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1.
Abstract

Context: Osteoarthritis (OA) is a degenerative joint disease with damage to the articular cartilage. Active production of inflammatory cytokine/chemokine and matrix metalloproteinases may be found during the progression of OA. Isorhamnetin had the effects of anti-inflammatory, antioxidant, anti-ischemia, anti-atherosclerotic hepatoprotective and anticancer activities.

Objective: Our study was focused on the effects of isorhamnetin treatment in OA.

Materials and methods: We used monosodium iodoacetate (MIA)-induced OA rats to evaluate the effects of isorhamnetin related anti-inflammatory process. The rats in all groups were sacrificed on four weeks post-MIA injection. The measurements of knee joint swelling, histological analysis, serum inflammatory biomarkers and western blot were evaluated.

Results: We found that isorhamnetin may reduce MIA-induced knee swelling by significantly reduction of articular cartilage damage.in rats. Suppression of pro-inflammatory cytokines production was found after isohamnetin treatment. Isorhamnetin inhibited the production of NO and PGE2, and the expression of iNOS and COX-2. The production of COMP, CTX-II and osteopontin (OPN) were also inhibited in MIA-induced OA rats.

Discussion and conclusions: Isorhamnetin may modulate the inflammatory progression of OA in MIA-induced OA rats. The prevention of cartilage damage was found in OA after adequate isorhamnetin treatment. Isorhamnetin may serve as a potential agent for the management of OA.  相似文献   

2.
Osteoarthritis (OA) is one of the most common musculoskeletal disorders and is characterized by degeneration of articular cartilage. Sulfation of extracellular ma-trix proteins in articular cartilage is an important step in maintaining normal cartilage metabolism. Two sulfation-related genes have been reported as the causal genes of severe chondrodysplasias: mutations in PAPSS2 (3′-phosphoadenosine 5′-phosphosulfate synthase 2) cause spondylo-epimetaphyseal dysplasia (SEMD), and mutations in SLC26A2 (solute carrier family 26, member 2) cause diastrophic dysplasia. Given their critical roles in cartilage metabolism and the severe phenotypes that result from mutations in these genes, we examined PAPSS2 and SLC26A2 as candidate susceptibility loci for OA. We identified sequence polymorphisms in the coding and core promoter regions of these genes and analyzed their potential association with knee OA within the Japanese population. Ten sequence polymorphisms were detected in PAPSS2 and five in SLC26A2. An association analysis showed suggestive association of one minor polymorphism in the promoter region of SLC26A2. This 4-bp adenine deletion allele, del4A, was over-represented in knee OA (P = 0.043, odds ratio = 3.43) and is thought to confer a minor susceptibility to knee OA within the Japanese population. Haplotype analysis showed no evidence of association with the two genes, however, excluding them as major susceptibility loci for knee OA. Received: May 7, 2001 / Accepted: June 21, 2001  相似文献   

3.
BackgroundOsteoarthritis (OA) is a joint disease of multifactorial etiology, affecting mainly the knees. We aimed to evaluate the effects of two different doses of gaseous ozone intra-articularly on the knee cartilage morphology of rats with osteoarthritis (OA).MethodsThe articular lesion was induced by sodium monoiodoacetate (MIA). 40 Wistar rats were divided into 4 groups: G1 control (without lesion and without treatment), G2 articular lesion (AL) (only lesion MIA-induced), G3 AL + treatment with 5 μg/mL of ozone intra-articular, and G4 AL + treatment with 10 μg/mL of ozone intra-articular. The experiment was carried out for 60 days.ResultsBoth doses of ozone intra-articular demonstrated less reduction in joint space (G3 and G4) compared to the G2, formation of osteophytes, but without subchondral sclerosis. Ozone decreased the volumetric density of the articular lesion (VV(AL)) of tibial. The treatments recovered VV(AL) of the femur similar to G1. Ozone lower dose (G3) showed lower tibia and femur macroscopic scores.ConclusionIntra-articular gaseous ozone can delay the degeneration of articular cartilage and can represents an integrative therapy in the OA treatment of knee after 60 days of treatment. For the first time the role of ozone in articular cartilage degeneration was evaluated helping to understand this therapy.  相似文献   

