97 results about "Synovial Cell" patented technology

There is provided a synovial cell growth inhibitor, or a pharmaceutical composition for treatment of chronic rheumatoid arthritis based on the synovial cell growth inhibitor.The pharmaceutical composition for treatment of chronic rheumatoid arthritis or synovial cell growth inhibitor contains an IL-6 antagonist, such as IL-6 antibody or IL-6R antibody, as an effective component.

A human T cell clone recognizing an antigen expressed by a synovial cell of a rheumatoid arthritis (RA) patient in HLA-DR-restricted manner is disclosed, which clone is very useful in exploring the pathogenesis of RA and developing a method for treating and preventing RA.

Compositions and methods are provided for treatment of cartilage defects in animals and humans. The compositions of the invention include synovial tissue, synovial cells and matrices containing synovial (or cambium) tissue or cells for use in filling a cartilage defect. The matrix and synovial tissue or cell preparations may also contain a proliferation agent, transforming factor or other active agents to promote healing. A controlled-release delivery system may be used to administer the transforming factor. The compositions of the invention also include a synovial covering membrane or devitalized fascial sheet for covering the cartilage defect. The methods of this invention are those in which a minimally invasive surgical intervention is performed to remove a small portion of synovial membrane from a joint. Portions of the synovial membrane, or cells expanded in vitro, are implanted alone or within a matrix, into the defect site, where they produce new cartilage tissue and repair the defect. Alternatively, partially transformed synovial-derived tissue may be formed in situ and implanted into the defect site.

The present invention provides an agent for treatment of arthritic diseases such as rheumatoid arthritis that has for its active ingredient a complex of hyaluronic acid and zinc. This complex synergistically inhibits proliferation of synovial cells and suppresses matrix metalloproteinase MMP-9, which is produced by synovial cells, as compared with its constituents, hyaluronic acid and zinc, alone.

The invention relates to the field of treatment of osteoarthritis, and in particular relates to a preparation method of an adipose mesenchymal stem cell preparation for treating osteoarthritis. The method comprises: step 1, preparing microencapsulated adipose mesenchymal stem cells; step 2, preparing animal origin cartilage cells and synovial cells; step 3, performing inflammatory induction on the adipose mesenchymal stem cells; and step 4, treating the adipose mesenchymal stem cells. According to the preparation method of the adipose mesenchymal stem cell preparation for treating osteoarthritis, provided by the invention, the adipose mesenchymal stem cell preparation for treating osteoarthritis origin cells and the adipose mesenchymal stem cells are co-cultured, and a new in vitro co-culture system is invented, so that the adipose mesenchymal stem cells can obtain treatment characteristics for osteoarthritis outside a body, and can significantly promote the treatment effect on the osteoarthritis after being transplanted in to a body.

The invention discloses PLAC1 (placenta-specific 1) genes which can serve as a molecular marker for early diagnosis of osteoarthritis. Expressions of the PLAC1 genes in synovial tissue of a normal person and a patient suffering from osteoarthritis prove to be different in terms of the transcriptional level and the protein level, and accordingly, the disease risk and the disease state of a subject can be judged according to the identified expression level of the PLAC1 genes. Additionally, experiments prove that interference to expression of the PLAC1 genes or inhibition on the function of PLAC protein can inhibit proliferation of synovial cells, and a new target is provided for development of medicines for treating osteoarthritis clinically.

The invention provides a method for isolating and cultivating mouse cells, which includes the following steps: (1) sterilizing tissue processing equipment; (2) selecting male BALB / c mice aged 1 to 2 months, killing them by breaking their necks, and using surgical scissors. Separate the synovial layer and fibrous layer of the joint capsule, then remove the synovial layer tissue, put the tissue into pre-cooled sterile PBS solution containing double antibody and wash it several times to remove blood stains and fatty tissue; (3) Cut the tissue into pieces, and use Digest with preheated type II collagenase and trypsin respectively; (4) Stop digestion, centrifuge, and discard the supernatant; (5) Inoculate into the coated culture flask by manual adhesion method; (6) After incubation for 1 to 2 hours, Cultivate in a 37°C, 5% CO2 environment; (7) Cell morphology observation; (8) Cell subculture; (9) Cell identification. The method for isolating and culturing mouse synovial cells provided by the invention is simple to operate, has a large number of cells obtained, and has a high survival rate. It is an ideal primary method for isolating and cultivating mouse synovial cells and provides reliable results for experiments. Cell resources.

