97 results about "Synovial Cell" patented technology

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.

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.

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 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 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 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.

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.