TABLE 5.
Effects and mechanism of Salvia miltiorrhiza and its active ingredients on osteoarthritis.
| Ingredient | In vivo/In vitro | Model | Administration | Dose/Time | Treatment effect | Mechanism | Diseases | References |
|---|---|---|---|---|---|---|---|---|
| Tanshinone ⅡA | In vivo | OA rat model established by ACLT and MMx | Intraperitoneal injection | 0.25∼0.5 mg/kg/d for 28 days | Suppress articular cartilage degradation through inhibition of apoptosis and expression levels of inflammatory cytokines | - | OA | Jia et al. (2017) |
| Salvia miltiorrhiza injection | In vivo | OA rabbit model established by ACLT | Oral gavage | 3 g/kg/d for 6 weeks | Glutathione levels in synovial and articular cartilage were increased and malondialdehyde levels were decreased | - | OA | Bai and Li (2016) |
| Salvia miltiorrhiza injection | In vivo | OA rat model established by ACLT and MMx | Intra-articular injection | 1.05 g/d for 5 weeks | Reduce the destruction of OA articular cartilage | Activate JAK2/STAT3 and AKT pathways | OA | Xu et al. (2018) |
| Cryptotanshinone | In vivo; In vitro | mouse OA models; OA chondrocytes | Oral gavage | 10 mg/kg/d for 16 days; 5, 10 and 20 μM for 24 h | Prevent cartilage degradation and subchondral osteosclerosis in mice OA models; Significantly inhibit the IL-1β-induced NO, GE2, COX-2, iNOS, MMP-3, MMP-13, and ADAMTS-5 | Inhibit both NF-κB and MAPK signaling pathways | OA | Feng et al. (2017) |
| Tanshinone ⅡA | In vitro | LPS-induced ATDC5 | - | 5, 10, 15 and 20 μM for 24 h | Significantly alleviated LPS-induced ATDC5 cell inflammatory injury and downregulated the expression of miR-203a | Downregulate miR-203a and suppress JAK/STAT and JNK pathways | OA | Luan and Liang (2018) |
| Tanshinone ⅡA | In vitro | Human primary chondrocytes | - | 0.1, 1, 5, and 10 μM | Inhibit LPS-induced inflammation and cell apoptosis of chondrocytes | Regulate the expression of miR-155 and FOXO3 | OA | Zhou et al. (2021) |
Note: OA, osteoarthritis; NF-κB, Nuclear factor kappa-B; MAPK, mitogen-activated protein kinase; VEGF, Vascular endothelial growth factor; LPS, Lipopolysaccharide; IL-1β, Interleukin-1β; MMP-13, Matrix metallopeptidase 13; ACLT, Anterior cruciate ligament resection; MMx, medial meniscus; JNK, c-Jun N-terminal kinase; NO, Nitric Oxide; PGE2, Prostaglandin E2; COX-2, cyclooxygenase-2; iNOS, Inducible Nitric Oxide Synthase; MMP-3, Matrix metallopeptidase 3; MMP-13:Matrix metallopeptidase 13; ADAMTS-5, Recombinant A Disintegrin And Metalloproteinase With Thrombospondin 5; JAK, Janus Kinase; STAT, Signal transducer and activator of transcription.