Cts Nerve Guidance Conduit Material Nerve Defects Properties Regeneration Effect Activity Bioactive Chitosan Conduit Tube Scaffold Inner Cross Sponge Texture

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Cts Nerve Guidance Conduit Material Nerve Defects Properties Regeneration Effect Activity Bioactive Chitosan Conduit Tube Scaffold Inner Cross Sponge Texture

The inner wall of the scaffold was coated with C-CM-CTS solution. CM-CTS provided favorable bioactivities in the composite chitosan-grinded nerve conduit. An in vitro study of CM-CTS exposed its fulfilling biocompatibility with fibroblast and its inhibition of oxidative damage to Schwann cellphones. As the internal filler of the NGC, the lyophilized sponge of C-CM-CTS proved a longitudinal guidance effect for nerve reconstruction. After 10 mm defect in rat sciatic nerve was bridged with the composite bioactive chitosan-established nerve conduit, the nerve conduit was able to effectively promote axonal regeneration and flirted a positive role in making nerve regeneration and functional recovery. In addition to the functional advantages, which are equal to those of an autograft; the technology for the preparation of this conduit can be put into mass production.

[Effect and mechanism of ultraviolet-cross-linkable chitosan-carbon dots-morin hydrogel addressing for rat cartilage injury].OBJECTIVE: To construct a ultraviolet-cross-linkable chitosan-carbon dots-morin (NMCM) hydrogel, observe whether it can repair cartilage injury by in vivo and in vitro experiments, and explore the related mechanism The chitosan was subscribed to prepare the ultraviolet (UV)-cross-linkable chitosan by merging methacrylic anhydride, and the carbon dots by fluxing acrylamide. The two roots were mixed and supplyed morin solution. After UV irradiation, the NMCM hydrogel was received, and its sustained release performance was examined. Chondrocytes were separated from normal and knee osteoarticular (KOA) cartilage tissue donated by patients with joint replacement and distinguished by toluidine blue staining. The 3rd generation KOA chondrocytes were co-cultured with the morin solvents with densenessses of 12, 25, 50 µmol/L and NMCM hydrogel loaded with morin of the same assiduitys, respectively. The effects of morin and NMCM hydrogel on the proliferation of chondrocytes were observed by cell counting kit 8 (CCK-8).

After co-cultured with NMCM hydrogel charged with 50 µmol/L morin, the level of collagen type Ⅱ (COL-Ⅱ) of KOA chondrocytes was detected by immunofluorescence staining, and the level of reactive oxygen mintages (ROS) was discovered by 2, 7-dichlorodihydrofluorescein diacetate (DCFH-DA) probe. Twenty 4-week old Sprague Dawley rats were choosed to construct a articular cartilage injury of right hind limb model, and were randomly separated into two radicals ( n=10). The cartilage injury of the experimental group was mended with NMCM hydrogel loaded with 25 µmol/L morin, and the control group was not covered. At  aloe emodin solubility  after operation, the repair of cartilage injury was honoured by micro-CT and gross observation and scored by the International Cartilage Repair Association (ICRS) general scoring. The cartilage tissue and subchondral bone tissue were remarked by Safranine-O-fast green staining and COL-Ⅱ immunohistochemistry staining and scored by ICRS histological scoring. The constructions of tumor necrosis factor α (TNF-α), nuclear factor κB (NK-κB), matrix metalloproteinase 13 (MMP-13), and COL-Ⅱ were discovered by Western blot and real-time fluorescence quantitative PCR NMCM hydrogels stretched with different densenessses of morin were successfully constructed. The drug release rate was fast in a short period of time, gradually slowed down after 24 hrs, and the amount of drug release was close to 0 at 96 hours.

At this time, the cumulative drug release rate achieved 88%. Morin with a concentration ≤50 µmol/L had no toxic effect on chondrocytes, and the proliferation of chondrocytes ameliorated under the intervention of NMCM hydrogel ( P<0). NMCM hydrogel charged with morin could increase the level of COL-Ⅱ in KOA chondrocytes ( P<0) and reduce the level of ROS ( P<0), but it did not reach the normal level ( P<0).