Figure 8.

A hypothetical scheme for the mechanism of HupA protection against iron overload induced neurotoxicity. Excessive iron treatment increases the level of LIP, in turn stimulates ROS generation and causes mitochondria dysfunction, which induces more ROS formation and eventually causes neuronal death. HupA significantly reduces the level of LIP and cellular ROS formation and ameliorates the mitochondrial function, and improves the cell viability. Interestingly, the mechanism of HupA protecting against iron overload neurotoxicity may not relevant to its cholinergic effect, in respect that inhibition of AChE activity by another specific AChE inhibitor–Don, to the same extent as that of HupA treatment, has no influence on iron overload induced LIP enhancement, ROS generation and mitochondrial dysfunction. HupA, huperzine A; Don, donepezil.