Knee osteoarthritis (KOA) lacks disease-modifying non-surgical treatments. This study evaluated whether Xue-Fu-Zhu-Yu (XFZY) decoction attenuates KOA-related synovial inflammation and apoptosis through MAPK signaling. UPLC-MS/MS profiling identified phenylpropanoids/polyketides, benzenoids, lipid-like compounds, and representative bioactive constituents including formononetin. Network pharmacology was combined with LPS-treated human synovial cells and a Freund's complete adjuvant-induced rat KOA model. XFZY reduced LPS-induced IL-6 and TNF-alpha, restored mitochondrial membrane potential, increased Bcl-2, reduced Caspase-3, and improved SOD and GSH levels. In silico analyses highlighted overlapping KOA-XFZY targets enriched in MAPK-related pathways; experimentally, XFZY decreased phosphorylation of p38, ERK, and JNK, whereas anisomycin weakened and SB203580 enhanced its anti-apoptotic effects. In rats, oral XFZY reduced inflammatory indices, improved synovial tissue integrity, and suppressed p38-MAPK activation. These findings extend known anti-inflammatory actions of XFZY to KOA synovial apoptosis and suggest MAPK suppression as a functional mediator, although validation in primary joint cells and clinical studies remains necessary.

Objectives:Knee osteoarthritis (KOA) is a persistent degenerative disease affecting the joints, significantly reducing the quality of life for individuals afflicted. This study explores the therapeutic effects of total saponin Achranthes (TSA) on KOA rats and its underlying mechanism. Materials and Methods:Forty-eight rats were randomly assigned to six experimental groups: a blank control group, a model group, a sham-operated group, and a TSA treatment group (low, medium, and high dose), with eight rats in each group. The rats were treated continuously for four weeks. The degree of joint swelling was quantified, and the Lequesne MG score was evaluated. Network pharmacology approaches were employed to pinpoint potential TSA targets and related pathways for managing KOA. Additionally, histopathological examinations were conducted on the knee cartilage of the rats. Serum levels of TNF-α and IL-1β were assessed through the ELISA assay. Results:The network pharmacology results indicate that TSA may effectively treat KOA through the MAPK and PI3K/Akt signaling pathways. Moreover, TSA significantly decreased the serum concentrations of pro-inflammatory cytokines such as TNF-α and IL-1β, and TSA down-regulated the P38 MAPK, PI3K/Akt, and NF-κB pathways, whereas the KOA model showed up-regulation. The treatment also significantly reduced MMP-9, MMP-13, and ADAMTS-5 protein levels. Conclusion:TSA can potentially ameliorate inflammation, safeguard knee cartilage tissue, and alleviate symptoms of KOA by inhibiting the MAPK/Akt/NF-κB signaling pathway.

Although observational studies have suggested associations between cathepsins and inflammatory wrist diseases, critical controversies persist regarding the causality, directionality, and disease-specific mechanisms of these relationships. Conventional clinical studies are unable to determine whether cathepsin-disease associations reflect true causality or spurious links driven by confounding factors or reverse causation. Moreover, systematic causal analyses focusing on protease-mediated mechanisms in wrist-specific inflammatory pathologies remain notably absent. To address these gaps, this study employs bidirectional 2-sample Mendelian randomization (MR) to investigate the causal effects of cathepsins on inflammatory wrist diseases and elucidate their disease-specific roles, thereby providing genetic evidence for targeted therapeutic strategies. We performed bidirectional 2-sample MR using public genome-wide association study summary statistics to assess causal relationships between 10 cathepsins and 4 inflammatory wrist diseases. Instrumental variables (single nucleotide polymorphisms) were selected at genome-wide significance (P < 5 × 10⁻⁶, and r² < 0.001) for exposure-outcome associations. Causality was evaluated via inverse-variance weighted, MR-Egger, and Weighted Median methods. Sensitivity analyses included Cochran Q, MR-Pleiotropy Residual Sum and Outlier, MR-Egger and leave-one-out validation. Univariate MR analysis demonstrated a causal association between genetically determined levels of cathepsin S and the development of carpal tunnel syndrome (odds ratio [OR], 0.954 [95% CI, 0.925-0.984]; P = .003), wrist synovitis (OR, 0.708 [95% CI, 0.529-0.949]; P = .021), and rheumatoid arthritis (RA; OR, 1.048 [95% CI, 1.005-1.092]; P = .029). Similarly, a causal link was established between cathepsin L and RA (OR, 0.948 [95% CI, 0.906-0.991]; P = .019), and between cathepsin F and De Quervain tenosynovitis (OR, 1.213 [95% CI, 1.003-1.466]; P = .046). A reverse MR analysis suggested a causal relationship between cathepsin O and wrist synovitis (OR, 1.047 [95% CI, 1.003-1.093]; P = .038). No causal associations were found for other cathepsins with the diseases studied. The reliability of these findings was confirmed through various robustness tests. Genetic evidence confirms cathepsin S protects against carpal tunnel syndrome and wrist synovitis but increases RA risk. Cathepsin F is positively associated with De Quervain tenosynovitis. Conversely, wrist synovitis elevates cathepsin O levels through reverse causation. These findings validate pathogenic mechanisms of wrist inflammatory disorders and suggest targeted inhibition of specific cathepsins as a promising therapeutic strategy.