Disclosed is a novel use of apigenin as a chondroregenerative agent, which has the effects of reducing elevated of cartilage destruction markers including total synovial fluid volume and proteoglycan, total proteins and prostaglandin in a synovial fluid, improving the condition of synovial cells, and regenerating cartilage. Also, the present invention discloses a therapeutic agent for osteoarthritis comprising apigenin as an agent regenerating articular cartilage, and a method of treating osteoarthritis using such a therapeutic agent.

A synthetic tetrapeptide having an amino acide sequence, Glycine-Proline-Arginine-Proline (GPRP) has pro-inflammatory effects on human fibroblastic cells, including synovial cells. An amide analog of GPRP is ineffective in inducing, or effective in causing a loss of, pro-inflammatory effects.

The invention discloses a bifidobacterium breve strain capable of relieving rheumatoid arthritis, and application of the bifidobacterium breve strain, and belongs to the technical field of microorganisms. According to the invention, the bifidobacterium breve strain CCFM1078 is screened out; the bifidobacterium breve strain CCFM1078 has the effect of relieving rheumatoid arthritis and is specifically embodied in that: RAW264.7 cells are remarkably promoted to secrete an anti-inflammatory factor IL-10; the joint thickness, clinical score and morbidity of a rat suffering from rheumatoid arthritisare remarkably reduced; the content of pro-inflammatory cytokines TNF alpha and IL-1 beta in serum of the rat suffering from rheumatoid arthritis is remarkably reduced; the content of short-chain fatty acid in excrement of the rat suffering from rheumatoid arthritis is remarkably adjusted; the proportion of Th17 cells in mesenteric lymph nodes of the rat suffering from rheumatoid arthritis is remarkably reduced; and, a pro-inflammatory factor IL-6 secreted by synovial cells is remarkably reduced.

The invention relates to the field of biotechnology, and provides an aptamer specifically targeting to inflammatory synovial cells of human rheumatoid arthritis (RA), wherein the aptamer has a nucleotide sequence shown as SEQ ID NO.1. The invention further provides applications of the aptamer in preparing a biological probe for identifying the inflammatory synovial cells and applications of the aptamer in preparing medicines or medicine carriers for resisting rheumatoid arthritis in a targeting manner. The aptamer has high selectivity for the inflammatory synovial cells, and the combination with hepatic cells is eliminated or weakened. The biological probe containing the aptamer can identify in-vitro human inflammatory synovial cells, such as the inflammatory synovial cells in a synovial tissue slice of an RA patient, and thus a basis is provided for the clinical diagnosis and targeting therapy of RA.

Compositions and methods are provided for treatment of cartilage defects in animals and humans. The compositions of the invention include synovial tissue, synovial cells and matrices containing synovial (or cambium) tissue or cells for use in filling a cartilage defect. The matrix and synovial tissue or cell preparations may also contain a proliferation agent, transforming factor or other active agents to promote healing. A controlled-release delivery system may be used to administer the transforming factor. The compositions of the invention also include a synovial covering membrane or devitalized fascial sheet for covering the cartilage defect. The methods of this invention are those in which a minimally invasive surgical intervention is performed to remove a small portion of synovial membrane from a joint. Portions of the synovial membrane, or cells expanded in vitro, are implanted alone or within a matrix, into the defect site, where they produce new cartilage tissue and repair the defect. Alternatively, partially transformed synovial-derived tissue may be formed in situ and implanted into the defect site.

The invention relates to a chronic articular inflammation-modulating composition which uses collagen-polyvinylpyrrolidone. Collagen turnover is modulated using collagen-PVP in patients with rheumatoid arthritis and osteoarthritis, since the biocomplex negatively regulates collagenolytic activity and increases the content of type III collagen and TIMP-1 to levels similar to those observed in normal synovia. In this way, the chronic inflammatory process is altered by the collagen-PVP, as described above, owing to the negative regulation of IL-1β, the TNF-α of IL-8 and the adhesion molecules, since said molecules can induce the expression and activation of collagenolytic enzymes, as well as the proliferation and migration of synovial cells by means of the adhesive mechanisms including the adhesion molecules, and the induction and activation of Cox-1. In addition to cellular anchoring, the interaction of the extracellular matrix integrins generates signals which regulate the expression of M MPs, suggesting that the adhesion molecules can also play a part in tissue destruction associated with rheumatoid arthritis. Moreover, the decrease in the synthesis of TNF-α and IL-1β appears to stimulate the cell death of synoviocytes by means of apoptosis, which, in turn, seems to contribute to the inhibition of the proliferation of synovial cells, the formation of pannus and the destruction of the articular tissue.

