Composition for improving joint inflammation and derivatives thereof

Abstract

Composition for improving inflammation in osteoarthritis, characterized in that the composition comprises the following components, measured in parts by weight: 1 to 5 parts by weight of N-acetylglucosamine and 0.1 to 2 parts by weight of calcium element in a calcium source.

Description

Technical field

[0001] The present utility model belongs to the technical field of functional compositions and specifically relates to a composition for improving inflammation in osteoarthritis as well as a product containing the composition. State of the art

[0002] Osteoarthritis (OA), also known as degenerative arthritis, is one of the most common diseases among older adults and people with obesity. OA is a joint disease, but it differs from rheumatoid arthritis (RA) in that it is not systemic and usually affects only one or a few joints. This disease leads to extensive destruction of the articular cartilage, sclerosis of the underlying bone, and the formation of osteophytes, causing loss of mobility and pain. The main pathological changes commonly involve bony growths in the cervical spine, lumbar spine, and knee joints; the primary symptom is pain. The end result is often the need for total joint replacement.

[0003] The inflammatory response plays a central role in the pathological progression of osteoarthritis. An increase in inflammatory mediators such as interleukin-6 (IL-6) promotes the expression of a number of degrading enzymes, including matrix metalloproteinases (MMPs) and A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS). These enzymes destroy the collagen network and proteoglycans in the cartilage matrix, causing the cartilage to lose its structural and functional integrity. Furthermore, the inflammatory environment can induce programmed cell death processes in chondrocytes (including apoptosis and pyroptosis), further weakening the cartilage's self-repair capacity. Simultaneously, the originally smooth surface of the articular cartilage becomes rough and uneven, and the bone beneath the cartilage also exhibits abnormal changes, including subchondral bone sclerosis and osteophyte formation.These changes not only intensify joint pain but also further restrict joint mobility.

[0004] Currently, treatment methods for osteoarthritis essentially comprise the following approaches: Western medicine frequently uses non-steroidal anti-inflammatory drugs and pain relievers (such as aspirin, ibuprofen, indomethacin, etc.); however, due to pronounced side effects, these often cause significant psychological distress for patients. Physiotherapy and acupuncture have fewer side effects, but their long-term effectiveness is still difficult to definitively confirm. While the oral administration of traditional Chinese medicine can overcome the aforementioned disadvantages, patients are often unwilling to accept it due to its perceived inconvenience.Furthermore, while common products on the market, such as "musk tiger bone patches," are convenient to use, their effectiveness is significantly limited due to the scarcity of certain raw materials (like tiger bones). Therefore, there is an urgent need to develop a formulation that can effectively treat inflammation in osteoarthritis, is highly palatable, and improves patient adherence. Content of the present utility model

[0005] The purpose of this section is to summarize some aspects of the embodiments of the present utility model and to briefly present some preferred embodiments.

[0006] In view of the aforementioned problems and / or the problems existing in the prior art, the present utility model is proposed.

[0007] Therefore, the purpose of the present utility model is to overcome the shortcomings of the prior art and to provide a composition for improving inflammation in osteoarthritis.

[0008] To achieve the aforementioned purposes, the following technical solution is used in the present utility model: a composition for improving inflammation in osteoarthritis, wherein the composition comprises the following components, measured in parts by weight: 1 to 5 parts by weight of N-acetylglucosamine and 0.1 to 2 parts by weight of calcium element in a calcium source.

[0009] As a preferred embodiment of the composition of the present utility model, the composition for improving inflammation in osteoarthritis comprises the following components, measured in parts by weight: 1 to 2 parts by weight of N-acetylglucosamine and 0.19 to 1.52 parts by weight of calcium element in a calcium source.

[0010] As a preferred embodiment of the composition of the present utility model, the composition for improving inflammation in osteoarthritis further comprises chondroitin sulfate sodium; the weight parts of chondroitin sulfate sodium are 0.1 to 3 parts by weight.

[0011] In a preferred embodiment of the composition of the present utility model, the parts by weight of chondroitin sulfate sodium are 0.37 to 2.97 parts by weight.

[0012] As a preferred embodiment of the composition of the present utility model, the composition for improving inflammation in osteoarthritis further comprises vitamin D and / or low molecular weight peptides.

