Comparison of early curative effects of lateral unicompartmental knee arthroplasty with total knee arthroplasty and the legacy constrained condylar knee arthroplasty in the treatment of isolated lateral osteoarthritis: a single-center retrospective study.

BACKGROUND: Aims of this study were to compare the functional and radiographic results, perioperative complication after lateral unicompartmental knee arthroplasty (LUKA) with total knee arthroplasty (TKA) and the legacy constrained condylar knee (LCCK) arthroplasty for the treatment of lateral compartmental knee osteoarthritis (LCKOA), and to provide a basis for the treatment of LCKOA. METHODS: From January 2021 to January 2024, analyzed retrospectively clinical data of 74 patients with LCKOA treated with LUKA, TKA and LCCK arthroplasty. According to the operation plan, the patients were divided into three groups: LUKA group (23 cases), TKA group (23 cases) and LCCK group (28 cases). The changes of hip-knee-ankle (HKA) angle of the affected knee before and after operation were measured. All patients were assessed using the operation time, blood loss during operation, incision length, visual analogue scale (VAS) score before operation and after operation, Hospital for Special Surgery score (HSS), Oxford Knee Score (OKS), range of motion (ROM). RESULTS: All 74 patients were followed up for (2.38 ± 0.33) years. The operation time, blood loss during operation, incision length and VAS score after operation in the LUKA group were significantly less than those in the TKA group and LCCK group (P < 0.05); HKA valgus angle, ROM, HSS score and OKS score of the three groups after operation were significantly better than those before operation (P < 0.05); There was no significant difference among the three groups in HSS score and OKS score (P > 0.05). CONCLUSION: LUKA, TKA and LCCK arthroplasty have good clinical effect in the treatment of LCKOA; Compared with TKA and LCCK arthroplasty, LUKA has the advantages of less trauma, less bleeding, less pain and quick recovery. The short-term effect is satisfactory, and the long-term effect remains to be observed.

Interference with SPARC inhibits Benzophenone-3 induced ferroptosis in osteoarthritis: Evidence from bioinformatics analyses and biological experimentation.

The aim of this study is to conduct a thorough evaluation of the association between Benzophenone-3 (BP-3) exposure and OA, offering critical insights into the underlying mechanisms involved. The National Health and Nutrition Examination Survey (NHANES) database was utilized to investigate the correlation between BP-3 and osteoarthritis. Proteomic sequencing from clinical sample and the PharmMapper online tool were employed to predict the biological target of BP-3. Cellular molecular assays and transfection studies were performed to verify the prediction from bioinformatics analyses. Through cross-sectional analysis of the NHANES database, we identified BP-3 as a risk factor for OA development. The results of proteomic sequencing showed that Secreted Protein Acidic and Rich in Cysteine (SPARC) was significantly elevated in the area of damage compared to the undamaged area. SPARC was also among the potential biological targets of BP-3 predicted by the online program. Through in vitro cell experiments, we further determined that the toxicological effects of BP-3 may be due to SPARC, which elevates intracellular GPX4 levels, activates the glutathione system, and promotes lipid peroxidation to mitigate ferroptosis. Inhibiting SPARC expression has been shown to reduce inflammation and ferroptosis in OA contexts. This research provides an expansive understanding of BP-3's influence on osteoarthritis development. We have identified SPARC as a potent target for combating chondrocyte ferroptosis in BP-3-associated osteoarthritis.

miR-7/EGFR/MEGF9 axis regulates cartilage degradation in osteoarthritis via PI3K/AKT/mTOR signaling pathway.