BackgroundThe relationship between visceral adipose tissue and osteoarthritis is not clear. The purpose of our study was to explore the relationship between visceral adipose tissue and osteoarthritis.MethodsWe used a two-sample Mendelian randomization method to select single-nucleotide polymorphisms (SNPs) significantly associated with visceral adipose tissue as instrumental variables to explore the relationship between visceral adipose tissue and all osteoarthritis, hand osteoarthritis, hip osteoarthritis, knee osteoarthritis, and spine osteoarthritis. The reliability of the results was tested using sensitivity analysis.ResultsOur findings indicated that visceral adipose tissue was associated with all osteoarthritis, hip osteoarthritis, knee osteoarthritis, and spine osteoarthritis (all osteoarthritis: OR = 1.399, 95% CI: 1.335–1.467, p = 7.95e-44; hip osteoarthritis: OR = 1.399, 95% CI: 1.284–1.524, p = 1.41e-14; knee osteoarthritis: OR = 1.794, 95% CI: 1.662–1.937, p = 1.33e-50; and spine osteoarthritis: OR = 1.445, 95% CI: 1.314–1.589, p = 2.89e-14). Sensitivity analysis demonstrated the reliability of these results.ConclusionOur study suggests that genetically predicted visceral adipose tissue is associated with osteoarthritis. Reducing the accumulation of visceral adipose tissue could potentially have an impact on the incidence of osteoarthritis.

BACKGROUND:Arthritis seriously affects people's quality of life, and there is an urgent clinical need to improve the efficacy of medications as well as to reduce the adverse effects induced by treatment. Combined colchicine therapy is gradually being embraced in clinical care, but the evidence remains insufficient. METHODS:English databases were searched from the establishment to September 4, 2024. Eleven eligible Randomized controlled trials (RCTs) were included. The quality of the literature was assessed by the risk of bias tool in the Cochrane Handbook. Relative risk (RR) and Cohen's d (SMD) were used for categorical and continuous variables, respectively, at 95% confidence interval (CI), and Stata 17.0 software was used for statistical analysis. Sensitivity analyses were used to verify the stability of the analyzed results, and heterogeneity analyses were used to explore the sources of heterogeneity in the studies. Funnel plots and Egger's test were used to assess publication bias. RESULTS:Eleven eligible RCTs were included in this study. Compared with conventional treatment, combined colchicine treatment improved patient's global assessment results (SMD = 1.24, 95% CI [0.01, 2.47], P = 0.05, I2 = 0]), stiffness (SMD = -0.81, 95% CI [-1.43, -0.19], P = 0.01, I2 = 63.91%]) and did not increase adverse effects (RR = 0.79, 95% CI [0.31, 1.27], P = 0.36, I2 = 0.00%). However, combined colchicine treatment did not improve visual analog scores (VAS) (SMD = -0.96, 95% CI [-2.85, 0.93], P = 0.13, I2 = 97.99%]), Western Ontario and McMaster Universities Arthritis Index (WOMAC) pain (SMD = 0.01, 95% CI [-0.24, 0.27], P = 0.91, I2 = 0]), WOMAC function (SMD = -0.01, 95% CI [-0.36, 0.16], P = 0.44, I2 = 0]), Total WOMAC scale (SMD = -0.05, 95% CI [-0.33, 0.22], P = 0.70, I2 = 0]), physician 's global assessment (SMD = 0.36, 95% CI [-2.27, 3.00], P = 0.79, I2 = 97.04%]) and Modified Clinical Health Assessment Questionnaire (ModHAD) (SMD = -1.72, 95% CI [-4.90,1.45], P = 0.29, I2 = 99.11%]). CONCLUSION:Compared with colchicine alone, combination therapy improves patients' quality of life without increasing the incidence of adverse events.