[0013] In a preferred embodiment of the composition of the present utility model, the parts by weight of vitamin D are 0.000005 to 0.00004 parts by weight; the parts by weight of low molecular weight peptides are 0.1 to 0.8 parts by weight.

[0014] In a preferred embodiment of the composition of the present utility model, the proportion of peptide fragments with a relative molecular mass ≤ 10,000 Da in low molecular weight peptides is ≥ 90%.

[0015] In a preferred embodiment of the composition of the present utility model, the low molecular weight peptides comprise low molecular weight collagen peptides.

[0016] A preferred embodiment of the composition of the present utility model consists of the low molecular weight peptides collagen tripeptides.

[0017] In a preferred embodiment of the composition of the present utility model, the calcium source comprises at least one of milk minerals, calcium citrate, calcium gluconate, calcium carbonate, calcium lactate, tricalcium phosphate, calcium citrate malate, calcium malate and calcium succinate.

[0018] As a preferred embodiment of the composition of the present utility model, the composition is any combination of instant drink, tablet, jelly, soft gum, capsule and beverage.

[0019] N-acetylglucosamine (hereinafter referred to as NAG) is the basic structural unit of chitin in the exoskeleton of crustaceans and represents a monosaccharide derivative with functional bioactivity. This substance exhibits anti-inflammatory, antitumor, and antioxidant effects. In recent years, NAG has gained attention in the field of osteoarthritis due to its bioactivity in cartilage repair and inflammation reduction. From a mechanistic perspective, NAG can effectively stimulate chondrocytes to synthesize type II collagen and proteoglycans, thereby improving the structural integrity and elasticity of articular cartilage; at the same time, NAG can inhibit the expression of inflammatory mediators (such as IL-6, IL-1β, and TNF-α) as well as matrix metalloproteinases (such as MMP-13), thus slowing down degenerative changes in joint tissue.

[0020] Calcium is a fundamental building block for maintaining healthy bones and is particularly important for the subchondral bone and deep cancellous bone, which are crucial for joint stability and mechanical cushioning. Strong bones provide the articular cartilage with the necessary mechanical support and a stable foundation. In the pathological process of osteoarthritis, lesions of the subchondral and cancellous bone, as well as cartilage degeneration, mutually reinforce each other.First, the effects of calcium and N-acetylglucosamine are different, yet they have a synergistic effect: NAG nourishes, protects, and repairs articular cartilage, improves cartilage metabolism, and alleviates symptoms of osteoarthritis; calcium aims to maintain the mineral density, strength, and microstructural health of the entire skeleton (including subchondral bone and deep cancellous bone in the joint area), as well as to prevent and treat osteoporosis. Second, the integrity of the bone-cartilage unit as a whole is protected: healthy cartilage requires healthy subchondral bone and cancellous bone as a stable and elastic supporting base.

[0021] Chondroitin sulfate sodium (hereinafter referred to as CS) is an acidic mucopolysaccharide widely distributed in human connective tissue and is one of the main components of the articular cartilage matrix. It is predominantly derived from animal cartilage and is frequently used for joint health and supportive treatment, for example, to relieve joint pain, reduce inflammation, and even offer some benefits for the cardiovascular system. CS does not merely serve as a "building material" but rather plays a key role in structural support, anti-inflammatory regulation, and cell protection. CS can effectively inhibit the formation of inflammatory mediators (such as PGE2 and NO) and, by regulating p65-mediated signaling pathways, significantly reduce the level of inflammation in osteoarthritis (OA).Furthermore, CS can downregulate the expression of matrix metalloproteinases (MMPs) and collagenases, preventing excessive degradation of the cartilage matrix and thereby slowing cartilage wear. In in vitro experiments, chondroitin sulfate sodium has been shown to upregulate the expression of genes related to cartilage formation, promote chondrocyte proliferation and survival, and improve the cartilaginous microenvironment.

