Fig. 3
From: Targeting SARM1 as a novel neuroprotective therapy in neurotropic viral infections
Inhibition or deletion of SARM1 significantly delays axonal degeneration in cerebral cortex neurons infected with neurotropic viruses. (A) Representative double immunostaining was performed on coronal cerebral cortex sections from 8-week-old wild type (WT) and Sarm1KO mice, 5 days after infection with JEV or HSV-1, or 8 days after RABV infection. The sections were stained for JEV-NS1, RABV-G or HSV-1-gD (green, virus marker) and Nf-M (red, axonal markers), and mounted with Vectashield containing DAPI (blue; nuclear marker). (B) Quantification of neurofilament immunostaining intensity in the axonal fluorescence images from experiments shown in panel A, indicated by Nf-M antibody. IntDen: Integrated Density. (C) Immunoblot analysis of the Nf-M and SARM1 levels in cerebral cortex with JEV, HSV-1 or RABV-infected WT or Sarm1KO mice. (D) Plasma neurofilament light chain (Nf-L) levels were quantified from WT and Sarm1KOmice and mice receiving JEV, or HSV-1 infection (5 days) or RABV infection for 8 days. (E and F) Cerebral cortex NAD+ (E) and cADPR (F) levels in WT or Sarm1KOmice after JEV, HSV-1, or RABV infection. Data represent mean ± SEM; individual data points are shown. Statistical analysis was performed with one-way ANOVA and Holm-Bonferroni multiple comparison. ns, P > 0.05; *, P < 0.05; **, P < 0.01; ***, P < 0.001