Osteoarthritis (OA) is a common degenerative disease in middle-aged and elderly people. Our previous study has proved that microRNA-7 (miR-7) exacerbated the OA process. This study was aimed to explore the downstream genes and mechanism regulated by miR-7 to affect OA. Multiple EGF-like-domains 9 (MEGF9) was the predicted target of miR-7 by databases. Luciferase report experiment results confirmed that MEGF9 could bind to miR-7. Among the 10 collected pairs of OA and healthy samples, the expression levels of miR-7 and MEGF9 were both up-regulated when compared with healthy subjects by qRT-PCR and immunohistochemistry (IHC). The increased MEGF9 levels were due to the interaction with epidermal growth factor receptor (EGFR) by co-immunoprecipitation. Evaluations found that upregulation of miR-7 or MEGF9 can increase the expression of EGFR, matrix metalloproteinase-13 (MMP-13) and a disintegrin like and metallopeptidase with thrombospondin type 1 motif 5 (ADAMTS-5), so as to aggravate cartilage degradation. In addition, this effect induced by miR-7/EGFR/MEGF9 axis was by activation of PI3K/AKT signaling. The IHC and western blot assay results on OA model mice also demonstrated that miR-7/EGFR/MEGF9 axis regulated cartilage degradation in vivo. In summary, miR-7/EGFR/MEGF9 axis may perform a crucial function in the regulation of OA, providing potential for OA treatment.

circFAM160A2 Promotes Mitochondrial Stabilization and Apoptosis Reduction in Osteoarthritis Chondrocytes by Targeting miR-505-3p and SIRT3.

Competitive endogenous RNAs (ceRNAs), as a newly identified regulating mechanism, have been demonstrated to play a crucial role in various human diseases. An increasing number of recent studies have revealed that circular RNAs (circRNAs) can function as ceRNAs. However, little is known about the role of circFAM160A2 in the pathological process of osteoarthritis (OA). This study is the first to examine the crucial role of the circFAM160A2-miR-505-3p-SIRT3 axis in osteoarthritis progression. miR-505-3p was selected from the interaction of a microRNA (miRNA) microarray comparing chondrocytes in OA and normal conditions and prediction results from TargetScan. RT-qPCR was performed to assess the expression of circFAM160A2, miR-505-3p, and SIRT3. A dual luciferase assay was used to validate the binding of circFAM160A2, miR-505-3p, and SIRT3. We used lentivirus and adeno-associated virus to establish in vitro and in vivo overexpression models. Western blotting, apoptosis assay, ROS detection assay, Safranin O staining, and CCK-8 assay were employed to assess the role of circFAM160A2, miR-505-3p, and SIRT3. We found that miR-505-3p was upregulated and circFAM160A2 was downregulated in OA. While overexpression of circFAM160A2 decreased the production of extracellular matrix (ECM) degrading enzymes and ameliorated chondrocyte apoptosis and mitochondrial dysfunction, inhibition of miR-505-3p could reverse the protective effect of circFAM160A2 on the OA phenotype both in vitro and in vivo. In conclusion, circFAM160A2 can promote mitochondrial stabilization and apoptosis reduction in OA chondrocytes by targeting miR-505-3p and SIRT3, which might be a potential therapeutic target for OA therapy.

The elevated expression of IL-38 serves as an anti-inflammatory factor in osteoarthritis and its protective effect in osteoarthritic chondrocytes.

The objective of this study is to investigate the role of IL-38 in osteoarthritis (OA). IL-38 levels in serum and synovial fluid (SF) of patients with OA were examined to identify the correlation between IL-38 expression and OA activity and to determine its anti-inflammatory effects in IL-1ß-induced chondrocytes. A total of 75 patients with OA who underwent joint replacement surgery and 25 age- and sex-matched healthy volunteers were recruited. The levels of IL-38 in serum and SF are shown to be significant elevated in OA patients compared with that of healthy controls. Serum and SF IL-38 levels of OA patients are positively correlated with Kellgren-Lawrence (K-L) grades 2 to 3, as well as with pro-inflammatory cytokines IL-6, IL-23, and TNF-α, but are negatively correlated with the anti-inflammatory cytokine IL-10 in K-L grades 3 to 4. Furthermore, overexpression of IL-38 in vitro is shown to attenuate the expression of pro-inflammatory cytokines such as COX-2, IL-6, IL-8, IL-36Ra, IL-36α/ß/γ, iNOS, and TNF-α, as well as matrix degrading enzymes such as MMP3, MMP13, and ADAMTS5, and apoptosis-related indicators Bax/Bcl-2, cleaved caspase 3/pro-caspase 3, and cleaved caspase 9/pro-caspase 9. IL-38 overexpression also reduces expression of the signaling proteins p-p38, p-p65, p-JNK, and RhoA significantly. Taken together, our results show that expression of IL-38 is increased in OA tissues and OA rat chondrocytes, and is positively correlated with early disease activity. This increased IL-38 expression lead to the inactivation of MAPK, NF-κB, JNK, and RhoA signaling pathways, which might have impletion on OA chondrocytes apoptosis, degradation and inflammatory effect. Thus, IL-38 probably serves as a novel therapeutic target for the treatment of OA.

