<p>The basal level of activated mTOR promoted NF-κB activation during inflammation, which induced the retinal expression of the inflammatory cytokines, interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1). Activated NF-κB elevated the activated and phosphorylated mTOR (pmTOR) level during inflammation, which may have exacerbated the pathogenesis. The subsequent retinal activation of signal transducer and activator of transcription 3 (STAT3), at least partly, reduced the rhodopsin protein expression in a post-transcriptional manner and impaired rod photoreceptor function. Rapamycin also attenuated inflammatory leukocyte adhesion to the vessel walls, and increased potentially neuroprotective autophagy in the retina during inflammation.</p
