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. Author manuscript; available in PMC: 2010 Mar 1.
Published in final edited form as: Nat Immunol. 2009 Aug 16;10(9):958–964. doi: 10.1038/ni.1775

Figure 2.

Figure 2

Inhibition of PARP-1 suppresses axonal loss and progressive disability in secondary progressive EAE. (a) Activity of recombinant PARP-1 (recPARP-1) incubated with DNA pretreated with 15-HC (+; row 3) or 7-KC (+; row 4). DNA without pretreatment (N) serves as a negative control; DNA with single-strand breakage (ssb-DNA) serves as a positive control. P values, one-way ANOVA. Data are representative of three independent experiments (mean and s.e.m.). (b,c) Clinical scores (b) and histopathological analysis of EAE (c) in 10-week-old NOD mice in which secondary progressive EAE was induced by immunization with MOG(35–55) in CFA (100 μg per mouse), with pertussis toxin (150 ng per mouse) given at the time of immunization and 48 h later, and AIQ (3 mg per kg body weight) or PBS (control) administered daily beginning on day 20. (c) Spinal cord sections at day 55, stained with Luxol fast blue or Bielschowsky's silver stain (left) for analysis of demyelination or axonal loss (right), respectively. P values, Student's t-test. Data are representative of two independent experiments (mean and s.e.m.).