SIRT3 ameliorates osteoarthritis via regulating chondrocyte autophagy and apoptosis through the PI3K/Akt/mTOR pathway.

Osteoarthritis (OA) is the most common form of joint disease. The aim of this study was to explore the functions of SIRT3 on OA pathophysiology and the mechanism involved. Rat chondrocytes and destabilized medial meniscus (DMM) rat OA model were used as in vitro and in vivo models. In addition, lentivirus and plasmid were used to overexpress SIRT3, while siRNA was applied to establish SIRT3 knockdown. IL-1ß induced inflammation, apoptosis, mitochondrial dysfunction, and chondrocyte degeneration were inhibited by SIRT3 overexpression, which were enhanced in SIRT3-knockdown rat chondrocytes. Furthermore, overexpression of SIRT3 could restore IL-1ß-induced autophagy inhibition. We also found that IL-1ß-induced PI3K/Akt/mTOR signaling pathway activation was inhibited by SIRT3 overexpression, which was enhanced by SIRT3 knockdown. Last, intra-articular SIRT3 overexpression alleviated the severity of OA-induced rat joint damage. Our results demonstrated that SIRT3 is an important protective agent against OA pathophysiology via inhibiting PI3K/Akt/mTOR signaling.

Tricetin Protects Rat Chondrocytes against IL-1ß-Induced Inflammation and Apoptosis.

Tricetin is a well-studied flavonoid with a wide range of pharmacological activities in cancer and inflammation. However, the ability of tricetin to ameliorate the inflammation that occurs in osteoarthritis (OA) has not been determined. This study explored the effects of tricetin on interleukin- (IL-) 1ß-induced rat chondrocytes. Chondrocytes harvested from rat cartilage were incubated in vitro with tricetin in the presence of IL-1ß. The expression of matrix metalloproteinase- (MMP-) 1, MMP-3, MMP-13, nitric oxide (NO), prostaglandin E2 (PGE2), Bax, and Bcl-2 was evaluated by real-time-PCR, ELISA, Griess reaction, and western blotting. Caspase-3 activity in chondrocytes was determined using a caspase-3 activity assay and MAPK pathway activity by western blotting. Tricetin decreased the expression of MMP-1, MMP-3, and MMP-13 at both the gene and protein level in IL-1ß-induced rat chondrocytes. It also inhibited IL-1ß-induced NO and PGE2 production, by modulating inducible NO synthase and cyclooxygenase 2 gene expression. An antiapoptotic role of tricetin involving the Bax/Bcl-2/caspase-3 pathway was also determined. The chondroprotective effect of tricetin was shown to be partly related to the suppression of the MAPK signaling pathway. The results of this study demonstrate the chondroprotective role of tricetin, based on its anticatabolic, anti-inflammatory, and antiapoptotic effects in chondrocytes. The therapeutic potential of tricetin in OA patients should be explored in future studies.

The 10-year outcomes of the ASR XL Acetabular System: a single-center experience from China.

