Table 1.

Anti-inflammatory ingredients and their mechanisms in IVDD.

	Ingredient	Mechanism	Main results
Drug	Glucocorticoids	inhibit phospholipase A2 suppress NK-κB	decrease expression of pro-inflammatory cytokines
	NSAID	inhibit cyclooxygenase	inhibit the expression of inflammatory mediators
	Curcumin	modulate pro-inflammatory cytokines, apoptotic proteins, NF–κB, COX-2	inhibit TNF-α and IL-1β production alleviate oxidative stress
	Ferulic acid	suppress the activation of NF-κBmodulate Sirt1/AMPK/PGC-1 pathway	suppress inflammatory response reduce oxidative stress
Biotherapy	IL-1ra and TNF-α inhibitors	selective inhibition of TNF-α and IL-1	inhibit inflammatory responses and ECM degradation
	Lactate oxidase	consume excess lactate	modification of the acidic microenvironment
	mRNA	Transcribing cells produce anti-inflammatory mediators	inflammatory factor receptor antagonist
	miRNA and siRNA	mediates target mRNA degradation or inhibits mRNA translation	inhibit inflammatory signaling pathways
	MSCs	paracrine and immunomodulatory effects	secrete anti-inflammatory cytokines polarize macrophages to M2 type
	Extracellular vesicles	transport an abundance of proteins, mRNAs, miRNAs, and short non- RNAs	suppress the expression of inflammatory factors and ECM-degrading enzymes
	Platelet-rich plasma	inhibit NF-κB activation, reduce pro-inflammatory cytokines IL-6 and IL-8	alleviate inflammation, inhibit apoptosis, promote cell proliferation, and increase ECM synthesis