The invention discloses a pharmaceutical composition of bezafibrate and application thereof to rheumatoid arthritis. The pharmaceutical composition of bezafibrate provided by the invention contains bezafibrate and a natural compound (I) with novel structure and isolated from the dried clove buds; when bezafibrate and the compound (I) are combined for action, the synovial cells arrest in a G1 phase of a cell cycle, thereby inhibiting the proliferation of synovial cells for the treatment of rheumatoid arthritis. The treatment effect of the pharmaceutical composition is better than the individual effect of bezafibrate or compound (I). The composition of bezafibrate and compound (I) can be developed into drugs for the treatment of rheumatoid arthritis. Compared with the prior art, the invention has prominent substantive features and obvious progress.

The invention discloses a mesenchymal stem cell preparation for repairing articular cartilage injury or coloboma, a preparation method and application thereof. According to the preparation method, mesenchymal stem cells and synovial cells are indirectly cocultured, so as to obtain the mesenchymal stem cells after coculture, and then the mesenchymal stem cells are cryopreserved, umbilical cord mesenchymal stem cells, which are acquired after the synovial cells and the umbilical cord mesenchymal stem cells are inoculated at density ratio of 4:1 and cocultured, are easier to differentiate towardcartilage direction under a same induction condition. The preparation method utilizes a constructed animal knee joint cartilage injury or coloboma model to prove that the umbilical cord mesenchymal stem cells cocultured with the synovial cells have an obvious effect of facilitating the repairing of articular cartilage injury or coloboma. The invention further provides a preparation which is prepared from the cocultured mesenchymal stem cells. The preparation can be applied to clinic repairing of articular cartilage injury or coloboma; the preparation can effectively promote the repairing of articular cartilage injury or coloboma through anticular injection; the therapeutic effect of the preparation is obviously better than that of a pure mesenchymal stem cell preparation.

The invention discloses a guaiane-type sesquiterpenes compound, of which the structural formula is represented as follows, and also discloses a preparation method of the compound and an application thereof in preparation of an anti-rheumatoid arthritis medicines. The invention, for the first time, develops the activity of the guaiane-type sesquiterpenes compound in inhibition on rheumatoid arthritis synovial cell proliferation. The compound can be used for preparing the anti-rheumatoid arthritis medicines.

The present invention discloses a novel protein called Synoviolin and a gene that encodes it. This protein is expressed specifically by synovial tissue and also accompanies the presence of an auto-antibody that recognizes this protein in rheumatoid arthritis (RA) patients. The protein according to the present invention and its antibody can be expected to be used as specific diagnostic markers for RA. In addition, the gene or protein according to the present invention may be used to permit the screening of drugs to treat RA. Moreover, the present invention provides synoviolin gene transgenic animals. The transgenic animals according to the present invention can be used as RA model animals in the development of pharmaceuticals to treat RA.

It is suggested that recombinant galectin 9 (rGal 9), produced in host Escherichia coli, exhibits an immune system-mediated action and a direct action on tumor cells (i.e., activity of inducing the intercellular adhesion and apoptosis of the tumor cells), thereby potent in inducing the inhibition of cancer metastasis and reduction. Moreover, the rGal 9 exerts no efficacy on non-activated lymphocytes but can induce apoptosis in activated T cells, in particular, CD4-positive T cells causing an excessive immune response. The rGal 9 has a further potent apoptosis-inducing property on synovial cells participating in joint deformation in rheumatism, etc. In the rGal 9, however, a link domain linking two CRDs is highly susceptible to protease and, therefore, is very easily digestible with the enzyme, thereby losing the above activities. Thus, there is a need for a more stabilized molecule in view of further studies. Modification of the link domain linking two CRDs in galectin 9 provides a modified molecule having an elevated activity without any undesirable effects on the above activities.

The invention provides a modified base aptamer for specifically targeting osteoarthritis synovial cells. The aptamer has a nucleotide sequence as shown in SEQ ID NO.1 or 2. Through modifying an aptamer library, performing positive selection on the osteoarthritis synovial cells and performing negative reverse screening on various kinds of skeletal muscle derived cells, the modified base aptamer forspecifically targeting the osteoarthritis synovial cells is finally obtained. The synovial cell aptamer sequence is screened from the modified aptamer library; the screening process is simple and convenient; complicated steps of a traditional method are greatly reduced; due to the modified structure, the binding force with target cells is higher; the specificity of the synovial cell aptamer is specifically and greatly enhanced; the aptamer targeted binding defect of existing osteoarthritis disease derived synovial cells is overcome; and in the subsequent process, modified groups AminedU in the target aptamer can directly carry nanometer particles to deliver drugs, interfering RNA, miRNA, exosomes and the like to act on different target points to perform specific treatment on synovitis.

