Sequential surgery for the treatment of type I knee ankylosis: a series of 62 cases.

BACKGROUNDS: The lack of systematic classification and standard treatment principles for knee ankylosis prevents optimal treatments. This study explored treatments for type I (mild) knee joint ankylosis. METHOD: This retrospective study analysed patients with knee joint ankylosis admitted from March 2013 to January 2018 who underwent sequential arthroscopic release. RESULT: The 62 patients had 12-36 (average, 18) months of follow-up. Thirty-eight patients were released; of these, 18 were assisted by limited incision with partial quadriceps femoris expansion myotomy and released according to arthroscopy. Six patients underwent lengthening and release of the quadriceps femoris. All surgeries combined with full-course rehabilitation resulted in improved joint mobility. The range of motion (ROM) of the knee joint recovered to a range of 0° to 85°-140° (mean: 118.32 ± 9.42°) from the preoperative range of 30°-70° (mean: 45° ± 15.50°). The clinical effect was evaluated according to the Judet criteria at the final follow-up. The outcomes at the last follow-up (at least for 1 year) were excellent in 55 cases, good in six cases, and fair in one case. CONCLUSION: Sequential arthroscopic release, minimal selective invasion of limited incision of partial quadriceps femoris expansion myotomy, assisted by pie-crusting technique to release, or quadriceps femoris lengthening, and release surgery for type I knee joint ankylosis, accompanied by early rehabilitation training provided satisfactory results without significant complications.

Dose-Response Relationships of Resistance Training in Adults With Knee Osteoarthritis: A Systematic Review and Meta-analysis.

BACKGROUND AND PURPOSE: To determine the effects of resistance training (RT) on symptoms, function, and lower limb muscle strength in patients with knee osteoarthritis (KOA), and to determine the optimal dose-response relationships. DATA SOURCES: We searched the PubMed, MEDLINE, Embase, Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science, and ClinicalTrials.gov databases from inception to January 23, 2022. ELIGIBILITY CRITERIA: Randomized controlled trials that examined the effects of RT in KOA patients (mean age ≥50 years) were included. DATA SYNTHESIS: We applied Hedges' g of the random-effects model to calculate the between-subject standardized mean difference (SMDbs). A random-effects metaregression was calculated to explain the influence of key training variables on the effectiveness of RT. We used the Grading of Recommendations Assessments, Development and Evaluation (GRADE) method to appraise the certainty of evidence. RESULTS: A total of 46 studies with 4289 participants were included. The analysis revealed moderate effects of RT on symptoms and function (SMDbs =-0.52; 95% CI: -0.64 to -0.40), and lower limb muscle strength (SMDbs = 0.53; 95% CI: 0.42 to 0.64) in the intervention group compared with the control group. The results of the metaregression revealed that only the variable "training period" (P< .001) had significant effects on symptoms, function, and lower limb muscle strength, and the 4 to 8 weeks of training subgroup showed greater effects than other subgroups (SMDbs =-0.70, -0.91 to -0.48; SMDbs = 0.76, 0.56 to 0.96). CONCLUSIONS: Compared with inactive treatments, RT is strongly recommended to improve symptoms, function, and muscle strength in individuals with KOA. Dose-response relationship analysis showed that 4 to 8 weeks of RT had more benefits.

Irreversible Electroporation Improves Tendon Healing in a Rat Model of Collagenase-Induced Achilles Tendinopathy.

BACKGROUND: Treatment of painful chronic tendinopathy is challenging, and there is an urgent need to develop new regenerative methods. Irreversible electroporation (IRE) can lead to localized cell ablation by electrical pulses and induce new cell and tissue growth. Previously, the authors' group reported that electroporation-ablated tendons fully regenerated. PURPOSE: To assess the efficiency of IRE in improving tendon healing using a collagenase-induced Achilles tendinopathy rat model. STUDY DESIGN: Controlled laboratory study. METHODS: After screening for the IRE ablation parameters, a collagenase-induced Achilles tendinopathy rat model was used to assess the efficacy of IRE in improving tendon healing via biomechanical, behavioral, histological, and immunofluorescence assessments. RESULTS: The experiments showed that the parameter of 875 V/cm 180 pulses could ablate most tenocytes, and apoptosis was the main type of death in vitro. In vivo, IRE promoted the healing process of chronic tendinopathy in the Achilles tendon of rats, based on biomechanical, behavioral, and histological assessments. Finally, immunofluorescence results revealed that IRE improved blood supply in the early stages of tendon repair and could potentially reduce neuropathic pain. CONCLUSION: IRE enhanced tendon tissue healing in a rat model of collagenase-induced Achilles tendinopathy. CLINICAL RELEVANCE: IRE may as a potential alternative treatment for tendinopathy in clinical usage.