4.
目的 制备一种仿生正常关节滑液流变学特征的组织黏附性可注射水凝胶,并研究该水凝胶抑制膝关节创伤后软骨退变的效果及其可能的机制。方法 以聚乙烯醇溶液(PVA)、淀粉和氯化钠为主要原料制备可注射、组织黏附性水凝胶(PWN)。通过流变学测试、注射器推出实验、体外降解实验、CCK-8实验、活/死细胞染色、细菌黏附实验、组织黏附实验分别对其流变学性能、可注射性、降解性能、细胞相容性、抗细菌黏附性能和组织黏附性能进行表征。构建大鼠膝关节力学失稳模型,并分为正常组、PWN组、透明质酸组(HA组)与未治疗组,其中PWN组、HA组术后1周时注射PWN与HA进行治疗。治疗4周后取大鼠膝关节标本进行Micro-CT分析和组织学染色分析,对比评估PWN对关节软骨退变的抑制作用。结果 PWN具有良好的细胞相容性和可注射性。此外,相比于HA,PWN的流变学特征更接近正常关节滑液,并且PWN具有缓慢降解的特性、更高的组织黏附性能和抗细菌黏附的能力。动物实验Micro-CT分析结果显示,PWN组软骨下骨的骨密度和骨体积/组织体积均显著高于未治疗组和HA组(P<0.05)。同时,番红快绿染色结果显示,相比于HA组,PWN组软骨表面连续性较好,未见明显破损、侵蚀,蛋白聚糖分布丰度接近正常组。结论 相比于临床使用的HA产品,PWN水凝胶具有仿生正常关节滑液的流变学特征、缓慢降解的特性和较强的组织黏附性能,可延缓大鼠膝关节力学失稳下关节骨软骨的退变,有望单独或与HA联合应用于骨关节炎等关节软骨病变的临床治疗。  相似文献   

5.
The aim of the present study was to evaluate in vivo modulatory effect of S-methylisothiourea (SMT), a preferential inhibitor of inducible nitric oxide synthase (iNOS) on pain and pathology in the surgical model of osteoarthritis (OA) in rats. The OA was produced by the anterior cruciate ligament transection (ACLT) and medial meniscectomy (MMx) of right knee. SMT was administered 1 day prior to the production of OA and continued up to day 42 postoperation. Mechanical hyperalgesia, thermal hyperalgesia, tail flick latency after repeated flexion and extension of OA knee and knee diameter of right knee were determined at weekly intervals. Serum levels of IL-1β, TNF-α and nitrite concentration were determined at the end of the experiment. Glycosaminoglycan (GAG) content, collagen content and histopathological evaluation of articular cartilage were also determined at the end of the experiment. SMT reduced mechanical hyperalgesia and the serum levels of IL-1β, TNF-α and nitrite. Further, SMT reduced the loss of GAG from articular cartilage. Microscopically, SMT reduced the severity of the cartilage lesion. The results indicate the effectiveness of SMT in attenuating the pain and pathology of experimental OA phase by reducing the production of nitric oxide and interleukin-1β and tumor necrosis factor-α, which are known to play a major role in the pathophysiology of OA.  相似文献   

6.
《Acta histochemica》2022,124(7):151933
BackgroundGreater bone resorption increases TGF-β1 release and nestin-positive BMSC recruitment to the subchondral bone marrow, leading to excessive subchondral osteophyte formation and severe wear to articular cartilage. Our previous research demonstrated that BMSCs-ExoTGF-β1 attenuated cartilage damage in osteoarthritis (OA) rats through carrying highly expressed miR-135b.MethodsThe bone marrow mesenchymal stem cells (BMSCs) were isolated from mouse bone marrow, and BMSC-derived exosomes (BMSCs-Exo) were isolated from BMSCs. OA mouse models were established by anterior cruciate ligament transection (ACLT) surgery on the left knee of mice. Then we explored the therapeutic effect of BMSCs-ExoTGF-β1 on ACLT mice.ResultsBMSCs-ExoTGF-β1 attenuated cartilage damage in OA mice in vivo by ameliorating articular cartilage degeneration and suppressing calcification of the cartilage zone. BMSCs-ExoTGF-β1 also inhibited osteoclastogenesis by suppressing the MAPK pathway in vitro. Micro-computed tomography indicated that BMSCs-ExoTGF-β1 impeded uncoupled subchondral bone remodeling. BMSCs-ExoTGF-β1 also reduced CD31hiEmcnhi vessel activity in the subchondral bone and attenuated OA pain behaviors.ConclusionsIn conclusion, BMSCs-ExoTGF-β1 maintains the microarchitecture, inhibits abnormal angiogenesis in subchondral bone and exerts protective effect against OA-induced pain and bone resorption on ACLT mice.Data availabilityThe datasets are available from the corresponding author on reasonable request.  相似文献   