The invention provides a primary culture method of rheumatoid arthritis synovial fibroblasts. The method comprises the steps of sufficiently crushing pretreated synovial tissue; adding type-III collagenase and type-II collagenase into the synovial tissue and conducting blowing and beating; after culture digestion, scattering the synovial tissue into single cells; after filtering, centrifuging a filtrate, taking a substratum precipitate, and inoculating the substratum precipitate into a DMEM high-glucose culture medium for adherent culture; adopting a natural purification method and a repeatedadherent method for purifying the cells to obtain the rheumatoid arthritis synovial fibroblasts. By means of the culture method, about 1,010 RASFs can be obtained within 30 days, the cell yield is greatly increased, multiple experiment demands can be met, and therefore, the primary culture method is a quick and effective primary RASFS isolation culture method. In the meanwhile, compared with synovial cell lines of in-vitro construction lines, the RASFs obtained through primary culture have higher study value, and have a good practical application prospect.

It is suggested that recombinant galectin 9 (rGal 9), produced in host Escherichia coli, exhibits an immune system-mediated action and a direct action on tumor cells (i.e., activity of inducing the intercellular adhesion and apoptosis of the tumor cells), thereby potent in inducing the inhibition of cancer metastasis and reduction. Moreover, the rGal 9 exerts no efficacy on non-activated lymphocytes but can induce apoptosis in activated T cells, in particular, CD4-positive T cells causing an excessive immune response. The rGal 9 has a further potent apoptosis-inducing property on synovial cells participating in joint deformation in rheumatism, etc. In the rGal 9, however, a link domain linking two CRDs is highly susceptible to protease and, therefore, is very easily digestible with the enzyme, thereby losing the above activities. Thus, there is a need for a more stabilized molecule in view of further studies. Modification of the link domain linking two CRDs in galectin 9 provides a modified molecule having an elevated activity without any undesirable effects on the above activities.

The invention discloses a pharmaceutical composition of buspirone hydrochloride and its medical application. The pharmaceutical composition of buspirone hydrochloride provided by the invention contains buspirone hydrochloride and a kind of dried rhizome of Anemarrhena anemarrhena The isolated natural product compound (I) with a novel structure, when buspirone hydrochloride and the compound (I) provided by the present invention act in combination, can make the synoviocytes stagnate in the G1 phase of the cell cycle, thereby inhibiting the proliferation of the synoviocytes, Treating synovitis; the therapeutic effect is better than that of buspirone hydrochloride or compound (I) alone. The composition of buspirone hydrochloride and compound (I) can be developed into a drug for treating synovitis, which has outstanding substantive features and significant progress compared with the prior art.

An object of the present invention is to provide a novel marker for rheumatoid arthritis (RA), and more specifically, to provide a marker whose expression may be specifically increased or decreased in RA. Another object of the present invention is to confirm whether or not miRNA serving as the marker is involved as the etiology of RA, and to provide an inspection method for RA and a therapeutic agent for RA each using the miRNA involved. The marker includes miRNA (for example, miR124a) whose expression is specifically increased or decreased in RA synovial cells based on a small RNA expression profile in the RA synovial cells. In addition, the therapeutic agent for RA includes miRNA (for example, miR124a) as an active ingredient.

The invention relates to the field of disease diagnosis technology and preparation of therapeutic drugs, in particular to application of a marker in preparation of a diagnostic kit or therapeutic drug for rheumatoid arthritis. In the application, the marker is a synovial cell supernate exosome lncRNA SNHG5 or a truncated sequence thereof; and the sequence of the lncRNA SNHG5 is as shown in SEQ ID NO: 1. The research finds that the expression of the synovial cell exosome lncRNA SNHG5 in rheumatoid arthritis patients is obviously increased compared with that in osteoarthritis patients, and by means of the exosome lncRNA SNHG5, a therapeutic target and an important basis are provided for not only early-stage rapid detection of the rheumatoid arthritis, but also clinical application such as gene therapy and drug therapy.