Long noncoding RNA NAV2-AS5 relieves chondrocyte inflammation by targeting miR-8082/TNIP2 in osteoarthritis.

Osteoarthritis (OA) is a common chronic and frequently occurring orthopedic disease in the middle-aged and elderly individuals. Numerous studies have shown that long noncoding RNAs (lncRNAs) play major roles in various diseases. However, the potential molecular mechanism of action of NAV2-AS5 in OA remains unclear. The present study was designed to explore the influence of NAV2-AS5 on the progression of chondrocyte inflammation and its underlying molecular mechanisms. To simulate the inflammatory environment in OA, the human chondrocyte cell line was treated with LPS. Cell proliferation, cell cycle progression, and apoptosis were assessed using Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine analysis, and flow cytometry. Proliferation- and cycle-related proteins and the release of inflammatory factors were examined by western blot analysis and enzyme-linked immunosorbent assay. The downstream targets of NAV2-AS5 were determined using bioinformatics and confirmed by a luciferase reporter assay. In our study, patients with OA showed downregulation of NAV2-AS5, upregulation of miR-8082, and downregulation of TNFAIP3 interacting protein 2 (TNIP2). Moreover, we found that both overexpression of NAV2-AS5 and miR-8082 inhibitor promoted cell proliferation, inhibited apoptosis, and released inflammatory cytokines in LPS-treated chondrocytes. MiR-8082 was predicted to be a target of both NAV2-AS5 and TNIP2. In addition, rescue experiments showed that silencing of TNIP2 reversed the effects of the miR-8082 inhibitor on proliferation, cell cycle, apoptosis, and inflammatory factors in sh-NAV2-AS5-treated chondrocytes. In conclusion, these findings indicate that NAV2-AS5 relieves chondrocyte inflammation by targeting miR-8082/TNIP2 in OA, which provides a new theoretical basis for OA therapy.

Pan-Cancer Transcriptome and Immune Infiltration Analyses Reveal the Oncogenic Role of Far Upstream Element-Binding Protein 1 (FUBP1).

Despite increasing evidence to support the relationship between FUBP1 and tumorigenesis in some types of cancers, there have been no analyses from a pan-cancer perspective. Here, we are the first to investigate the putative oncogenic role of FUBP1 in 33 cancer types based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Dysregulated FUBP1 expression was observed in most cancer types, and high FUBP1 expression suggests poor prognosis in cancers such as ACC, KICH, LIHC, LUAD, LUSC, SARC, CESC, and SKCM. Missense mutation is the most common type of FUBP1 mutation, and R430 in KH_4 is a predominant mutation site. Enhanced phosphorylation of FUBP1 at the S120 site has been observed in clear cell RCC, lung adenocarcinoma, and pediatric brain cancer specimens from African-American and Asian individuals. The expression of FUBP1 was found to be negatively correlated with the infiltration of CD8+ T lymphocytes in GBM, HNSC-HPV- and UCEC but positively correlated with that of tumor-associated fibroblasts in CESC, ESCA, HNSC, LIHC, LUAD, PAAD, and THYM. Furthermore, RNA splicing and spliceosome signaling were predominantly enriched in both GO and KEGG analyses of the functional mechanism of FUBP1. Briefly, this pan-cancer analysis comprehensively revealed the multifaceted characteristics and oncogenic role of FUBP1 in different human cancers.

Healthcare and Scientific Treatment of Knee Osteoarthritis.

Knee osteoarthritis is a chronic degenerative disease companied with chronic knee pain and dysfunction. However, the etiology and pathogenesis of knee osteoarthritis were unclear. Currently, age, diet, trauma, obesity, and inheritance are the main risk factors. The major pathological hallmarks of knee osteoarthritis included subchondral bone sclerosis, articular cartilage degeneration, arthrosynovitis, and osteophyte. With the acceleration of the aging process in China, the treatment of knee arthritis and the methods to improve the quality of life have become the focus of medical staff. Currently, therapies in clinical practice include surgery and nonoperative treatment; however, the clinical effects of different individuals at different stages will still be very different. This article reviews the recent advances in the treatment of knee osteoarthritis from three aspects: nonsurgical treatment, surgical treatment, and modern new medical means.