BACKGROUND: The revision rate of articular surface replacement (ASR) implants continues to rise in China because of metal debris. However, there are few reports on the clinical results of ASR implants with prolonged follow-up time in China. This study investigated the clinical outcomes and the risk factors of revision surgery in patients with ASR implants. METHODS: In total, 74 patients (74 hips) who underwent primary total hip arthroplasty (THA) with ASR implants over the past 4 to 10 years were retrospectively analyzed. Relevant clinical, radiographic, and biochemical data were examined. RESULTS: The average follow-up time was 88.46 (range 23-114) months, and the ASR implants of 18 hips (24.3%) were revised. Patients who received revision surgery had worse joint function with significantly lower Harris Hip Score and Western Ontario and McMaster Universities index than non-revision patients (61.11 ± 6.68 vs 85.30 ± 9.16, p < 0.001; 61.00 ± 3.83 vs 79.04 ± 14.49, p < 0.001; respectively). Higher acetabular abduction angle and serum Co and Cr concentration were significantly relevant to worse joint function as measured by HSS (p = 0.018, 0.009, 0.043, respectively). ROC curve analysis was applied to categorize the optimal cutoff values of acetabular abduction angle and serum Cr and Co concentration for revision surgery, which were settled as 47.80°, 98.44 µg/L, and 6.95 µg/L, respectively. Overall survival of the prostheses with high acetabular abduction angle (> 47.80°, HR = 70.145, 95% CI 1.558-3158.213, p = 0.029), high serum Cr concentration (98.44 µg/L, HR = 58.956, 95% CI 1.294-2685.203, p = 0.036), and high serum Co concentration (> 6.95 µg/L, HR = 179.511, 95% CI 2.360-13656.941, p = 0.019) decreased significantly than the lower groups. CONCLUSIONS: Evaluation of the DePuy ASR XL articulation demonstrated increased rates of revision following a longer follow-up period. High acetabular abduction angle and serum Cr and Co concentration correlated with worse clinical outcomes and high revision rate. Therefore, we advocate that patients with DePuy ASR XL implants be followed up more closely than those with other implants, especially with high acetabular abduction angle and serum Cr or Co concentration.

Association between interleukin-17A/F single nucleotide polymorphisms and susceptibility to osteoarthritis in a Chinese population.

Interleukin-17A/F (IL-17A/F) might play a role in the pathophysiology of osteoarthritis (OA), but several studies exploring the association between IL-17A/F single nucleotide polymorphisms and OA in different populations present inconsistent results. Thus, this case-control study, involving 410 OA cases and 507 controls, was aimed to investigate such association in a Chinese population. Genotyping was performed using standard polymerase chain reaction and restriction fragment length polymorphism. It was found that AA genotype or A allele carriers of IL-17A gene rs2275913 polymorphism were associated with OA susceptibility. Stratified analyses showed IL-17A rs2275913 polymorphism was evidently associated with a significantly increased risk for OA among males, <60 years old patients, smokers, and drinkers. No significant association was observed between IL-17F gene rs763780 polymorphism and OA risk. In conclusion, IL-17A rs2275913 polymorphism is involved in the development of OA in Chinese Han population. This finding should be confirmed by a larger study from diverse ethnic populations.

Paeoniflorin inhibits IL-1ß-induced MMP secretion via the NF-κB pathway in chondrocytes.

Paeoniflorin serves important cellular roles, exerting anti-cancer, anti-inflammatory and anti-pulmonary fibrosis effects and possesses immune-modulatory properties. However, the exact role of paeoniflorin in the pathogenesis of osteoarthritis (OA) remains unclear. The aim of the present study was to investigate the effects of paeoniflorin on articular surfaces in vitro. Rat chondrocytes were cultured in vitro and an MTT assay was performed to assess chondrocyte survival. Following treatment with interleukin (IL)-1ß and paeoniflorin, the production of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases-1 (TIMP-1) was examined using reverse transcription-quantitative polymerase chain reaction and western blotting. The interleukin (IL)-1ß-induced nuclear factor (NF)-κB pathway activation was also investigated. The results demonstrated that paeoniflorin was able to downregulate the expression of MMP and increase the expression of TIMP-1ntmRNA and protein in IL-1ß-induced rat chondrocytes. Furthermore, treating chondrocytes with paeoniflorin blocked the activation of NF-κB. These results suggest that paeoniflorin may serve am anti-catabolic role in the progression of OA and may be an effective preventative treatment for OA.