[0022] Vitamin D (especially its active form 1,25-dihydroxyvitamin D3, calcitriol) not only participates in mineral metabolism but also exerts multiple biological effects in the regulation of cellular functions in bone and cartilage tissue, in immune regulation, and in joint protection. Vitamin D binds to the vitamin D receptor (VDR) and regulates the active absorption of calcium and phosphorus by epithelial cells of the small intestine, thereby maintaining homeostasis of calcium and phosphate concentrations in the blood. This is crucial for the mineralization process of bone tissue. Vitamin D also has an important regulatory function in the immune system, which is particularly evident in joint diseases (such as rheumatoid arthritis and osteoarthritis): It inhibits the expression of pro-inflammatory cytokines (such as TNF-α, IL-6, and IL-1β).It inhibits the maturation of dendritic cells and the polarization of Th1 / Th17 T helper cells, and slows down autoimmune reactions. It reduces the inflammatory response of synovial cells and mitigates synovial hyperplasia and its destruction.

[0023] Low-molecular-weight collagen peptides are small fragments formed by the enzymatic hydrolysis of collagen protein and are more readily absorbed and utilized by the human body. They are primarily derived from terrestrial animals (such as cattle and yak bones) as well as marine organisms (such as cod and Antarctic krill). Low-molecular-weight collagen tripeptides are small-molecular-weight breakdown products of collagen protein, consisting of three amino acids, and exhibit good bioavailability. In the inflammatory environment of osteoarthritis, they can exert a protective effect through several mechanisms. First, collagen tripeptides can promote the proliferation and differentiation of chondrocytes and enhance their synthesis of extracellular matrix components such as type II collagen and proteoglycans, thereby maintaining the structural integrity of cartilage tissue.Secondly, they can inhibit the activation of the NF-κB signaling pathway induced by inflammatory stimuli (such as IL-1β or TNF-α), reduce the expression of inflammatory mediators (such as IL-6, COX-2, and iNOS), and mitigate the local inflammatory response in the joint. Furthermore, collagen tripeptides can downregulate the expression of matrix metalloproteinases (such as MMP-3 and MMP-13), inhibit the degradation of the cartilage matrix, and thereby slow the progression of osteoarthritis. These effects indicate that low-molecular-weight collagen tripeptides have some potential for use in relieving inflammation in osteoarthritis and protecting cartilage tissue.

[0024] Due to the synergistic effect between the respective components, such as N-acetylglucosamine and calcium element in calcium source, within a specific weight ratio range, the present utility model can effectively improve the repair effect on chondrocytes and inhibit inflammatory joint damage compared to a single component, thereby achieving a significantly improved effect in reducing inflammation in osteoarthritis.

[0025] Another purpose of the present utility model is to overcome the shortcomings of the prior art and to provide a product containing the composition for improving inflammation in osteoarthritis.

[0026] As a preferred embodiment of the product of the present utility model, the product comprises ordinary food, food supplements, animal feed or pharmaceuticals.

[0027] For the purposes of this utility model, ordinary foodstuffs are understood to be finished products and raw materials intended for consumption or drinking by humans, including processed foods, semi-finished products and unprocessed foods.

[0028] Compared to the prior art, the present utility model has the following advantageous effects: (1) The present utility model provides a composition for improving inflammation in osteoarthritis; through the synergistic action between several material components, inflammation in osteoarthritis can be effectively improved. At the same time, a better effect in reducing the release of the cellular inflammatory cytokine IL-6 can only be achieved if the ratio between the material components in the composition for improving inflammation in osteoarthritis is kept within a suitable range. (2) The composition for improving inflammation in osteoarthritis according to the present utility model, wherein all raw material components are among the raw materials permitted as ordinary foodstuffs, exhibits a high level of safety; furthermore, the composition of the present utility model can be manufactured in various dosage forms, thereby significantly improving its palatability and consumer adherence. Brief description of the characters

[0029] To clarify the technical solutions of the embodiments of this utility model, the drawings required for the description of the embodiments are briefly presented below. Obviously, the drawings mentioned in the following description represent only some embodiments of this utility model; a person skilled in the art can derive further drawings from these without any creative effort. The following applies: Fig. Figure 1 is a schematic representation of the results of the chondrocyte inflammation experiment for the exemplary embodiments and comparative examples in the present utility model. Here, #### means P < 0.0001 compared to the control group; **** means P < 0.0001 compared to the model group; *** means P < 0.001 compared to the model group; ** means P < 0.01 compared to the model group; * means P < 0.05 compared to the model group. Detailed descriptions

[0030] The technical solutions in the embodiments of this utility model are clearly and completely described below in conjunction with the embodiments of this utility model. Obviously, the described embodiments are only a subset of the embodiments of this utility model and not all embodiments. Based on the embodiments of this utility model, all other embodiments that a person skilled in the art could obtain without inventive activity are within the scope of protection of this utility model.