An experimental study on stress-shielding effects of locked compression plates in fixing intact dog femur.

BACKGROUND: In orthopedic application, stress-shielding effects of implant materials cause bone loss, which often induces porosis, delayed bone healing, and other complications. We aimed to compare the stress-shielding effects of locked compression plate (LCP) and limited-contact dynamic compression plate (LC-DCP) in dogs with plate-fixed femurs. METHODS: Bilateral intact femurs of 24 adult dogs were fixed by adult forearm 9-hole titanium plates using minimally invasive plate osteosynthesis (MIPPO) technology, with LCP on the left and LC-DCP on the right femurs. Dogs were sacrificed at 6 weeks, 12 weeks, and 24 weeks after surgery, and bone specimens were used to evaluate the efficacies of different fixing methods on bones through X-ray, dual-energy X-ray absorptiometry (DEXA), histology, MicroCT, and biomechanics analyses. RESULTS: X-ray results showed significant callus formation and periosteal reaction in the LC-DCP group. Bone cell morphology, degree of osteoporosis, and bone mineral density (BMD) changes of the LCP group were significantly better than that of the LC-DCP group. MicroCT results showed that the LCP group had significantly reduced degree of cortical bone osteoporosis than the LC-DCP group. Tissue mineral density (TMD) in the LCP group was higher than that in the LC-DCP group at different time points (6 weeks, 12 weeks, and 24 weeks). Biomechanics analyses demonstrated that the compressive strength and flexural strength of bones fixed by LCP were better than that by LC-DCP. CONCLUSIONS: Stress-shielding effects of LCP are significantly weaker than that of LC-DCP, which is beneficial to new bone formation and fracture healing, and LCP can be widely used in clinic for fracture fixation.

microRNA-mediated GAS1 downregulation promotes the proliferation of synovial fibroblasts by PI3K-Akt signaling in osteoarthritis.

Hyperplastic synovial fibroblasts (SFs) serve a critical role in the pathogenesis of knee osteoarthritis (OA); however, the molecular mechanism involved in OA during synovial tissue hyperproliferation remains unclear. Growth arrest-specific gene 1 (GAS1), a cell growth repressor gene, was found to be downregulated in OASFs according to previous preliminary experiments. It was therefore hypothesized that reduced GAS1 expression may participate in the hyperproliferation of SFs in OA development, downstream of possible microRNA (miR) regulation, in hyperplastic OASFs. In the present study, GAS1 expression was indeed decreased in OASFs and interleukin-1ß-induced SFs by reverse transcription-quantitative PCR and western blot analysis. Further cell viability assays, cell cycle and apoptosis analyses revealed that the overexpression of GAS1 can inhibited proliferation, induced cell cycle arrest and promoted apoptosis in SFs. In contrast, GAS1 knockdown in SFs accelerated cell proliferation, enhanced cell cycle progression and suppressed apoptosis. Notably, the suppressive effects of GAS1 were mediated through the inactivation of the PI3K-Akt pathway. Finally, miR-34a-5p and miR-181a-5p were predicted and subsequently verified to directly target the 3'-untranslated region of the GAS1 gene, downregulating GAS1 levels in OASFs and IL-1ß-induced SFs. In conclusion, the present study demonstrated that downregulation of GAS1 can lead to the hyperproliferation of SFs in OA pathogenesis through the PI3K-Akt pathway, and miR-34a-5p and miR-181a-5p are potential regulators of GAS1 expression in OA. Therefore, it may be promising to investigate the potential of GAS1 as a novel therapeutic target for preventing SF hyperplasia in OA.

Microwave Ablation of Primary Malignant Pelvic Bone Tumors.