Paeoniflorin inhibits IL-1ß-induced chondrocyte apoptosis by regulating the Bax/Bcl-2/caspase-3 signaling pathway.

Apoptosis serves a pivotal role in the pathogenesis of osteoarthritis (OA). Increasing evidence has demonstrated that paeoniflorin exerts key properties (including anticancer, anti-inflammation and neuroprotective) for clinical applications. However, the precise role of paeoniflorin in articular cartilage apoptosis remains unknown. The present study explored the effects and potential molecular mechanism of paeoniflorin on rat chondrocyte apoptosis. Rat articular chondrocytes were cultured in monolayers. The lactate dehydrogenase (LDH) release rate of cells was determined by an LDH release assay. Annexin V-fluorescein isothiocyanate and propidium iodide staining were performed to detect early and advanced apoptotic cells by flow cytometry. The activity of caspase-3 in chondrocytes was determined using a caspase-3 activity assay. The expression of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) was examined by reverse transcription­quantitative polymerase chain and western blotting. The present study also examined the protein kinase B (Akt) signaling pathway by western blotting. Treatment with 25 or 50 µM paeoniflorin markedly decreased the release of LDH and the ratio of apoptotic cells in interleukin (IL)-1ß-induced rat chondrocytes. Paeoniflorin treatment decreased the mRNA and protein levels of Bax, and increased the level of Bcl-2. Paeoniflorin also reduced the activity of caspase-3 in chondrocytes. Furthermore, paeoniflorin was determined to regulate the Akt signaling pathway by increasing Akt phosphorylation. Therefore, paeoniflorin may exert its protective effect by inhibiting apoptosis in IL-1ß-induced rat chondrocytes and thus, may be an effective agent in the prevention and treatment of OA.

Rosmarinic acid down-regulates NO and PGE2 expression via MAPK pathway in rat chondrocytes.

Rosmarinic acid (RosA) is a water-soluble polyphenol, which can be isolated from many herbs such as orthosiphon diffuses and rosmarinus officinalis. Previous studies have shown that RosA possesses various biological properties. In this study, we investigate the anti-osteoarthritic effects of RosA in rat articular chondrocytes. Chondrocytes were pre-treated with RosA, followed by the stimulation of IL-1ß. Real-time PCR and Western blot were performed to detect the expression of matrix metalloproteinase (MMP)-1, MMP-3 and MMP-13. Nitric oxide and PGE2 production were measured by Griess reagent and enzyme-linked immunosorbent assay (ELISA). The expression of mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) was also investigated by Western blot analysis. We found that RosA down-regulated the MMPs expression as well as nitric oxide and PGE2 production in IL-1ß-induced chondrocytes. In addition, RosA inhibited p38 and JNK phosphorylation as well as p65 translocation. The results suggest that RosA may be considered a possible agent in the treatment of OA.

Vaspin prevents leptin­induced inflammation and catabolism by inhibiting the activation of nuclear factor­κB in rat chondrocytes.

The present study aimed to investigate the function and possible underlying mechanism of various concentrations of visceral adipose tissue­derived serine protease inhibitor (vaspin) on leptin­induced inflammatory and metabolic responses in rat chondrocytes. Rat articular chondrocytes were isolated and treated with different concentrations of vaspin, which was followed by stimulation with leptin. The expression of genes, secretion of nitric oxide and tumor necrosis factor­α, and activation of the nuclear factor (NF)­κB pathway were analyzed by reverse transcription­quantitative polymerase chain reaction, ELISA and western blotting. The results demonstrated that vaspin inhibited the leptin­induced upregulated gene expression levels of leptin receptor (OB­Rb), a disintegrin and metalloprotease with thrombospondin motifs (ADAMTS)­4, ADAMTS­5, matrix metalloproteinase (MMP)­2 and MMP­9, and the secretion of NO and TNF­α, in a dose­dependent manner. The phosphorylation of inhibitor of NF­κB (IκB), IκB kinase (IKK)α, IKKß and NF­κB were also promoted by leptin in the chondrocytes, which were also suppressed by increased concentration of vaspin. Taken together, results demonstrated that vaspin prevented leptin­induced inflammation and catabolism by inhibiting the activation of NF­κB in rat chondrocytes.

