| Therapeutic Agent | Experimental Model | Effects | References |
| Isorhapontigenin (ISO) | Rat Chondrocytes | Suppressed the IL-1β-induced inflammation and cartilage matrix damage | [36] |
| Kinsenoside (Kin) | Chondrocytes | Attenuated IL-1β-induced chondrocyte damage | [37] |
| Anthocyanins and Metabolites | Chondrocytes | Inhibited IL-1β-induced matrix metalloproteinases expression | [38] |
| Emodin | Rat Chondrocytes | Induced chondrocytes proliferation and downregulated the expression of several inflammatory mediators | [39] |
| Kaempferol | Rat Chondrocytes | Inhibited the IL-1β-induced expression of inflammatory mediator proteins such as COX2 and the common matrix-degrading enzymes MMP-1, MMP-3, and MMP-13 | [40] |
| Schisandrin B | Rat Chondrocytes; Rat | Decreased IL-1β-induced upregulation of MMP-3, MMP-13, IL-6, and iNOS, and increased IL-1β-induced downregulation of collagen II and aggrecan | [41] |
| Echinocystic Acid (EA) | Chondrocytes | Inhibited IL-1β-stimulated the production of MMP-13, NO, and PGE2, as well as the expression of iNOS and COX-2 | [42] |
| Gentiopicroside | Rat Chondrocytes | Inhibited IL-1β-induced inflammation response and increased Collagen type II expression | [43] |
| Hydrogen Sulfde (H2S) | Chondrocytes | Reversed the effect of IL-1β on the MMP-13, PGE2, and NO production and on the gene expression of COX-2, MMP-13, and iNOS | [44] |
| Nicotine | Chondrocytes | Inhibited MIA- or IL1β-induced chondrocyte activation via the α7 nicotinic acetylcholine receptor (α7-nAChR) | [45] |
| ERK Inhibitor U0126 | Chondrocytes | Abrogated lactoferrin (LF) activation of BMP7 gene expression | [46] |
| Melatonin | Rabbit OA Model | Induced cytoprotection and anti-inflammatory effect against H2O2-stimulated the expression of cytotoxicity, iNOS, and COX-2 | [47] |
| Inhibition of ERK with PD98059 | Rabbit Chondrocytes | Suppressed SIRT2-induced dedifferentiation and COX-2 expression | [48] |
| Transduction of Lysyl Oxidase Like-2 (LOXL2) | OA Chondrocytes | Inhibited chondrocyte apoptosis and increased the mRNA levels of chondroitin sulfate proteoglycan (CSPG4), aggrecan (ACAN), sex-determining region Y-box containing gene 9 (SOX9), and COL2A1, but reduced the levels of MMP-1, MMP-3, and MMP-13 | [49] |
| Physiological Concentration of Soluble Uric Acid (sUA) | Chondrocytes | Showed anti-inflammatory and chondro-protective effect | [50] |
| ERK Inhibition | Chondrocytes | Exert therapeutic effect against the harmful effects of macrophage inhibition factor (MIF)-CD74 signal in human degenerated cartilage endplate (CEP) degeneration | [51] |
| Glycoprotein 130 (gp130) | Chondrocytes; Rat Partial Meniscectomy Model | Reduced apoptosis and hypertrophic responses, and the breakdown of cartilage matrix in regenerated cartilage | [52] |
| The Inhibitor of Angiopoietin-Like Protein 2 (aNgPtl2) | Chondrocytes | Downregulated the expression of the inflammation-related factor gene | [53] |
| IL?37 | Chondrocytes | Suppressed the expression of pro?inflammatory factors via IL?1R8 | [54] |
| Cilengitide | Chondrocytes | Inhibited the stimulation of excessive mechanically induced inflammatory reaction by upregulating the expression of IL?1β, TNF?α, MMP?3, and MMP?13 | [55] |
| Semaphorin 3A (Sema3A) | Chondrocytes | Inhibited the gene expression of inflammatory cytokines upregulated by CTS | [56] |
| Focal Adhesion Kinase (FAK) | Chondrocytes | Suppressed inflammation-related factors such as COX-2, IL-1β, and TNF-α in chondrocytes under CTS | [57] |
| miR-125b mimic | Chondrocytes | Inhibited several pro-inflammatory cytokines and chemokines and growth factors secretion, such as IL-6, IL-8, INF-γ, IGFBP-1, and PGDF-BB | [58] |
| Mesenchymal Stem Cell Derived Exosomes (MSC-Exos) | Chondrocytes | Promoted the viability of chondrocytes | [59] |