Background: En bloc tumor resection followed by reconstruction is a widely used surgical treatment for malignant pelvic bone tumors. High rates of complications and mechanical instability often contribute to poor postoperative results. We attempted en bloc microwave ablation (MWA) in situ to improve the outcome. Methods: From May 1995 to December 2015, 104 patients with primary pelvic malignancy received radical MWA in our department. After careful dissection of the tumor-bearing bone from surrounding normal tissues with safe margins, a microwave antenna array was inserted into the tumor mass to emit electromagnetic energy, inducing tumor cellular death via thermocoagulation. The loose, devitalized tumor tissues were removed by cutting or curettage, leaving a defective bone scaffold. Re-strengthening by autograft or allograft was needed in most patients. Results: The over 3 years survival rate was 51.5% for high-grade malignancies (among them, 26.9% were osteosarcoma) and 94.8% for low-grade malignancies (chondrosarcoma). In most of the living patients, cosmetic and useful limbs were preserved. The mean functional score (Musculoskeletal Tumor Society) was 27 or 90% (range: 25-30, 75-100%). Among the 56 patients who belonged to the excellent function group, 11 were followed up for more than 10 years. The local recurrence rate was 8.6%. Among the 9 patients with recurrence, 5 died from disease, 2 were treated by hemipelvic amputation, and 2 underwent revision surgery with MWA and gained local control. The deep infection rate was 5.6%. All six patients with infection were healed by irrigation, debridement, and systemic antibiotic administration. Conclusion: Local, microwave-induced hyperthermia for treating malignant pelvic bone tumors is an effective alternative method. The oncological and functional results are encouraging. The use of MWA should be continued to evaluate and improve this new therapeutic system.

A20 inhibits the release of inflammatory cytokines by suppressing the activation of the nuclear factor-kappa B pathway in osteoarthritic fibroblast-like synoviocytes.

A growing number of studies suggest that synovitis plays an important role in the pathogenesis and progression of osteoarthritis (OA). As a negative mediator of the nuclear factor-kappa B (NF-κB) signaling pathway, the zinc finger protein A20 has significant anti-inflammatory properties. In this study, the differential expression of A20 was investigated at the mRNA and protein levels in human normal OA fibroblast-like synoviocytes (FLSs) and normal FLSs pretreated with TNF-α. We then measured the activation of the NF-κB pathway and expression of pro-inflammatory cytokines in the above three groups by western blotting, a human cytokine array and ELISA. We found that TNF-α activated the NF-κB pathway, increased the expression of the pro-inflammatory cytokines IL-6 and IL-8, and A20 expression in human normal FLSs. However, the role of A20 in FLSs was unclear. To clarify this, we investigated the effect of A20 overexpression in human normal FLSs. The results indicate that A20 inhibits the NF-κB signaling pathway activation and OA-associated pro-inflammatory cytokines release. The results of this study indicate that A20 has anti-inflammatory effects in FLSs, which makes it a potential target for OA synovitis treatment.

The effect of temperature-control microwave on HELA and MG-63 cells.

CONTEXT: Hyperthermia has now been used to treat many kinds of solid malignancies. However, the applied thermal parameters about heat temperature and time varied all over the world, and no consensus about the optimal formula had been reached. Microwave ablation, as one of thermal ablation methods, is usually applied based on the fixed parameters of power and duration. As a result, too high temperature or overheating might not be avoided and excessive heating might cause some additional side effects to normal tissues. AIMS: To explore the optimal parameters of power and duration for the HELA and MG-63 cells in vitro. SETTINGS AND DESIGN: With a temperature-controlled microwave workstation, a microwave thermal ablation experiment was performed in vitro. SUBJECTS AND METHODS: The HELA and MG-63 cells were heated with 40°C, 45°C, 50°C, 55°C, and 60°C lasting for 5-30 min, respectively. Then, the cell viability was detected using four methods: Flow cytometer assay, nicotinamide adenine dinucleotide-diaphorase staining, Calcein-acetoxymethyl ester staining immediately after treatment, and CCK-8 assay 24 h later. RESULTS: The temperature-controlled microwave has an excellent ablation effect on both cell lines. Furthermore, when the thermal stimulation reached 55°C 25 min and 55°C 20 min for the HELA and MG-63 cells, respectively, or 60°C 5 min for both, all the viability indexes indicated immediately devitalization. CONCLUSION: It presented a preliminary minimum lethal dose of heat was validated on the cellular level in vitro, which should be verified and corrected further in vivo.

Modulation of TGF­ß activity by latent TGF­ß­binding protein 1 in human osteoarthritis fibroblast­like synoviocytes.