Background: Knee osteoarthritis (KOA) is a persistent degenerative condition characterized by the deterioration of cartilage. The Chinese herbal formula Radix Rehmanniae PraeparataAngelica Sinensis-Radix Achyranthis Bidentatae (RAR) has often been used in effective prescriptions for KOA as the main functional drug, but its underlying mechanism remains unclear. Therefore, network pharmacology and verification experiments were employed to investigate the impact and mode of action of RAR in the treatment of KOA. Methods: The destabilization of the medial meniscus model (DMM) was utilized to assess the anti-KOA effect of RAR by using gait analysis, micro-computed tomography (Micro -CT), and histology. Primary chondrocytes were extracted from the rib cartilage of a newborn mouse. The protective effects of RAR on OA cells were evaluated using a CCK-8 assay. The antioxidative effect of RAR was determined by measuring reactive oxygen species (ROS), superoxide dismutase (SOD), and glutathione (GSH) production. Furthermore, network pharmacology and molecular docking were utilized to propose possible RAR targets for KOA, which were further verified through experiments. Results: In vivo, RAR significantly ameliorated DMM-induced KOA characteristics, such as subchondral bone sclerosis, cartilage deterioration, gait abnormalities, and the degree of knee swelling. In vitro, RAR stimulated chondrocyte proliferation and the expression of Col2a1, Comp, and Acan. Moreover, RAR treatment significantly reduced ROS accumulation in an OA cell model induced by IL -113 and increased the activity of antioxidant enzymes (SOD and GSH). Network pharmacology analysis combined with molecular docking showed that Mapk1 might be a key therapeutic target. Subsequent research showed that RAR could downregulate Mapk1 mRNA levels in IL-113-induced chondrocytes and DMM-induced rats. Conclusion: RAR inhibited extracellular matrix (ECM) degradation and oxidative stress response via the MAPK signaling pathway in KOA, and Mapk1 may be a core target.

Objective This meta-analysis aims to assess the efficacy and safety of platelet-rich plasma (PRP) for osteonecrosis of the femoral head (ONFH). Methods We comprehensively searched randomized controlled trials in PubMed, Web of Science, EMBASE, the Cochrane Central Register of Controlled Trials, Chinese National Knowledge Infrastructure, China Science and Technology Journal Database, WanFang, and Chinese BioMedical Literature Database from inception until October 25, 2024. The literature on the clinical efficacy of autologous PRP for ONFH was collated. According to the inclusion and exclusion criteria, the literature was screened, quality evaluated and the data was extracted. Meta-analysis was carried out with the software Review Manager 5.4.1 software and Stata 17.0 software. In addition, potential publication bias was detected by the funnel plot test and Egger’s test. The GRADE system was used to evaluate the quality of evidence for outcome indicators. Results Fourteen studies involving 909 patients were included in this study. Compared with non-PRP, PRP exhibited significant improvements in the Harris hip score (HHS) at 3 months (MD = 3.58, 95% Cl: 1.59 to 5.58, P = 0.0004), 6 months (MD = 6.19, 95% Cl: 3.96 to 8.41, P < 0.00001), 12 months (MD = 4.73, 95% Cl: 3.24 to 6.22, P < 0.00001), ≥ 24 months (MD = 6.83, 95% Cl: 2.09 to 11.59, P = 0.0003), and the last follow-up (MD = 6.57, 95% Cl: 4.81 to 8.33, P < 0.00001). The PRP also showed improvement in HHS compared to baseline than the non-PRP at 3 months (MD = 3.60, 95% Cl: 1.26 to 5.94, P = 0.003), 6 months (MD = 6.17, 95% Cl: 3.74 to 8.61, P < 0.00001), 12 months (MD = 5.35, 95% Cl: 3.44 to 7.25, P < 0.00001), ≥ 24 months (MD = 8.19, 95% Cl: 3.76 to 12.62, P = 0.0003), and the last follow-up (MD = 6.94, 95% Cl: 5.09 to 8.78, P < 0.00001). The change in visual analog scale (VAS) score 3 months post intervention (MD = -0.33, 95% Cl: -0.52 to -0.13, P = 0.001), 6 months (MD = -0.69, 95% Cl: -0.90 to -0.48, P < 0.00001), 12 months (MD = -0.75, 95% Cl: -1.05 to -0.46, P < 0.00001), ≥ 24 months (MD = -1.05, 95% Cl: -1.20 to -0.89, P < 0.00001), and the last follow-up (MD = -0.75, 95% Cl: -0.97 to -0.54, P < 0.00001). The PRP also showed a decrease in VAS score compared to baseline than the non-PRP at 3 months (MD = -0.29, 95% Cl: -0.41 to -0.17, P = 0.003), 6 months (MD = -0.63, 95% Cl: -0.96 to -0.30, P = 0.0002), 12 months (MD = -0.78, 95% Cl: -1.22 to -0.33, P = 0.0006), ≥ 24 months (MD = -1.11, 95% Cl: -1.27 to -0.96, P < 0.00001), and the last follow-up (MD = -0.74, 95% Cl: -1.05 to -0.43, P < 0.00001). Additionally, it was found that the PRP group had the advantages in the following aspects: collapse rate of the femoral head (RR = 0.33, 95% Cl: 0.17 to 0.62, P = 0.0006), rate of conversion to total hip arthroplasty (RR = 0.37, 95% Cl: 0.18 to 0.74, P = 0.005), and overall complications (RR = 0.33, 95% Cl: 0.13 to 0.83, P = 0.02). The GRADE evidence evaluation showed overall complication as very low quality and other indicators as low quality. Conclusion There is limited evidence showing benefit of PRP therapy for treatment of ONFH patients, and most of this evidence is of low quality. Caution should therefore be exercised in interpreting these results. It is recommended that future research involve a greater number of high-quality studies to validate the aforementioned conclusions. Systematic review registration https://www.crd.york.ac.uk/prospero/ #recordDetails, CRD42023463031.

