Research Paper Volume 13, Issue 14 pp 19048—19063

Combined treatment with C16 peptide and angiopoietin-1 confers neuroprotection and reduces inflammation in 3-nitropropionic acid-induced dystonia mice

Treatment with C16+Ang-l can alleviate 3-NP-induced TH and CHAT expression decline, neuronal death, and synaptophysin loss. Western blot semi-quantitative analyses of (A–B) TH (for dopamine neurons), (C–D) CHAT (for cholinergic neurons), (E–F) Syn (synapse-associated proteins that showed synaptic plasticity and correlate with cognitive decline), and (G–H) active caspase-3 (an enzyme involved in mammalian apoptotic cell death) in the control, 3-NP, and 3-NP+C16+Ang-1 groups. aP bP

Figure 6. Treatment with C16+Ang-l can alleviate 3-NP-induced TH and CHAT expression decline, neuronal death, and synaptophysin loss. Western blot semi-quantitative analyses of (AB) TH (for dopamine neurons), (CD) CHAT (for cholinergic neurons), (EF) Syn (synapse-associated proteins that showed synaptic plasticity and correlate with cognitive decline), and (GH) active caspase-3 (an enzyme involved in mammalian apoptotic cell death) in the control, 3-NP, and 3-NP+C16+Ang-1 groups. aP < 0.05 versus control; bP < 0.05 versus 3-NP-treated mice.