Acacetin inhibits expression of matrix metalloproteinases via a MAPK-dependent mechanism in fibroblast-like synoviocytes.

It is well known that rheumatoid arthritis (RA) is an autoimmune joint disease in which fibroblast-like synoviocytes (FLSs) play a pivotal role. In this study, we investigated the anti-arthritic properties of acacetin in FLSs. The expression of matrix metalloproteinase (MMP)-1, MMP-3 and MMP-13 were investigated by quantitative RT-PCR and western blot at gene and protein levels. At the same time, the phosphorylation of mitogen-activated protein kinases (MAPK) was investigated. The DNA-binding activity of NF-κB was investigated by electrophoretic mobility shift assay. We found that acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1ß-induced FLSs. Our results suggest that acacetin has antiarthritic effects in FLSs. Thus, acacetin should be further studied for the treatment of arthritis.

Cordycepin modulates inflammatory and catabolic gene expression in interleukin-1beta-induced human chondrocytes from advanced-stage osteoarthritis: an in vitro study.

Cordycepin is widely used as for its various pharmacological activities, such as anti-inflammation, anti-angiogenesis, anti-aging, anti-tumor and anti-proliferation. However, the precise role of cordycepin on chondrocytes is not clear. In the present study, we examined the inhibitory effects of cordycepin on interleukin-1 beta (IL-1ß)-induced glycosaminoglycan (GAG) release, nitric oxide production as well as gene expressions of inflammatory and catabolic mediators in human cartilage and chondrocytes. Cartilage explants and human chondrocytes were cultured in the absence or in the presence of IL-1ß (10 ng/ml) and with or without cordycepin (5-100 µM). GAG content in the cartilage explants was measured by using the dimethylmethylene blue method and Safranin O staining. Nitric oxide level was determined by Griess reaction. Expressions of MMP-1, MMP-13, cathepsin K, cathepsin S, ADAMTS-4 (a disintegrin and metalloproteinase with thrombospondin motifs-4) and ADAMTS-5, inducible nitric oxide synthase (iNOS) and cyclooxgenase-2 (COX-2) were evaluated by real-time quantitative PCR. We found that cordycepin suppressed IL-1ß-stimulated GAG release. Gene expressions of catabolic enzymes, including MMP-1, MMP-13, cathepsin K, cathepsin S, ADAMTS-4 and ADAMTS-5, were decreased by cordycepin in a dose-dependent manner. In addition, cordycepin inhibited IL-1ß-induced COX-2 and iNOS expression at the transcript level as well as blocked NO production. Our results suggest that cordycepin may possess chondroprotective effect by preventing cartilage denegation and interfering inflammatory response in the pathogenesis of OA.

Morin exerts antiosteoarthritic properties: an in vitro and in vivo study.

Morin is a flavonoid isolated from members of the Moraceae family. Morin has been reported to possess antioxidative and anticarcinogenic activities. However, the antiosteoarthritic properties of morin have not been investigated. In this study, we evaluate the antiarthritic properties of morin through in vitro and in vivo studies. We examined the effects of morin on the expression levels of matrix metalloproteinase (MMP)-3, MMP-13 and tissue inhibitors of metalloproteinase (TIMP)-1 in interleukin-1ß (IL-1ß)-induced rat chondrocytes by realtime polymerase chain reaction and Western blotting. The effects of morin on the phosphorylation of mitogen-activated protein kinases were also investigated. The in vivo antiosteoarthritic effects of morin were evaluated in the rat model of anterior cruciate ligament transection (ACLT)-induced osteoarthritis (OA). We found that morin inhibited the expression of MMP-3 and MMP-13 and increased the expression of TIMP-1 in IL-1ß-induced rat chondrocytes. In addition, morin inhibited IL-1ß-induced phosphorylation of extracellular signal-regulated kinase and p38. For the in vivo study in a rat model of OA induced by ACLT, in which morin was orally administered to rat, the results show that morin suppressed cartilage degradation. Our results suggest that morin may be considered as a possible therapeutic agent for the treatment of OA.

