Ginkgolide C inhibits ROS-mediated activation of NLRP3 inflammasome in chondrocytes to ameliorate osteoarthritis.

ETHNOPHARMACOLOGICAL RELEVANCE: Ginkgo biloba, as the most widely available medicinal plant worldwide, has been frequently utilized for treat cardiovascular, cerebrovascular, diabetic and other diseases. Due to its distinct pharmacological effects, it has been broadly applications in pharmaceuticals, health products, dietary supplements, and so on. Ginkgolide C (GC), a prominent extract of Ginkgo biloba, possesses potential in anti-inflammatory and anti-oxidant efficacy. AIMS OF THE STUDY: To determine whether GC mitigated the progressive degeneration of articular cartilage in a Monosodium Iodoacetate (MIA)-induced osteoarthritis (OA) rat model by inhibiting the activation of the NLRP3 inflammasome, and the specific underlying mechanisms. MATERIALS AND METHODS: In vivo, an OA rat model was established by intra-articular injection of MIA. The protective effect of GC (10 mg/kg) on articular cartilage was evaluated. Application of ATDC5 cells to elucidate the mechanism of the protective effect of GC on articular cartilage. Specifically, the expression levels of molecules associated with cartilage ECM degrading enzymes, OS, ERS, and NLRP3 inflammasome activation were analyzed. RESULTS: In vivo, GC ameliorated MIA-induced OA rat joint pain, and exhibited remarkable anti-inflammatory and anti- ECM degradation effects via inhibition of the activation of NLRP3 inflammasome, the release of inflammatory factors, and the expression of matrix-degrading enzymes in cartilage. Mechanically, GC inhibited the activation of NLRP3 inflammasome by restraining ROS-mediated p-IRE1α and activating Nrf2/NQO1 signal path, thereby alleviating OA. The ROS scavenger NAC was as effective as GC in reducing ROS production and inhibiting the activation of NLRP3 inflammasome. CONCLUSIONS: GC have exerted chondroprotective effects by inhibiting the activation of NLRP3 inflammasome.

The effect of thermal mineral waters on pain relief, physical function and quality of life in patients with osteoarthritis: A systematic review and meta-analysis.

BACKGROUND: To evaluate the effectiveness and safety of thermal mineral waters therapy for pain relief, and functional improvement, and quality of life (QoL) in patients with osteoarthritis (OA). METHODS: Cochrane Library, Web of science, EMBASE, ClinicalTrials.gov and PubMed were systematically searched for randomized controlled trials. Study inclusion criteria included assessment of the visual analog scale and Western Ontario and McMaster Universities scores and the lequesne index to evaluate the effects of thermal mineral waters on pain relief and functional improvement. Also, studies that used the European quality of life 5-dimension scale and health assessment questionnaire to assess the impact of thermal mineral waters therapy on improving QoL were included. RESULTS: Sixteen studies were included. A meta-analysis showed that thermal mineral waters therapy could significantly reduce pain as measured visual analog scale and Western Ontario and McMaster Universities assessments (P < .001). Thermal mineral waters significantly reduced the lequesne index (P < .001) and improved joint function. Finally, compared with a control group, European quality of life 5-dimension scale and health assessment questionnaire improved significantly in patients with OA receiving thermal mineral waters therapy (P  < .05). There is no evidence that thermal mineral waters is unsafe for treating OA. CONCLUSION: Thermal mineral waters therapy is a safe way to relieve pain, improve physical functions, and QoL in patients with OA.

Puerarin inhibits the development of osteoarthritis through antiinflammatory and antimatrix-degrading pathways in osteoarthritis-induced rat model.

Puerarin is an isoflavone isolated from the medicinal plant Pueraria lobata. The purpose of this study was to study the antiinflammatory and antimatrix-degrading effects of puerarin in a rat osteoarthritis (OA) model and its protective effects on joints. The rat OA model was established by anterior cruciate ligament transection (ACLT) surgery. Rats (n = 40) were divided into nontreated OA, OA + celecoxib (2.86 mg/kg), OA + puerarin (50 and 100 mg/kg), and control groups. Two weeks after surgical induction, puerarin was administered by gavage daily for 8 weeks. After 8 weeks, macroscopic observation and histopathological images showed that cartilage damage was reduced after puerarin and celecoxib treatment, the intensity of Safranin O staining was high, and the OARSI scores were significantly reduced compared to the OA group. Puerarin reduced the expression of MMP-3, MMP-13, ADAMTS-5, and COX-2 in the cartilage tissue of ACLT rats, inhibited the production of IL-1ß, IL-6, and TNF-α inflammatory factors, increased Type II collagen content, and altered the expression of serum OA cartilage degradation/bone turnover biomarkers (CTX-I, CTX-II, COMP, and PIINP). Based on these findings, we speculate that puerarin supplement to attain recovery from OA damage.

The effects of sodium usnic acid by topical application on skin wound healing in rats.

Wound healing is the process of repairing and remodeling damaged tissue. This is a public health problem that can influence the survival rate and quality of life of injured people. This attracts the attention of the medical community because it has high health care costs and there is presently a lack of successful therapy. Thus, the application of natural ingredients and medicinal plants has become a focus of research. The purpose of this study is to investigate the effectiveness of topically-applied sodium usnic acid on macroscopic and microscopic changes under dermal injury. These effects were measured using wound contraction experiments, histological analysis, and immunohistochemistry analysis, and gentamicin was used as a positive control medicine. Our results revealed that wound healing rates were higher and re-epithelialized times were shorter with topical application of sodium usnic acid, as compared to the negative control group. Histological results showed treatment with sodium usnic acid caused a reduction in inflammatory cells and an increase in fibroblast proliferation, granulation tissue, vascular regeneration. Sodium usnic acid treatment also resulted in earlier complete re-epithelialization, formation of well-organized bands of collagen, and epidermal keratinization. Furthermore, the levels of VEGF were significantly higher at day 1 post-wounding in those treated with sodium usnic acid. In conclusion, our results indicate that the topical use of sodium usnic acid could promote skin wound healing, and this mechanism might be related to anti-inflammatory effects at the wound site.