Table 1.

Natural molecules inhibit ferroptosis for NDD treatment.

Compounds	Models	Mechanisms	Administration	Ref.
Curcumin	6-OHDA induced PD rats	Suppressing the iron-induced degeneration of nigral dopaminergic neurons by iron-chelating activity	i.g.	[19]
7-O-Esters of taxifolin	Glutamate-induced HT22 cells; Aβ25-35-induced AD mice	Resisting oxytosis, ferroptosis and ATP depletion	i.p.	[22]
Ginkgolide B	SAMP8 mice as AD model	Mitigating ferroptosis by reducing iron content, decreasing TFR1 and NCOA4 expressions, increasing FTH1 expression, and activating the Nrf2/GPX4 signaling pathway	i.g.	[20]
Myricetin	Fe2+-induced SH-SY5Y cells; scopolamine-induced AD mice	Downregulating acetylcholinesterase and brain iron content; inhibiting TFR1 expression; increasing antioxidant enzyme activity	i.g.	[23]
Salidroside	Glutamate-induced HT22 cells; Aβ1-42-induced AD mice	Reducing lipid peroxidation and ROS levels; increasing GPX4 and SLC7A11 protein expressions; improving mitochondrial ultrastructure; attenuating neuronal ferroptosis by activating the Nrf2/HO1 signaling pathway	i.g.	[21]

ATP: adenosine triphosphate; TFR1: the receptor of transferrin to control cellular iron uptake. NCOA4 can mediate autophagic degradation of ferritin to maintain iron homeostasis; SLC7A11 can regulate GSH production; i.g. for intragastric administration; i.p. for intraperitoneal injection.