[0031] Unless otherwise specified in the exemplary embodiments and comparative examples, the experimental procedures used are conventional procedures; the materials, reagents and the like used can be obtained from commercial sources unless otherwise stated.

[0032] The manufacturing processes of the respective components in the exemplary embodiments and comparative examples are described below: N-Acetylglucosamine (NAG): Production is carried out using an existing biofermentation process, whereby Corynebacterium glutamicum RDG-2110 is selected to ferment raw materials such as glucose and dried corn steep liquor powder at a temperature of 30 to 40 °C; fermentation time is 48 to 96 h; subsequently, filtration for sterilization, filtration for protein separation, decolorization, concentration, crystallization, alcohol washing and drying are carried out to obtain N-acetylglucosamine.

[0033] Calcium source: Calcium carbonate and citric acid solution are mixed at 40 to 80 °C while stirring for 30 to 120 minutes; subsequently, centrifugation, drying and sterilization, mixing, sieving to remove impurities and metal detection are carried out, resulting in calcium citrate.

[0034] Chondroitin sulfate sodium (CS): Animal cartilage raw materials undergo pretreatment such as cleaning and grinding; the preprocessed raw materials are boiled (90 to 100 °C, 30 to 120 min) and enzymatically hydrolyzed (using an enzyme mixture of trypsin, alkaline lipase and alkaline protease or using other proteases such as pepsin, with the reaction taking place in a water bath at about 37 °C for several hours; after completion of the enzymatic hydrolysis, the enzyme is inactivated by heating); subsequently, filtration, centrifugation, ultrafiltration, purification, filtration, alcohol precipitation, dehydration, granulation, centrifugation and drying are carried out to obtain chondroitin sulfate sodium.

[0035] Vitamin D: D3 crude oil is esterified (acidic catalyst), saponified, crystallized, dried and mixed, resulting in vitamin D powder.

[0036] Low molecular weight peptides: Raw materials are thawed and crushed; this is followed by enzymatic hydrolysis (using a neutral protease, an alkaline protease or an enzyme mixture; hydrolysis time is 2 to 8 h), enzyme inactivation (enzyme inactivation at 85 to 95 °C, treatment time 5 to 15 min), cooling, vibratory sieving, adsorption, pressure filtration, concentration, sterilization, spray drying, powder collection and filling, resulting in low molecular weight collagen peptides; in the resulting low molecular weight collagen peptides, the proportion of peptide fragments with a relative molecular mass ≤ 10,000 Da is ≥ 90%.

[0037] The manufacturing processes for the respective components in the exemplary embodiments and comparative examples are all conventional manufacturing processes in the field. At the same time, in addition to selecting components produced by the aforementioned manufacturing processes, the respective components of the composition for improving inflammation in osteoarthritis in the present utility model can also be selected as existing commercial products, whereby the final effect of improving inflammation in osteoarthritis can also be achieved. Examples 1 to 16 and comparative examples 1 to 8

[0038] The quantities of the respective components used in the compositions for improving inflammation in osteoarthritis according to the exemplary embodiments 1 to 16 and the comparative examples 1 to 8 are shown in Table 1.

[0039] In embodiments 1 to 16, in addition to calcium citrate, one or more components can be selected as the calcium source, namely milk minerals, calcium gluconate, calcium carbonate, calcium lactate, tricalcium phosphate, calcium citrate malate, calcium malate, calcium succinate and the like, which are used in different masses but have the same calcium content as calcium citrate; thus, the same effect as with calcium citrate can ultimately be achieved.

