FIGURE 10

Schematic representation of protective effect of CGA, NCGA, and CCGA against Pb-induced developmental neurotoxicity co-treatment of CGA, NCGA, and CCGA alleviated developmental malformation, reduced toxicity score, increased the length of DA neuron region, protected brain vasculature and neuron differentiation in the CNS, ameliorated locomotor impairment, modulated neurodevelopmental genes (c-fos, gfap, mbp, pparγ, tuba1b, bdnf, and dat), oxidative stress-related genes (sod2, sod1, cat, gclm, gsto2, and gpx4a), and parkinsonian and autophagy-related genes (dj1, pink1, parkin, ambra1a, ulk1b, ulk2, and atg5). Summing up, our study demonstrates that co-treatment with CGA and its analogues NCGA and CCGA protects against Pb-induced developmental neurotoxicity. The protective mechanism of CGA, NCGA, and CCGA co-treatment might not be only due to the inhibition of apoptosis also protection of brain vasculature but also due to the inhibition of Pb exposure induced oxidative stress and autophagy in zebrafish (Figure 10). Our results provide proof of concept that CGA, NCGA, and CCGA might represent the future treatment against Pb poisoning.