Osteoarthritis (OA) is a widespread chronic degenerative joint disease characterized by the degeneration of articular cartilage or inflamed joints. Our findings indicated that treatment with artemisinin (AT) downregulates the protein levels of MMP3, MMP13, and ADAMTS5, which are cartilage degradation-related proteins in OA, and inhibits the expression of inflammatory factors in interleukin-1β (IL-1β)-stimulated chondrocytes. However, the mechanism of the role of AT in OA remains unclear. Here, we performed gene sequencing and bioinformatics analysis in control, OA, and OA + AT groups to demonstrate that several mRNA candidates were enriched in the PI3K/AKT/mTOR signaling pathway, and TNFSF11 was significantly downregulated after AT treatment. TNFSF11 was downregulated in the OA + AT group, whereas it was upregulated in rat OA tissues and OA chondrocytes. Therefore, we confirmed that TNFSF11 was the target gene of AT. In addition, our study revealed that AT relieved cartilage degradation and defection by activating mitochondrial autophagy via inhibiting the PI3K/AKT/mTOR signaling pathway in IL-1β-induced chondrocytes. Furthermore, an OA model was established in rats with medial meniscus destabilization. Injecting AT into the knee joints of OA rat alleviated surgical resection-induced cartilage destruction. Thus, these findings revealed that AT relieves OA by activating mitochondrial autophagy by reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling.

Osteogenic differentiation (OD) of bone marrow mesenchymal stem cells (BMSCs) contributes significantly to the regeneration of bone defects. Resistin, an adipose tissue-specific secretory factor, has been shown to involve many different functions, including metabolism, inflammation, cancer, and bone remodeling. However, the effects and mechanisms of resistin on OD of BMSCs remain unclear. Herein, we demonstrated that resistin was highly expressed in BMSCs with OD. Upregulation of resistin contributed to the progression of OD of BMSCs by activating PI3K/AKT/mTOR signaling pathway. In addition, resistin facilitated OD by targeting transcriptional co-activator with PDZ-binding motif (TAZ). In a rat femoral condyle bone defect model, local injection of resistin significantly promoted bone repair and improved bone formation. This work contributes to better understanding the mechanism of resistin directly involved in the OD and might provide a new therapeutic strategy for bone defect regeneration.

The aim of this study is to observe the therapeutic effect of percutaneous endoscopic discectomy and its influencing factors for lumbar disc herniation and compare the advantages and disadvantages of transforaminal and interlaminar of percutaneous endoscopy. Data from 143 patients with lumbar disc herniation were respectively collected, including demographic and clinical data. Study population were divided into curative effect group and poor curative effect group, and logistic regression was used to explore the influencing factors of curative effect. The operation data and pre-and post-operation scores were compared to explore the effect of transforaminal and interlaminar approach on surgery efficacy. The rate of curative effect was 93.7%. 120 patients were classified as curative group and 23 patients were categorized as poor effective group. Univariate analysis found that the patients in the curative effect group tended to receive the interlaminar approach (58.3% vs 34.8%, P = .038). Multivariate logistic regression did not find operation approach was not related to curative effect of operation (transforaminal and interlaminar). But age ≥45 (odd risk (OR) = 6.43, P = .016), course of disease >12 month (OR = 3.77, P = .003), back and leg pain (OR = 3.46, P = .026), history of trauma (OR = 3.88, P = .014), Pfirrmann level IV (OR = 4.84, P = .004), and pre-Visual Analogue Scale (VAS) <5.3 (OR = 3.63, P = .015) were associated with operation efficacy. Compared with transforaminal group, the interlaminar group has less operative time (P = .000), less fluoroscopy time (P = .000), less puncture time (P = .000), less blood loss (P = .011). The transforaminal or interlaminar did not affect the treatment efficacy of percutaneous endoscopic discectomy for lumbar disc herniation. The selection of surgery approach depended on anatomical structure and physiological characteristics. It should be noted that 45 years of age or older, in the course of more than 12 months, both lumbocrural pain and lumbar disc herniation with grade IV, with history of trauma, may have impact on the efficacy of surgery.

Osteoporosis is a result of the imbalance between osteoblasts and osteoclasts quantities, which is closely correlated with osteogenic differentiation (OD). Leucocyte cell-derived chemotaxin 2 (LECT2) has been reported as a regulatory factor in some chronic diseases such as hepatitis through mediating downstream target gene β-catenin. Additionally, Wnt/β-catenin is also the crucial modulatory signal pathway in OD. Mesenchymal stem cells (MSC) is a kind of mesodermal stem cells; its differentiation direction is discovered affected by Wnt/β-catenin. However, the function of LECT2 in osteoporosis still remains exploration, which encourages us to lucubrate its functional effect in regulating the OD of MSCs. In this study, we found that LECT2 was expressed at low level in MSCs with osteogenic differentiation, and knockdown of LECT2 would activate Wnt/β-catenin pathway and therefore promoting OD in MSCs. It is the first time to report that LECT2 participates in regulating OD via mediating Wnt/β-catenin. Our discovery would affirmatively help provide a novel strategy for the diagnosis and therapy methods for osteoporosis.