Background: Previous observational studies have demonstrated an association between grip strength and detrimental pregnancy and perinatal outcomes. However, the causality of this relationship remains uncertain. Objective: This study aims to investigate if there is a causal relationship between grip strength and adverse pregnancy and perinatal outcomes, providing evidence to support active intervention for adverse pregnancy outcomes. Study design: A two-sample Mendelian randomization method was used to select GWAS data from the UK Biobank and the FinnGen Biobank as data sources. The inverse variance weighting method was used as the main analysis method. The reliability of the results was verified through sensitivity analysis, including Cochran's Q test, MR-egger intercept regression analysis, leave-one-out analysis, and funnel plot. Independent queues are also used to verify the reliability of the results. Results: The study demonstrated a significant positive correlation between genetically predicted hand grip strength and offspring birth weight, specifically left-hand grip strength (β = 0.193, 95 % CI: 0.099–0.286, p = 0.0001) and right-hand grip strength (β = 0.310, 95 % CI: 0.235–0.384, p = 3.27E-16). Sensitivity analysis indicated no horizontal multi-effect, and leave-one-out analysis along with the funnel plot showed no abnormalities. The verification queue also yielded similar results. Conclusion: This study revealed a significant association between grip strength-related traits and offspring birth weight, suggesting a potential protective effect. Moreover, a negative predictive trend was observed for other adverse pregnancy outcomes. Modifying grip strength through an active lifestyle and continuous monitoring of pregnant women's grip strength may have implications for improving pregnancy outcomes. However, further research is warranted to investigate these findings more comprehensively.

BackgroundThe association between depression and musculoskeletal diseases has long been a subject of contentious debate. However, the causal relationship between the two remains uncertain. This study employs a two-sample Mendelian randomization (MR) analysis to investigate the causality between depression and six musculoskeletal diseases.MethodsIn this study, we performed MR analysis to systematically explore the causal relationship between depression and six musculoskeletal disorders. Single nucleotide polymorphisms (SNPs) that are linked to depression were employed as instrumental variables. To ensure robust and reliable conclusions, multiple analytical approaches were utilized, including inverse variance weighting(IVW), weighted median, and MR-Egger regression. Additionally, sensitivity analysis methods such as the MR-Egger intercept test, Cochran’s Q test, leave-one-out analysis, and funnel plot were employed.ResultsOur MR analysis revealed a significant association between depression and cervical spondylosis (depression: OR 1.003, 95% CI 1.002–1.005, P = 8.32E-05; major depressive disorder: OR 1.003, 95% CI 1.001–1.005, P = 0.0052). Furthermore, a strong correlation was noted between major depressive disorder (MDD) and knee osteoarthritis (KOA) (OR 1.299, 95% CI 1.154–1.463, P = 1.50E−5). Sensitivity analysis confirmed the robustness of these findings. Our independent validation study also corroborated these results.ConclusionThe MR analysis conducted in this study provides evidence supporting a genetic link between depression and cervical spondylosis, as well as KOA. Targeted interventions to manage depression in susceptible populations may contribute to lowering the risk of cervical spondylosis and KOA in these cohorts.

