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Indirect calorimetry demonstrates higher fatty-acid oxidation and resting energy expenditure after dosing, consistent with an ERR-driven shift toward oxidative metabolism
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Basing on the secondary injury mechanism, anti-oxidation and anti-excitatory amino have been used in releasing the neurological dysfunction, not showing effect, and currently, there are no effective treatments approved by clinical trials for TBI patients (Pearn et al., 2017)
For example, flubendazole combined with 5-FU can induce CRPC death by promoting ferroptosis [28]
Research models focus on pathway convergence signalling sequencing and molecular cooperation between cytoprotective and structural regulatory systems