In this study, we demonstrate that HD, Ber, and Jas elevated the LC3-II/LC3-I, beclin-1, Atg-3, Atg-5, Atg-7, and Atg-12 levels, decreased the expression of p62 and restrained the activation of mTOR (one of the most important proteins to negatively regulate autophagy), and upregulated the phosphorylation of AKT and its related substrate GSK-3β at 24 h of reperfusion. The gene discussed is ATG3; the disease is Huntington disease.