ObjectiveHyperuricaemia and gout are common metabolic disorders. However, the causal relationships between blood metabolites and serum urate levels, as well as gout, remain unclear. A systematic evaluation of the causal connections between blood metabolites, hyperuricemia, and gout could enhance early screening and prevention of hyperuricemia and gout in clinical settings, providing novel insights and approaches for clinical treatment.MethodsIn this study, we employed a bidirectional two-sample Mendelian randomization analysis utilizing data from a genome-wide association study involving 7,286 participants, encompassing 486 blood metabolites. Serum urate and gout data were sourced from the Chronic Kidney Disease Genetics consortium, including 288,649 participants for serum urate and 9,819 African American and 753,994 European individuals for gout. Initially, LDSC methodology was applied to identify blood metabolites with a genetic relationship to serum urate and gout. Subsequently, inverse-variance weighting was employed as the primary analysis method, with a series of sensitivity and pleiotropy analyses conducted to assess the robustness of the results.ResultsFollowing LDSC, 133 blood metabolites exhibited a potential genetic relationship with serum urate and gout. In the primary Mendelian randomization analysis using inverse-variance weighting, 19 blood metabolites were recognized as potentially influencing serum urate levels and gout. Subsequently, the IVW p-values of potential metabolites were corrected using the false discovery rate method. We find leucine (IVW P FDR = 0.00004), N-acetylornithine (IVW P FDR = 0.0295), N1-methyl-3-pyridone-4-carboxamide (IVW P FDR = 0.0295), and succinyl carnitine (IVW P FDR = 0.00004) were identified as significant risk factors for elevated serum urate levels. Additionally, 1-oleoylglycerol (IVW P FDR = 0.0007) may lead to a substantial increase in the risk of gout. Succinyl carnitine exhibited acceptable weak heterogeneity, and the results for other blood metabolites remained robust after sensitivity, heterogeneity, and pleiotropy testing. We conducted an enrichment analysis on potential blood metabolites, followed by a metabolic pathway analysis revealing four pathways associated with serum urate levels.ConclusionThe identified causal relationships between these metabolites and serum urate and gout offer a novel perspective, providing new mechanistic insights into serum urate levels and gout.

目的 研究腰腿痛宁胶囊对木瓜蛋白酶诱导的兔膝骨性关节炎模型炎症因子的调控机制.方法 20只实验兔随机分为空白组、模型组、仙灵骨葆组和腰腿痛宁组,各5只.各组左膝关节腔注射木瓜蛋白酶混合液0.5 mL·kg-1,并驱赶运动14 d,然后分别采用对应药物给予治疗28 d.同时,各组在治疗前(造模成功后)和治疗后用量角器测量左膝关节活动角度.实验结束后,拍摄X线片观察各组左膝关节损伤情况;HE染色法观察各组关节软骨病理改变,进行Mankin评分;ELISA法测定各组血清和关节液中IL-1β、IL-6、TNF-α的水平.结果 治疗前,与空白组比较,其他各组左膝关节活动度明显降低(P<0.05),X线片显示左膝关节间隙明显变窄、骨赘形成;治疗后,与空白组比较,模型组左膝关节软骨损伤程度及Mankin评分明显增高(P<0.05),炎症因子水平均显著升高(P<0.05);治疗后,与模型组比较,仙灵骨葆组和腰腿痛宁组左膝关节活动度均改善(P<0.05),左膝关节软骨损伤程度及Mankin评分明显降低(P<0.05),炎症因子水平水平显著降低(P<0.05).结论 腰腿痛宁胶囊能降低兔早期膝骨关节炎血清和关节液中IL-1β、IL-6、TNF-α的水平,提示腰腿痛宁胶囊可通过抑制炎症反应延缓膝骨关节炎病理发展.

