in vivo study deciphered that olanzapine attenuated brain damage after focal cerebral ischemia [24] and case report showed that an adolescent with abulia from left middle cerebral artery stroke was treated successfully by using short duration olanzapine [25] . Recent literature has verified that propofol plays a protective role on regulatory T cells, suppresses neurotoxic astrogliosis, and enhances neurological recovery after IS [26] . Propofol is also reported to protect against cerebral ischemia/reperfusion injury though inhibiting long noncoding RNA SNHG14 [27] .…”

Mild hypothermia combined with dexmedetomidine reduced brain, lung, and kidney damage in experimental acute focal ischemic stroke

“…In an animal model, propofol was comparable to dexmedetomidine to minimize brain injury, since it reduced oxidative stress, apoptosis [ 33 ], microglia-mediated proinflammatory cytokines [ 34 ], as well as increased expression of heme-oxygenase-1 in ischemic penumbra and core [ 35 ]. Furthermore, propofol potentiates neurologic recovery [ 36 ] and neurobehavioral outcome [ 37 , 38 ] through a decrease in myeloperoxidases, nuclear factor (NF)-κB, cyclooxygenase (COX)-2, and TNF-α [ 39 ], which reduces cerebral edema and protects the blood–brain barrier. In pre-clinical studies, dexmedetomidine increased anti-inflammatory and neuroprotective effects more than propofol [ 40 , 41 ], and this is in accordance to our findings; however, in the clinical setting, dexmedetomidine and propofol appeared equally effective on brain recovery and outcome [ 42 , 43 ].…”

“…Statistical significance was considered for p < 0.0125. DEX dexmedetomidine, HYPO hypothermia, NORMO normothermia, PRO propofol Furthermore, propofol potentiates neurologic recovery [36] and neurobehavioral outcome [37,38] through a decrease in myeloperoxidases, nuclear factor (NF)-κB, cyclooxygenase (COX)-2, and TNF-α [39], which reduces cerebral edema and protects the blood-brain barrier. In pre-clinical studies, dexmedetomidine increased anti-inflammatory and neuroprotective effects more than propofol [40,41], and this is in accordance to our findings; however, in the clinical setting, dexmedetomidine and propofol appeared equally effective on brain recovery and outcome [42,43].…”