Table 1.

Mechanisms of quercetin for treating damage induced by various factors.

Inductive Factors	Damage Name	Protection Mechanisms	Result
LPS/d-GalN	Acute liver injury	Inhibits the activation of NF-κB and MAPK signaling pathways and inhibits the expression of apoptosis-related proteins induced by LPS/d-GalN	Decreases the production of LPS/d-GalN induced by oxidation markers [33]
Toosendanin	Liver toxicity	Induces Nrf2/GCL/GSH antioxidant signal transduction pathways	Increases Nrf2-mediated GCLC/GCLM expression, thereby increasing GSH content in cells [34]
Alcohol	Liver damage	Regulates phosphoinositide 3-kinase/Akt/NF-κB and STAT3 pathways	Enhances the body’s antioxidant, anti-inflammatory, and anti-apoptotic effects [35]
A variety of liver toxins	Liver toxicity	Induces p62 expression and inhibits the binding of Keap1 and Nrf2	Increases the transcription expression of Nrf2-targeted antioxidant genes [36]
Doxorubicin	Heart toxicity	Upregulates Bmi-1 expression to reduce oxidative stress	Reduces DNA damage at ROS levels and maintains cardiomyocyte viability [37]
CCl4	Liver damage	Improves antioxidant activity and regulates TLR2/TLR4 and MAPK/NF-κB signaling pathways	Inhibits ROS production in the liver and attenuates CCl4-induced oxidative damage [38]
Lead	Liver damage	Reduces oxidative stress in liver, inhibits JNK phosphorylation, and increases PI3K and Akt levels	Effectively inhibits lead-induced endoplasmic reticulum stress [39]
Cadmium	Cerebral cholinergic dysfunction	Reduces the production of ROS and protects the integrity of the line by regulating the protein involved in apoptosis and MAPK signal conduction	Regulates molecular targets involved in the signal conduction of brain cholinergic energy and reduces the neurotoxicity of cadmium [40]
	Malignant cell transformation	Protects BEAS-2B cells from Cr (VI) induction by targeting miR-21-PDCD4 signaling	Reduces ROS production induced by Cr (VI) exposure in BEAS-2B cells [41]
d-lactose	Cognitive impairment and neuron degeneration or loss	Improves the Nrf2-ARE signaling pathway	Decreases free radicals, increases antioxidant enzyme activity, improves overall antioxidant capacity, and slows down aging by improving Nrf2 [42]
Receptor activator for NF-κB ligand	Osteoblast differentiation	Regulates the transcription activities of NF-κB and AP-1	Inhibits the NF-κB and AP-1 mechanism activation [43]