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在創傷性腦損傷模型中檢查熱處理過的人血小板沉澱裂解物的神經保護和神經修復功效

為了解決gk模型修復的問題，作者Ouada Nebie 這樣論述：

Traumatic brain injury (TBI) remains a global health challenge nowadays, impacting over 50million people per year globally. This situation is partly linked to the fact that TBI is among thecentral nervous system disorders whose management mostly requires long-term care. It incurs asubstantial econo

mic burden to health systems and costing the global economy more than $400million. In either high, middle, or low-income countries, TBI is associated with significanteconomic and societal changes that deserve attention. The disease is described as one of the mostcomplexes, inducing some disproportio

nate effects between the countries. Unfortunately, theintervention strategies are still facing several limitations at the global level despite all the healthsciences’ progress. These obstacles are the surge of neuroinflammation, leading to progressiveneuronal degeneration and cognitive deficit. Effo

rts are made to stop this “silent killer”, but thereis a failure to manage the long-term burden of TBI efficiently until now.Nowadays, there is growing evidence that platelet lysates are full of bioactive compounds, andthey could constitute a powerful natural neuroprotective agent. Few studies have

already showntheir therapeutic potential in stroke, amyotrophic lateral sclerosis, and Parkinson's disease. Thus,we hypothesized that the delivery of human platelet lysate at an injured area in the brain couldprovide a suitable environment for recovery.The current project is intending to develop an

innovative approach for the treatment of TBI. Weaim to give the proof-of-concept of the interest of using heat-treated human platelet pellet lysate(HPPL) as a neuroprotective agent in TBI using experimental models.We used cells and animal models of TBI to achieve our goal. We first prepared HPPL fro

m nonpathogen-reduced platelet concentrates (PCs) and pathogen-inactivated PCs (I-HPPL) accordingto a previously established procedure. We evaluated their safety and functionality using cellmodels relevant to TBI, including viability assays, wound healing, anti-inflammatory activity,protein expressi

ons, and anti-ferroptosis effect. The safety assessment of the platelet biomaterialwas done using neuronal and endothelial cells and its neuroprotective potential with primaryneurons, dopaminergic cells line and, a ferroptosis inducer.Mouse TBI models were used to assess the therapeutic potential of

HPPL. We targeted it impacton motor function, neuroinflammation, oxidative stress, and synaptic loss. Behavior tests, geneexpression, fluorescent staining, ELISA, Western blot, and proteomics have been used during theinvestigation.19The in vitro experiment performed to investigate the platelet lysa

te’s safety demonstrated clearlythat HPPL/I-HPPL contain bioactive molecules and did not affect cell’s viability or induced stress.Moreover, HPPL and I-HPPL did not affect synaptic and neuronal protein expression and revealedanti-ferroptosis potential. This finding leads to further investigation of

HPPL's beneficial effect invivo. HPPL administration to TBI mice improved their motor function, mitigated the inflammationand oxidative stress. HPPL also decreased the synaptic proteins lost.HPPL is safe and exerted neuroprotective activity in vitro. It successfully reversed the motordeficit, inflam

mation, and stress triggered by brain injury in mice.