[0040] The manufacturing process for the compositions for improving inflammation in osteoarthritis according to embodiments 1 to 16 and comparative examples 1 to 8 comprises the following steps: All components are mixed evenly, thus obtaining the composition for improving inflammation in osteoarthritis. Table 1 Actual amounts of the composition added / mg group NAG Calcium elementin calcium source CS Vitamin D Low molecular weight peptides Example 1 500 95 0 0 0 Example 2 500 190 0 0 0 Example 3 500 380 0 0 0 Example 4 500 760 0 0 0 Example 5 500 95 185 0 0 Example 6 500 190 370 0 0 Example 7 500 380 740 0 0 Example 8 500 760 1480 0 0 Example 9 500 95 185 0.0025 0 Example 10 500 190 370 0.005 0 Example 11 500 380 740 0.01 0 Example 12 500 760 1480 0.02 0 Example 13 500 95 185 0.0025 50 Example 14 500 190 370 0.005 100 Example 15 500 380 740 0.01 200 Example 16 500 760 1480 0.02 400 Comparative example 1 500 90 0 0 0 Comparative example 2 500 800 0 0 0 Comparative example 3 500 90 180 0 0 Comparative example 4 500 800 1500 0 0 Comparative example 5 500 90 180 0.002 0 Comparative example 6 500 800 1500 0.025 0 Comparative example 7 500 90 180 0.002 45 Comparative example 8 500 800 1500 0.025 450 Experiment 1I. Cell culture:

[0041] SW1353 cells from human chondrosarcoma are cultured in DMEM whole medium containing 10% fetal calf serum and penicillin / streptomycin and incubated at 37°C and 5% CO2. Cells in the logarithmic growth phase are used for subsequent experiments.

[0042] SW1353 cells in the logarithmic growth phase are seeded into a 24-well plate. When SW1353 cells cover approximately 50% of the 24-well plate, a control group with the addition of 500 µl DMEM, a model group with 500 µl DMEM + LPS (LPS solution concentration: 200 µg / mL), and a sample / treatment group with the addition of 500 µl DMEM + LPS + the composition according to Table 1 are set up and treated for 24 h.

[0043] The mixture is then centrifuged at 2 to 8 °C and 1000× g for 15 min; the supernatant is removed and used for subsequent experiments.

[0044] II. Experimental classification: Sample / treatment group (composition according to examples 1 to 16 and comparison examples 1 to 8 in Table 1 + LPS + culture medium), control group (culture medium), model group (LPS + culture medium). III. Experimental principle:

[0045] Purified antibodies are used to coat a microtiter plate to create a solid-phase support. Sample or standard, biotinylated anti-IL-6 antibody, and horseradish peroxidase (HRP)-labeled avidin are successively added to the wells coated with anti-IL-6 antibody. After thorough washing, the color reaction is performed using the substrate 3,3',5,5'-tetramethylbenzidine (TMB). TMB is converted to a blue color by peroxidase catalysis and then to the final yellow color upon treatment with an acid. The color intensity correlates positively with the IL-6 content in the sample. The optical density (OD) is measured using a microplate reader at a wavelength of 450 nm, and the sample concentration is calculated. The individual components of the kit are shown in Table 2. Table 2 ingredient Product specification and quantity ELISA plate (assay plate) 12 strips × 8 indentations Standard (Standard) 2 vials (lyophilized product) Biotin-labeled antibody (biotin antibody) 1 × 120 µl / vial (100×) Horseradish peroxidase-labeled avidin (HRP-avidin) 1 × 120 µl / vial (100×) Dilution buffer for biotin-labeled antibody (Biotin-antibody Diluent) 1 x 15 ml bottle Sample diluent buffer 1 x 50 ml bottle Concentrated Wash Buffer 1 × 20 ml / bottle (25×) Substrate solution (TMB substrate) 1 x 10 ml bottle Stop Solution 1 x 10 ml bottle Sheet film 4 IV. Reagent preparation: 1. Standard: (1) One vial of standard is removed from the kit and centrifuged at 6000 to 10000 rpm for 30 s. The standard is dissolved with 1 ml of sample dilution buffer, with the pipette tip directed towards the bottom of the cryovial and the solution repeatedly drawn up and expelled 5 times to aid dissolution. After thorough mixing, standard S7 is obtained and made available for further use. (2) Seven 1.5 mL centrifuge tubes (S0-S6) are arranged in series, and 250 mL of sample dilution buffer are added to each tube. 250 mL of standard S7 are pipetted into the first centrifuge tube (S6) and mixed thoroughly by gentle up-and-down pipetting. 250 mL are withdrawn from S6 and transferred to the second EP tube (S5) and mixed thoroughly by gentle up-and-down pipetting. The double serial dilution of the standard is continued in the same manner. S0 consists of sample dilution buffer. Specific information on the standards is given in Table 3. Table 3 Nr. S7 S6 S5 S4 S3 S2 S1 S0 pg / ml 500 250 125 62.5 31.2 15.6 7.8 0

[0046] 2. Preparation of the washing buffer working solution: Concentrated washing buffer is diluted with deionized water in a ratio of 1:25. For example, 240 ml of deionized water are measured using a graduated cylinder and poured into a beaker or other clean container; then 10 ml of concentrated washing buffer are measured, added evenly, and thoroughly mixed while stirring. The solution is freshly prepared before use. Salt precipitation may occur in the concentrated washing buffer at low storage temperatures; warming in a water bath can aid dissolution during dilution.