7.
Studies have determined the effects of joint immobilization on the articular cartilage of sedentary animals, but we are not aware of any studies reporting the effects of joint immobilization in previously trained animals. The objective of the present study was to determine whether exercise could prevent degeneration of the articular cartilage that accompanies joint immobilization. We used light microscopy to study the thickness, cell density, nuclear size, and collagen density of articular cartilage of the femoral condyle of Wistar rats subjected to aerobic physical activity on an adapted treadmill five times per week. Four groups of Wistar rats were used: a control group (C), an immobilized group (I), an exercised group (E), and an exercised and then immobilized group (EI). The right knee joints from rats in groups I and EI were immobilized at 90 °C of flexion using a plastic cast for 8 weeks. Cartilage thickness decreased significantly in group I (mean, 120.14 ± 15.6 μm, < 0.05), but not in group EI (mean, 174 ± 2.25), and increased significantly in group E (mean, 289.49 ± 9.15) compared with group C (mean, 239.20 ± 6.25). The same results were obtained for cell density, nuclear size, and collagen density (in all cases, < 0.05). We concluded that exercise can prevent degenerative changes in femoral articular cartilage caused by immobilization of the knee joint.  相似文献   

8.
We tested the hypothesis that swim exercise can protect the articular cartilage from damages induced secondary to insulin-dependent diabetes mellitus in rats using the scanning electron microscopy and to monitor the blood levels of oxidative and antioxidative stress biomarkers that are known to be modulated in osteoarthritis (OA). A profound damage to the cartilage was observed in the diabetic rats. Our findings also show that swim exercise protects the knee joints from damage induced by diabetes as well as significantly inhibiting OA-induced upregulation of thiobarbituric acid reactive substances (TBARS) and tumor necrosis factor alpha (TNF-α) and augmented superoxide dismutase (SOD) inhibition by OA. Thus, we demonstrated an effective protection by swim exercise against diabetes-induced OA in a rat model of the disease.  相似文献   

9.
《The Knee》2020,27(6):1848-1856
BackgroundPhysical inactivity is a global problem and patients with knee osteoarthritis (OA) are predisposed to inactivity and its health-related consequences. Current guidelines recommend exercise as primary treatment but whether this affects time spent physically inactive is unknown. The objective was to investigate changes in physical inactivity among individuals with knee OA following an educational and exercise program.MethodsPragmatic prospective cohort study performed in six physical therapy clinics in Denmark offering a nationwide education and exercise program for knee OA. The program consists of physiotherapy guided education and group-based or home exercise sessions, performed biweekly for approximately eight weeks. The exercises target knee and hip joint stability as well as focus on increasing muscle strength. Primary outcome was time spent physically inactive (min/day), measured with a tri-axial accelerometer mounted on the lateral side of the thigh during the entire exercise program duration. OA symptoms were assessed using the Knee injury and Osteoarthritis Outcome Score (KOOS).ResultsThirty-two individuals with knee OA were analyzed. From baseline to post-intervention, no changes occurred in average time spent physically inactive (mean change: + 16.2 min [95% CI − 15.7 to 48.1]; P = 0.31), but statistically significant improvements in KOOS pain (+ 6.7 points [95% CI 2.3 to 11.0]; P = 0.0032) and KOOS function (+ 5.8 points [95% CI 1.9 to 9.7]; P = 0.0046) were found.ConclusionsParticipating and completing a widely adopted education and exercise program are not associated with spontaneous improvements in physical inactivity despite changes in self-reported pain and function. Interventions specifically targeting physical inactivity are needed.Registration number: www.clinicaltrials.gov: NCT03125954.  相似文献   

10.
Abstract

Background: Osteoarthritis (OA) is a chronic joint-degeneration disease and accounts for the most frequent arthritis in aging people. OA is characterized by the degeneration of articular cartilage, subchondral bone sclerosis and synovitis. Inflammation as an important role in OA progression, in that anti-inflammatory agents could effectively inhibit the development of OA with minimal side effects, therefore developing a nature anti-inflammatory compound will be a promising therapy for treating OA.

Methods: We treated patient-derived chondrocytes and mouse models of OA with astragaloside, an effective component of astragalus membranaceus, and measured its effect on pro-inflammatory cytokines and OA progression in mice.

Results: In vitro, astragaloside induced a dose-dependent inhibition of IL-1β-induced the production of inflammatory factors, including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), nitric oxide (NO), prostaglandin E2 (PGE2), expression of MMP 13 and ADAMTS-5, and the activation of NF-κB signaling. In vivo, astragaloside ameliorate the degeneration of cartilage in mouse model of OA.

Conclusion: Astragaloside potentially serve as a promising and effective therapeutic agent for treating OA patients.  相似文献   

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