Jonathan M. Florentina, Yun Linb, Jasdeep Singha, Le Luo Guana
Abstract
Our study focused on understanding the critical role of the TLR-4/NF-κB pathway in cerebral ischemia-reperfusion injury. The study will explore the morphological changes in cerebral ischemia, the neurological deficit score after brain injury, TLR-4 and NF-κB protein expression, and mRNA levels in brain PI function changes, brain water, and urine. Serum levels of POV nanometer ozone concentration and TNF-α levels in mouse serum will assess the mouse brain tissue. Further examination will be done with morphological changes of TUNEL-POV/HE staining probe: TUNEL approaches to clarify the mechanism of cerebral ischemia-reperfusion injury. Hyperbaric oxygen through interference with NLRP3 gene and protein expression will be studied to provide new ideas for clinical treatment and to provide a theoretical basis for hyperbaric oxygen. Cerebral ischemia is a global health problem. Cerebral ischemia injury causes great harm to human society. Cerebral ischemia and reperfusion injury is a more complex pathological process, with a variety of factors involved. Cerebral ischemia has an irritable refractory time of onset, worsening patient illness. In particular, cerebral ischemia strongly Tumandu, oxygen free radicals are generated in the energy disorders, causing changes in the chemical structure of the cell and various structures. This leads to an accumulation of adverse reactions, including acidosis and intracellular Ca2+ overload. In the current research, neurocyte apoptosis and inflammation are considered to be the effectors of cerebral ischemia-reperfusion injury. Therefore, exploring the repair of animal models of cerebral ischemia-reperfusion injury and intervention and treatment has important theoretical and practical significance.
KeyWords: TLR-4; MCAO; NF-κB; HeN; HeJ
Copyright © 2020 by The American Society for BioMedicine and BM-Publisher, Inc.
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References
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