Table 2.

Summary of therapeutic agents that can be used to target ferroptosis and inflammatory pathways in neuroinflammation and neurological disorders.

Therapeutic agents	Characteristics	Anti-inflammatory and anti-ferroptosis mechanisms	References
Deferiprone	Antioxidant, iron chelator	Decreases oxidative stress (OS); reduces iron overload	[166,170,171]
Ferrostatin-1	Antioxidant, iron chelator	Inhibits reactive oxygen species (ROS) accumulation; activates angiotensin II type 1 receptor; suppresses ROS; activates the Keap1/Nrf2/HO-1 signaling	[67,171,175]
Liproxstatin-1	Antioxidant, iron chelator	Reduces serum inflammation mediators; decreases the in vivo rise of interleukin (IL)-1β, tumor necrosis factor alpha (TNF-α), and IL-6; inhibits lipid peroxidation	[[178], [179], [180]]
Alpha-lipoic acid	Antioxidant, iron chelator	Decreases the level of ROS; elevates the GPX4 expressions; decreases mitogen-activated protein kinase and nuclear factor kappa B (NF-κB) signaling; activates NLRP3 inflammasome; secretes pro-inflammatory cytokines, reduces iron overload	[70,181]
Quercetin	Antioxidant	Inhibits the generation of nitric oxide, suppresses NF-κB signaling, eliminates ROS and several oxidizing substances; decreases iron overload	[[185], [186], [187], [188], [189], [190]]
Baicalein	Antioxidant	Decreases various inflammatory cytokines such as IL-6, TNF-α, and IL-1β; provides protection against OS-induced damage, suppresses OS; suppresses glutathione (GSH) depletion, lipid peroxidation (LPO), and phosphatidylethanolamine oxidation	[191,192,194]
Puerarin	Antioxidant	Inhibits ROS production; regulates p38 MAPK-CREB pathway; suppresses iron overload; regulates iron homeostasis	[197,198]
Vitamin E	Antioxidant	Decreases synthesis of signaling molecules, signaling cascades, and transcription factors; terminates LPO; neutralizes peroxidative free radicals	[202,204,206]
Coenzyme Q10	Antioxidant	Degrades IκBα and nuclear translocation of p65 by decreasing prostaglandin E2 generation and cyclooxygenase-2 expression; suppresses NF–κB signaling; downregulates several pro-inflammatory mediators; decreases propagation and initiation of LPO; upregulates GSH	[211,212,215]