[0047] 3. Preparation of the working solution of the biotin-labeled antibody: The biotin-labeled antibody solution is diluted 1:100 with the dilution buffer for biotin-labeled antibody. For example, 10 µl of biotin-labeled antibody is added to 990 µl of dilution buffer for biotin-labeled antibody and mixed gently; the solution is freshly prepared within 10 minutes before use.

[0048] 4. Preparation of the working solution of HRP-labeled avidin: HRP-labeled avidin is diluted 1:100 with the dilution buffer for HRP-labeled avidin. For example, 10 µl of HRP-labeled avidin is added to 990 µl of dilution buffer for HRP-labeled avidin and mixed gently; the solution is freshly prepared within 10 minutes before use. V. Experimental method: 1) The reagents listed in Table 2 are brought to room temperature (18-25 °C) and left to stand for at least 30 minutes to equalize the temperature. 2) Sample preparation: Standard wells and wells for the samples to be tested are prepared (three of each). 100 µl of IL-6 standard S0-S7 (for later generation of the standard curve) or 100 µl of the sample to be tested is added to each well; the mixture is then gently swirled, covered with a foil plate, and incubated at 37 °C for 2 h. 3) Liquid is discarded, plate is spun out and beaten dry; no washing step takes place. 4) 100 µl of working solution of the biotin-labeled antibody is added to each well; then the plate is covered with a new foil and incubated at 37 °C for 1 h. 5) The liquid in the wells is discarded, the plate is centrifuged and beaten dry; the plate is washed 3 times. Each time, it is soaked for 2 minutes, 200 µl per well, then centrifuged and beaten dry. 6) 100 µl of working solution of the HRP-labeled avidin is added to each well; then the plate is covered with a new foil and incubated at 37 °C for 1 h. 7) The liquid in the wells is discarded, the plate is centrifuged and beaten dry; the plate is washed 5 times. Each time, it is soaked for 2 minutes, 200 µl per well, then centrifuged and beaten dry. 8) 90 µl of substrate solution is added to each well one after the other, and the color reaction is carried out at 37 °C, protected from light, for 15-30 min. 9) 50 µl of stop solution are added to each well one after the other to stop the reaction. 10) Within 5 minutes of the reaction being completed, the optical density (OD value) of each well is measured successively using a microplate reader at a wavelength of 450 nm. 11) After subtracting the OD value of the wells S0 from the standard values, a curve is created; if replicates are set up, the mean value is used for the calculation. The concentration of the standards is used as the ordinate (logarithmic axis), and the mean of the OD values ​​of the standards after subtracting the S0 OD value is used as the abscissa (logarithmic axis). Using the professional software "CurveExpert," a standard curve is created on logarithmic coordinate paper according to the instructions. The IL-6 concentration in the respective wells of the samples is then calculated from this standard curve. VI. Experimental Results

[0049] The improving effect of the compositions produced by embodiments 1 to 16 and comparative examples 1 to 8 on chondrocyte inflammation is described in Fig. 1 shown.

[0050] From the test results in Fig. It is evident from Figure 1 that the compositions produced in embodiments 1 to 16 of the present utility model can all significantly reduce the release of the cellular inflammatory cytokine IL-6, thereby achieving an effect to improve inflammation in osteoarthritis, and that they have a better effect in reducing the release of the cellular inflammatory cytokine IL-6 compared to the comparison examples.

[0051] The compositions in comparative examples 1 to 2 contain N-acetylglucosamine and a calcium source; since the ratio of the amounts added to these two components is not suitable, the effect of the compositions ultimately produced in reducing the IL-6 concentration is obviously worse than that of the exemplary embodiments.

