N-acetylcysteine (NAC) ameliorates Epstein-Barr virus latent membrane protein 1 induced chronic inflammation
Fig 3
NAC treatment delays phenotypic progression.
A to G photographs of ear skin phenotype: A: The phenotype of a transgenic mouse (right) at 42 days old, referred to as stage 1 (St1), compared to NSC (left). (B-G): The phenotypic effect of systemic treatment of transgenic mice with NAC (right) from 38 days old, compared to untreated (left: UT) at progressive ages and phenotypic stages. Age and stage details: B: 42 days old: left: untreated stage 1, right: 4 days NAC. C: 60 days old: left: untreated stage 2, right: 22 days NAC. D: 84 days old: left: untreated stage 3, right: 46 days NAC. E: 100 days old: left: untreated stage 3, right: 56 days NAC. F: 140 days old: left: untreated stage 4, right: 96 days NAC. G: 160 days old: left: untreated stage 5, right: 116 days NAC treatment. (H) The mean age of progression to the next phenotypic stage is shown graphically for untreated transgenic mice (n = 57, error bars show SD). (I) The average phenotypic stage with age is plotted for a cohort of transgenic mice treated with NAC (total n = 34, with at least n = 7 for each time point) compared to untreated (total n = 188, with at least n = 10 for each time point). Stage progression is significantly different between the two groups (P<0.0001) from 7 weeks of age onwards. Error bars show SE. Note: drops in the curve for untreated mice do not reflect phenotype reversal but are due to removal of mice from study.