The invneiton provides a cadinane sesquiterpene compound, and a preparation method and application thereof. The preparation method comprises the following steps: (1) preparation of fissistigma oldhamii extract: carrying out cold leaching or hot extracting on dried stem of the fissistigma oldhamii by using ethanol of which the volume concentration is 30 to 95 percent, thus obtaining an extracting solution; carrying out vacuum concentration, thus obtaining paste, i.e., the fissistigma oldhamii extract; (2) separation and purification: diluting the fissistigma oldhamii extract by using water to prepare a suspension solution, sequentially extracting by using petroleum ether and ethyl acetate, forming extractum by carrying out vacuum concentration on an ethyl acetate extracting solution, and carrying out column chromatography, thin layer chromatography, molecular sieve chromatographic separation and high-performance liquid-phase separation, thus obtaining the cadinane sesquiterpene compound. The invention also discloses the preparation method of the cadinane sesquiterpene compound and the application of the cadinane sesquiterpene compound in preparing medicine for resisting rheumatoid arthritis. According to the cadinane sesquiterpene compound disclosed by the invention, the activity of the cadinane sesquiterpene compound in inhibiting synovial cell proliferation of the rheumatoid arthritis is firstly discovered, and the cadinane sesquiterpene compound can be used for preparing the medicine for resisting the rheumatoid arthritis.

The invention discloses a monoclonal antibody for resisting Cyr61 protein, which is prepared from a hybridoma cell line CGMCC3299 or CGMCC3300 and can be specifically combined with an N end SEQ ID No 1of the Cyr61 protein. The monoclonal antibody for resisting Cyr61 protein can be used for inhibiting proliferation, adhesion and protraction of rheumatoid arthritis synovial cells and malignant tumor cells as well as in vitro detection of the Cyr61 protein.

The invention designs a pair of targeting DKK-1 (Dickkopf-related protein-1) specific siRNA (small interfering ribonucleic acid) capable of obviously down-regulating the DKK-1 expression of over-activated synovial fibroblasts in patients with rheumatoid arthritis (RA) and inhibiting the abilities of cell proliferation and inflammatory factor secretion and invasion, thereby attaching great significance to the immunotherapy for RA treatment.

The invention discloses a TGF-Beta3 (Transforming Growth Factor Beta3) loaded slow-release tissue engineering synovial sheath. The synovial sheath is characterized by consisting of a dense layer (1) and a porous layer (2), wherein the porous layer (2) is mesh-shaped, and chitosan microspheres containing TGF-Beta3 and synovial cells are loaded into the porous layer (2). According to the synovial sheath, the artificial synovialization of chitosan scaffolds is realized. The TGF-Beta3 loaded slow-release tissue engineering synovial sheath has the advantages that the slow release of the TGF-Beta3 can be realized, the cicatrization resisting effect of the TGF-Beta3 is exerted, the TGF-Beta3 with biological activity is released in a slow and sustained manner, and active substances, such as hyaluronic acid and the like, secreted by synovial survival cells can be utilized so as to be expected to play a role in adhesion prevention after tendon injury repair. The synovial sheath can serve as an ideal material for preventing adhesion after tendon injury repair, and has good preventing and treating effects when the synovial sheath is applied to tendon adhesion in orthopedics.

The onset ratios and pathological conditions of collagen-induced arthritis and adjuvant arthritis in model mice and rats, respectively, were successfully ameliorated by topically expressing the cyclin-dependent kinase inhibitors p16INK4a and p21Cip1 p in articular tissues using adenoviral vectors. In the synovial cells of CDKI-transduced mice, expression of inflammatory cytokines was inhibited. Described are the use of the p21Cip1 protein for inhibiting abnormal proliferation of synovial tissues, inflammation in synovial tissues and / or expression of inflammatory cytokines in synovial tissues; the p21Cip1 gene; compounds promoting the activity or expression of the p21Cip1 protein; and pharmaceutical compositions containing these molecules. Also provided are method of screening for compounds participating in the abnormal proliferation of synovial tissues, inflammation in synovial tissues and / or the expression of inflammatory cytokines in synovial tissues targeting the p21Cip1 protein. Rheumatoid arthritis and other disorders associated with inflammation of the synovial tissue can be prevented or treated by promoting expression or function of p21Cip1 protein.

An object of the present invention is to provide a novel marker for rheumatoid arthritis (RA), and more specifically, to provide a marker whose expression may be specifically increased or decreased in RA. Another object of the present invention is to confirm whether or not miRNA serving as the marker is involved as the etiology of RA, and to provide an inspection method for RA and a therapeutic agent for RA each using the miRNA involved. The marker includes miRNA (for example, miR124a) whose expression is specifically increased or decreased in RA synovial cells based on a small RNA expression profile in the RA synovial cells. In addition, the therapeutic agent for RA includes miRNA (for example, miR124a) as an active ingredient.