Protective effects of berberine in an experimental rat osteoarthritis model.

Berberine shows anticancer, antibacterial, antiinflammatory and antioxidant effects and may be useful in many clinical applications. The effects of berberine on articular cartilage metabolism remain unknown, so this study was performed to evaluate these effects in vitro and in vivo. For the in vitro work, rat articular chondrocytes were cultured in a monolayer and matrix metalloproteinase-1 (MMP-1), -3, -13 and tissue inhibitor of metalloproteinase (TIMP-1) expression was evaluated by real-time quantitative PCR. Nitric oxide (NO) levels were determined using the Griess reaction, and glycosaminoglycan (GAG) release was measured using the dimethylmethylene blue method. For the in vivo work, berberine was administered by intraarticular injection, and the effects on MMPs and TIMP-1 were examined at the gene and protein levels. Berberine was found to inhibit the expression of MMP-1, -3 and -13, and increased the level of TIMP-1 at the mRNA level in a dose-dependent manner. In IL-1ß-induced rat articular chondrocytes, berberine decreased IL-1ß-induced GAG release and NO production. Meanwhile, high-dose berberine exhibited an anticatabolic effect in an IL-1ß-induced rat osteoarthritis (OA) model. These findings suggest that berberine may play a protective role in the development of OA and may be useful in the treatment of OA.

Effects of diallyl sulphide in chondrocyte and cartilage in experimental osteoarthritis in rabbit.

Diallyl sulphide (DAS) is known for its antioxidant, anticancer and detoxifying properties. The aim of this study was to investigate the effect of DAS on rabbit articular chondrocytes and cartilage in experimental osteoarthritis (OA) induced by anterior cruciate ligament transection (ACLT). DAS inhibited matrix metalloproteinase-1 (MMP-1), MMP-3 and MMP-13 expression in interleukin-1beta (IL-1ß)-induced chondrocytes. In an in vivo study, DAS ameliorated cartilage degradation as assessed by morphological and histological examination. Messenger RNA expression of MMP-1, MMP-3, MMP-13 and IL-1ß was inhibited by DAS in cartilage. In addition, DAS increased the collagen II level in cartilage. The results suggest that DAS may protect cartilage in the development of OA.

Trichostatin A inhibits expression of cathepsins in experimental osteoarthritis.

The aim of this study was to investigate the effects of trichostatin A (TSA) on expression of cathepsins in cartilage in experimental osteoarthritis (OA). OA was induced in 18 rabbits by bilateral anterior cruciate ligament transection (ACLT). Four weeks after surgery, rabbits received intra-articular injection with TSA dissolved in the dimethylsulphoxide (DMSO) in the right knees and DMSO in the left knees once a week for 5 weeks. Rabbits were killed 7 days after the last injection. The knee joints were assessed by morphological and histological examination. Messenger RNA expression of cathepsins K, B, L, S and cystatin C was studied by real-time PCR. TSA inhibited the expression of cathepsins K, B, L, S and cystatin C accompanied with the less degradation in cartilage. The results suggest that TSA exhibits protective effects against cartilage degradation in rabbits with OA and the effects may be associated with the inhibition of cathepsins.

The emerging role of adipokines in osteoarthritis: a narrative review.

Osteoarthritis (OA) is a most common multifactorial degenerative joint disease in elderly individuals. OA is affecting severely the quality of life of patients, while the causes of OA are not completely understood. Age, obesity, the female sex, and previous injury are considered as significant risk factors. Recently, increased levels of adipokines which are mainly produced by adipocytes have been detected in patients with osteoarthritis. Moreover, studies on different adipokines all reveal that they have played proinflammatory and catabolic/anabolic roles during the pathophysiology of OA. In the present review, we summarize current data on the effect of the adipose tissue-derived hormones leptin, adiponectin, resistin and visfatin on initiation and progression of OA.