Osteoarthritis (OA) is a common degenerative joint disease; however, its underlying pathogenesis remains to be elucidated. Previous studies have demonstrated that the transforming growth factor­ß (TGF­ß) signaling pathway has a role in the initiation and development of OA. Additionally, latent TGF­ß­binding protein­1 (LTBP­1) modulates the activity of the TGF­ß­mothers against decapentaplegic (Smad) signaling pathway in numerous diseases, including malignant glioma. The present study demonstrated that expression of LTBP­1 is increased in OA synovial tissues compared with normal synovial tissues. The effect of TGF­ß was identified to be mediated by phosphorylated(p)­(Smad)2/3, which may activate activin­like kinase (ALK)5 receptor, and by p­Smad1/5/8, which may induce ALK1, thereby stimulating expression of matrix metalloproteinase­(MMP)­13 in OA fibroblast­like synoviocytes (FLS). Compared with normal FLS, OA FLS demonstrated an increased p­Smad1/5/8:p­Smad2 ratio, which led to elevated MMP­13 expression and aggravation of OA. Furthermore, knockdown of the LTBP­1 gene by siRNA transfection in OA FLS reduced p­Smad1/5/8 expression without affecting TGF­ß mRNA levels, although p­Smad2 expression increased. It was also demonstrated that OA FLS exhibited increased proliferation compared with normal FLS in vitro. Furthermore, siRNA­mediated downregulation of LTBP­1 reduced proliferation of OA FLS. In conclusion, the present study demonstrated that an alteration in the p­Smad1/5/8:p­Smad2 ratio as well as association between p­Smad1/5/8 and MMP­13 expression in human OA FLS, may contribute to the development of OA. The results of the present study suggested that LTBP­1 is a modulator of the TGF­ß signaling pathway in human OA FLS, which may aid in elucidating the mechanism underlying the pathology of OA.

Dual specificity phosphatase 1 has a protective role in osteoarthritis fibroblast­like synoviocytes via inhibition of the MAPK signaling pathway.

Increasing evidence indicates the important role of inflammation in the pathogenesis and progression of osteoarthritis (OA). Dual specificity phosphatase 1 (DUSP1), a negative regulator of the mitogen­activated protein kinase (MAPK) signaling pathway, has anti­inflammatory properties. In the present study, the expression of DUSP1 was investigated in human OA fibroblast­like synoviocytes (FLSs), human normal FLSs and OA FLSs pretreated with dexamethasone at the mRNA and protein levels. Then, the activation of MAPK pathway proteins and the expression of matrix metalloproteinase­13 (MMP­13) and cyclooxygenase­2 (COX­2) were measured by western blot analysis in the three groups of cells. Dexamethasone induced the expression of DUSP1 and inhibited the activation of the MAPK pathway and reduced the expression of MMP­13 and COX­2 in OA FLSs. However, the role of DUSP1 remained unclear. To clarify this, the effects of overexpression of DUSP1 in OA FLSs were determined using a DUSP1­overexpressing lentivirus. The results demonstrated that overexpression of DUSP1 in OA FLSs inhibited the activation of the MAPK pathway and expression of OA­associated mediators. The findings of the present study indicate that DUSP1 has a protective role in OA FLSs and may be a potential target in the treatment of OA.

Closed reduction and percutaneous annulated screw fixation in the treatment of comminuted proximal humeral fractures.

BACKGROUND: Displaced proximal humeral fractures remain a challenge to orthopedic surgeons. OBJECTIVES: The purpose of this study was to evaluate the functional and radiological outcomes of patients with comminuted proximal humeral fractures treated with closed reduction and percutaneous screw fixation (CRPF). MATERIAL AND METHODS: The authors retrospectively reviewed 38 cases of displaced proximal humeral fractures (2-, 3- or 4-part fractures according to the Neer classification) that were treated using the CRPF technique from May 2009 to April 2013. From this group 26 patients were followed up for a period ranging from 9 to 24 months (averaging 12.9 months) and evaluated for the functional and radiological outcomes by a series of standard questionnaires and measurements. RESULTS: The fractures in all 26 patients were healed within an average time of 14.6 weeks (ranging from 11 to 27 weeks), and the mean interval between the operation and fully functional activity was 18.6 weeks (ranging from 15 to 32 weeks). At the final follow-up visit, no patient showed shoulder instability; the mean range of abduction motion was 146.5° (ranging from 72° to 180°). For all patients, no statistically significant difference in the functional outcomes was observed between their 6-month and final follow-up visits; or in the radiological findings between their immediate post-operative and final follow-up examinations. CONCLUSIONS: The CRPF technique is a safe and effective therapeutic option for comminuted proximal humeral fractures. Good stability is obtained and aggressive impairment of the soft tissue and periosteum around the fracture is avoided, which allows for an early painless range of motion. The technique promotes bone healing, prevents ischemic osteonecrosis of the head of the humerus and leads to few complications.