ObjectiveObservational studies have suggested an increased risk of cardiovascular disease in individuals with ankylosing spondylitis. However, these studies are prone to confounding factors and reverse causality. To address these limitations, we conducted a Mendelian randomization study to assess the causal relationship between AS and CVD.MethodsThe study population comprises 9,069 individuals with ankylosing spondylitis and 509,093 individuals with either of six common cardiovascular diseases and a related indicator. Causal analysis using summary effect estimates and inverse variance weighting were employed as the main methods.ResultsThe CAUSE analysis showed no evidence of a causal relationship between AS and CVD. The odds ratios for total CVD, heart failure, myocardial infarction, valvular heart disease, ischemic heart disease, and venous thromboembolism, Arterial stiffness index, were as follows: OR, 1.01; 95% confidence interval, 0.96–1.05; P = 0.91; OR, 1.03; 95% CI, 0.99–1.08; P = 0.50; OR, 0.94; 95% CI, 0.86–1.03; P = 0.53; OR, 0.99; 95% CI, 0.94–1.04; P = 0.99; OR, 0.98; 95% CI, 0.91–1.04; P = 0.94; OR, 0.98; 95% CI, 0.91–1.04; P = 0.99; β, −0.0019; 95% CI, 0.97–1.01; P = 0.99. The IVW and weighted median methods also yielded consistent results, and no heterogeneity or pleiotropy was found. Likewise, a reverse Mendelian randomization analysis did not uncover a heritable causal relationship between AS and CVD.ConclusionThis Mendelian randomization study does not support a causal relationship between AS and CVD. Further research is needed to confirm this association.

腰椎间盘突出症是由于腰椎间盘及周围组织发生退行性病变后,纤维环破裂,髓核单独或者连同纤维环向外突出,压迫刺激神经根或窦椎神经而引起的以腰痛或腿痛腿麻为主要症状的一种综合征[1].腰间盘突出症在传统医学中没有专门的论述,根据该病的病位、病因、及临床表现等,此病应属于《黄帝内经》中"腰痛""痹病"及"肾虚"等范畴[2].临床上腰椎间盘突出症首选中医药保守康复疗法[3].赵文海教授40余年来致力于腰椎间盘突出症的临床研究,基于天池伤科流派"补肾、祛瘀、除痹"的学术观点,依据我国北方地域特点,提出了以"先后天同补"治疗腰椎间盘突出症的总纲及"补肝肾,健脾胃、祛寒湿、破瘀阻"的治疗原则,现将其用药经验总结整理如下.

Background:Sedentary behavior and physical activity are still ambiguous in their effects on osteoarthritis. We aimed to evaluate the effects of physical activity and sedentary behavior on osteoarthritis to provide a reference for the prevention of osteoarthritis.Methods:This study was conducted in Changchun, China in 2022. We used two-sample Mendelian randomization with the SNP as an instrumental variable to investigate the effect of physical activity and sedentary behavior on osteoarthritis. In addition, a two-step Mendelian randomization method was used to test whether mediating factors (BMI, smoking, Apolipoprotein B) were involved in mediating the effects of exposure factors on osteoarthritis.Results:TV watching was causally related to knee osteoarthritis and spine osteoarthritis, and they were positively correlated (knee osteoarthritis: OR=1.162,95 %CI: 1.027-1.315, P=0.017; spine osteoarthritis: OR=1.208,95 %CI: 1.033-1.413, P=0.018). BMI played a mediating role in the process of TV watching with knee osteoarthritis and spine osteoarthritis. ((The proportion of BMI mediating effect: knee osteoarthritis: 47.1% (95% CI: 36.7%~63.2%); spine osteoarthritis: 29.5% (95% CI: 19.3%~40.8%)). The proportion of Smoking mediating effect in the process of TV watching with spine osteoarthritis was 16.1% (95% CI: 3.7% ~ 31.6%).Conclusion:TV watching is a potential risk factor for osteoarthritis and plays a role through modifiable factors such as BMI and smoking, therefore, interventions on these factors have the potential to reduce the burden of osteoarthritis caused by longer TV watching times.

