Ugo Basile Grip Strenght Meter to find new therapeutic target in stroke related inflammation
Ugo Basile Grip Strength Meter to find new therapeutic target in stroke related inflammation
The recent study “SRGN amplifies microglia-mediated neuroinflammation and exacerbates ischemic brain injury”, revealed the important role of SRGN in triggering microglial activation and amplifying neuroinflammation after ischemic stroke, acting as a novel therapeutic target in microglia-boosted proinflammatory response following ischemic stroke. Targeting SRGN might provide new strategies for alleviating post-stroke brain injury.
Methods: Srgn knockout (KO), Cd44-KO and wild-type (WT) mice were subjected to middle cerebral artery occlusion (MCAO) to mimic ischemic stroke. Exogenous SRGN supplementation was achieved by stereotactic injection of recombinant mouse SRGN (rSRGN). Cerebral infarction was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Neurological functions were evaluated by the modified neurological severity score (mNSS) and grip strength. Microglial activation was detected by Iba1 immunostaining, morphological analysis and cytokines’ production. Neuronal death was examined by MAP2 immunostaining and FJB staining.
Neurological Behavior Test: The neurological functions were evaluated by the modified neurological severity score (mNSS) and grip strength tests. The mNSS test evaluates various domains: sensory, motor, reflex, and balance. The grip strength test was employed to assess the forelimb muscle strength of the mice.
Results: The expression of SRGN and its receptor CD44 was significantly elevated in the ischemic mouse brains, especially in microglia. In addition, lipopolysaccharide (LPS) induced SRGN upregulation in microglia in vitro. rSRGN worsened ischemic brain injury in mice and amplified post-stroke neuroinflammation, while gene knockout of Srgn exerted reverse impacts. rSRGN promoted microglial proinflammatory activation both in vivo and in vitro, whereas Srgn-deficiency alleviated microglia-mediated inflammatory response. Moreover, the genetic deletion of Cd44 partially rescued rSRGN-induced excessed neuroinflammation and ischemic brain injury in mice. Mechanistically, SRGN boosted the activation of NF-κB signal, and increased glycolysis in microglia.
Read the full research open access article SRGN amplifies microglia-mediated neuroinflammation and exacerbates ischemic brain injury
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