[0052] The compositions in comparative examples 3 to 4 contain N-acetylglucosamine, a calcium source, and chondroitin sulfate sodium; since the ratios between the respective components are not suitable, the effect of the ultimately produced compositions on lowering the IL-6 concentration is worse than that of the exemplary embodiments.

[0053] The compositions in comparative examples 5 to 6 contain N-acetylglucosamine, a calcium source, chondroitin sulfate sodium, and vitamin D; since the ratios between the respective components are not suitable, the effect of the ultimately produced compositions on lowering the IL-6 concentration is worse than that of the exemplary embodiments.

[0054] The compositions in comparative examples 7 to 8 contain N-acetylglucosamine, a calcium source, chondroitin sulfate sodium, vitamin D, and low molecular weight peptides; since the ratios between the respective components are not suitable, the effect of the ultimately produced compositions on lowering the IL-6 concentration is worse than that of the exemplary embodiments.

[0055] In the composition of comparison example 3, whose components include N-acetylglucosamine, a calcium source, and chondroitin sulfate sodium, as well as in the composition of comparison example 5, whose components include N-acetylglucosamine, a calcium source, chondroitin sulfate sodium, and vitamin D, the unsuitable ratios between the respective components may cause problems such as cellular stress, apoptosis, or metabolic dysregulation, leading to the upregulation of inflammatory mediators such as IL-6; this ultimately results in the manufactured compositions having a lesser effect on lowering IL-6 concentration than the model group.

[0056] The above test results show that the composition for improving inflammation in osteoarthritis in the present utility model can only significantly reduce the release of the cellular inflammatory cytokine IL-6 and achieve an effective effect in improving inflammation in osteoarthritis if the ratios between the selected respective components are kept within a suitable range.

[0057] The foregoing embodiments merely illustrate the principles and effects of the present utility model and are not intended to limit its scope. Any person familiar with this technology may make modifications or changes to the foregoing embodiments without deviating from the spirit and scope of the present utility model. Therefore, all equivalent modifications or changes made by a person skilled in the art, without deviating from the spirit and technical concept disclosed in the present utility model, shall continue to be covered by the scope of protection of the claims of the present utility model.

Claims

[1] Composition to improve inflammation in osteoarthritis, characterized by , that the composition includes the following components, calculated in parts by weight: 1 to 5 parts by weight of N-acetylglucosamine and 0.1 to 2 parts by weight of calcium element in a calcium source. [2] Composition for improving inflammation in osteoarthritis according to claim 1, characterized by , that the composition includes the following components, calculated in parts by weight: 1 to 2 parts by weight of N-acetylglucosamine and 0.19 to 1.52 parts by weight of calcium element in a calcium source. [3] Composition for improving inflammation in osteoarthritis according to claim 1 or 2, characterized by , that the composition for improving inflammation in osteoarthritis further includes chondroitin sulfate sodium; the weight parts of chondroitin sulfate sodium are 0.1 to 3 weight parts. [4] Composition for improving inflammation in osteoarthritis according to claim 3, characterized by , that the composition for improving inflammation in osteoarthritis also includes vitamin D and / or low molecular weight peptides. [5] Composition for improving inflammation in osteoarthritis according to claim 4, characterized by , that the parts by weight of vitamin D are 0.000005 to 0.00004 parts by weight; the parts by weight of low molecular weight peptides are 0.1 to 0.8 parts by weight. [6] Composition for improving inflammation in osteoarthritis according to claim 4, characterized by , that the proportion of peptide fragments with a relative molecular mass ≤ 10,000 Da in low molecular weight peptides is ≥ 90%; the low molecular weight peptides include low molecular weight collagen peptides. [7] Composition for improving inflammation in osteoarthritis according to claim 1, characterized bythat the calcium source includes at least one of the following: milk minerals, calcium citrate, calcium gluconate, calcium carbonate, calcium lactate, tricalcium phosphate, calcium citrate malate, calcium malate and calcium succinate. [8] Composition according to claim 7, characterized by , that the composition is any of instant drink, tablet, jelly, soft gum, capsule and beverage. [9] Product containing composition for improving inflammation in osteoarthritis according to any one of claims 1 to 7. [10] Product according to claim 9, characterized by that the product includes ordinary food, food supplements, animal feed or medicinal products.

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