Background Previous studies have suggested that antihypertensive drugs may play a role in the treatment of osteoarthritis, but these studies may be limited by confounding factors and lead to biased results. Therefore, we conducted a Mendelian randomization study to investigate the effects of blood pressure and antihypertensive drugs on osteoarthritis. Methods We used published large-scale genome-wide association data and applied univariate and multivariate Mendelian randomization methods. The main analysis model was inverse variance weighting, and the reliability of the results was tested using MR-Egger intercept analysis, Cochran's Q test, and leave-one-out analysis. We comprehensively evaluated the relationship between systolic blood pressure, diastolic blood pressure, 12 antihypertensive drugs, and osteoarthritis. We also conducted verification in the independent queue of UK Biobank and built a simple linear regression model to obtain an independent comparison. Results We found no evidence that systolic and diastolic blood pressure significantly affected osteoarthritis. However, among antihypertensive drugs, we observed a significant positive correlation between potassium-preserving diuretics and aldosterone antagonists and all osteoarthritis (OR: 0.560, 95% CI 0.406–0.772, P = 0.0004). Sensitivity analysis showed no horizontal pleiotropy or heterogeneity, and the leave-one-out analysis demonstrated the reliability of the results. This result was replicated with nominally statistical significance in the validation cohort and exhibited significant correlation in the linear regression analysis. Conclusions Our study suggested that controlling the protein targets of potassium-sparing diuretics and aldosterone antagonists may have beneficial results for osteoarthritis. These findings provide valuable medication strategies for the control of hypertension in patients with osteoarthritis.

目的:探讨缓释骨诱导因子的玉米醇溶蛋白(Zein)/左旋聚乳酸(PLLA)同轴静电纺丝纳米纤维支架对骨髓间充质干细胞(MSCs)成骨分化作用.方法:制备载有骨形态发生蛋白-2(BMP-2)和地塞米松(DEX)的壳-核型同轴静电纺丝支架,使用透射电子显微镜(TEM)验证纳米纤维的壳-核结构.分离原代骨髓间充质干细胞并培养,使用扫描电子显微镜(SEM)评估骨髓间充质干细胞的黏附、生长情况.检测碱性磷酸酶(ALP)活性并定量分析,茜素红染色(ARS)检测钙矿化沉积物并定量分析.结果:骨髓间充质干细胞经成骨诱导分化后,表现出成骨细胞的特性.透射电子显微镜观察到以玉米醇溶蛋白和左旋聚乳酸为原料,利用同轴静电纺丝技术制备的纳米纤维具有完整的壳-核结构.扫描电子显微镜观察到骨髓间充质干细胞在加载骨形态发生蛋白-2和地塞米松的纳米纤维支架显示出良好的细胞黏附、伸展能力.加载双重诱导因子的Zein-DEX/PLLA-BMP-2纳米纤维支架上骨髓间充质干细胞表现出更高的碱性磷酸酶活性和细胞外基质(ECM)矿物沉积,优于对照组.结论:以天然生物材料玉米醇溶蛋白和生物高分子材料左旋聚乳酸为原料制备了加载生物活性因子骨形态发生蛋白-2和地塞米松的壳-核结构的新型同轴静电纺丝纳米纤维支架,形成类似细胞外基质样结构,刺激骨髓间充质干细胞早期黏附、增殖、诱导成骨分化,适合骨组织工程的应用.

目的:观察针刺养老穴结合运动治疗急性外踝关节扭伤的临床疗效.方法:将60例急性外踝关节扭伤患者,用随机数字表法分为两组,各30例.对照组使用传统针刺方法结合运动治疗;观察组使用针刺养老穴结合运动治疗,观察两组的疗效,并比较治疗前后的疼痛评分(VAS)及有效率.结果:治疗后,两组VAS评分均降低,其中观察组VAS评分低于对照组,差异有统计学意义(P＜0.05).对照组有效率为93.34％,观察组有效率为96.67％,差异有统计学意义(P＜0.05).结论:针刺养老穴结合运动可以有效缓解急性外踝关节扭伤患者临床症状,疗效较优.

糖尿病骨质疏松症是全身代谢性疾病,在中医学范围内,将其归为"消渴"继发"骨痿"进行讨论,"消渴"患者患病日久,后期继发骨痿,涉及多脏腑,病久气阴亏虚,肾气虚衰,从而肝血化生不足,脾胃无法运化,进而筋骨无以所养,导致骨枯髓减.临床现阶段主要以对症治疗、病因论治、脏腑论治、分期辨证等进行治疗.