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After TBI, there is an activation of neuroinflammation response pathway mediated by microglia cells that were not initially damaged, and the activated microglial cells may promote the release of proinflammatory factors such as interleukin 1, tumor necrosis factor, nitric oxide, etc., (Kumar and Loane, 2012), inducing a progressive cycle of chronic inflammation (Sulhan et al., 2020)

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An investigation of the antidepressant-like effect of Jiaotaiwan in rats by nontargeted metabolomics based on ultra-high-performance liquid chromatography quadrupole time-of-flight mass spectrometry

HGF blood-brain barrier permeability BBB blood-brain barrier permeability Antagonists Improper activation of the c-Met receptor can be encouraged by genetic activating mutations, transcriptional upregulation or by ligand-dependent autocrine or paracrine mechanisms