Ginsenoside Rh2 enhances the antitumor immunological response of a melanoma mice model.

The treatment of malignant tumors following surgery is important in preventing relapse. Among all the post-surgery treatments, immunomodulators have demonstrated satisfactory effects on preventing recurrence according to recent studies. Ginsenoside is a compound isolated from panax ginseng, which is a famous traditional Chinese medicine. Ginsenoside aids in killing tumor cells through numerous processes, including the antitumor processes of ginsenoside Rh2 and Rg1, and also affects the inflammatory processes of the immune system. However, the role that ginsenoside serves in antitumor immunological activity remains to be elucidated. Therefore, the present study aimed to analyze the effect of ginsenoside Rh2 on the antitumor immunological response. With a melanoma mice model, ginsenoside Rh2 was demonstrated to inhibit tumor growth and improved the survival time of the mice. Ginsenoside Rh2 enhanced T-lymphocyte infiltration in the tumor and triggered cytotoxicity in spleen lymphocytes. In addition, the immunological response triggered by ginsenoside Rh2 could be transferred to other mice. In conclusion, the present study provides evidence that ginsenoside Rh2 treatment enhanced the antitumor immunological response, which may be a potential therapy for melanoma.

[CCR7 silence by siRNA inhibits proliferation, invasion and promotes apoptosis of human MG63 osteosarcoma cells].

Objective To investigate the effect of siRNA-mediated chemokine receptor 7 (CCR7) silence on the proliferation, migration, invasion and apoptosis of human MG-63 osteosarcoma cells. Methods The study designed and synthesized siRNA targeting CCR7 (CCR7-siRNA). After MG63 cells were transfected with CCR7-siRNA, the expression of CCR7 was identified by Western blotting; cell apoptosis was detected by annexinV-FITC/PI double staining combined with flow cemetery; cell proliferation was tested by MTT assay; and cell migration and invasion abilities were examined by TranswellTM migration/invasion assays. Results CCR7 expression in MG63 cells was significantly inhibited after transfected with CCR7-siRNA. At the same time, cell proliferation, migration and invasion abilities were distinctly suppressed, and cell apoptosis rate increased. Conclusion Down-regulating CCR7 expression in MG63 cells could apparently inhibit cell proliferation, migration and invasion abilities of MG63 cells, and also induce cell apoptosis.

[Estrogen exerts anti-inflammatory effects by inhibiting NF-κB pathway through binding with estrogen receptor ß on synovicytes of osteoarthritis].

Objective To investigate the mechanism of estrogen's anti-inflammatory effects on synovial cells during the pathogenic process of osteoarthritis. Methods We isolated synovicytes from synovium tissues and identified the cells with flow cytometry. Then we detected the expression level of estrogen receptor ß (ERß) in synovicytes with immunofluorescence staining. The synovicytes were divided into control group, group pretreated with 10 ng/mL IL-1ß, group pretreated with 10 ng/mL IL-1ß and 10-7 mol/L estrogen, group pretreated with 10 ng/mL IL-1ß, 10-7 mol/L estrogen and specific antagonist of ERß, 10-5 mol/L tetrahydrocannabinol (THC). Thirty-six hours later, we observed the mRNA and protein levels of IκBα, phospho-IκBα (p-IκBα) and IL-6. Results Immunofluorescence staining showed the high expression level of ERß in synovicytes. In IL-1ß treated cells, IL-6 mRNA and protein level, IκBα mRNA and p-IκBα protein levels were elevated compared with the control group, while IκBα protein level declined. In the cells pretreated with IL-1ß and estrogen, the mRNA and protein levels of IL-6, IκBα and p-IκBα were inhibited compared with IL-1ß treated cells. THC blocked the effects of estrogen on the IL-1ß and estrogen treated cells, and the mRNA and protein levels of IL-6, IκBα and p-IκBα had no significant difference compared with IL-1ß treated cells. Conclusion The estrogen can restrain the activation of NF-κB pathway in synovicytes via ERß, thus playing a vital role in anti-inflammation.