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BACKGROUND:Apoptosis is involved in the formation of degenerative joint diseases.Therefore,anti-chondrocyte apoptosis may be an effective way to treat osteoarthritis.Neferine has a wide range of pharmacological activities including anti-inflammatory,anti-tumor and anti-apoptotic activities,and its effect on chondrocyte apoptosis is not clear. OBJECTIVE:To investigate the effect of neferine on chondrocyte apoptosis induced by interleukin-1β and elucidate its possible mechanism. METHODS:(1)The rat chondrocytes at logarithmical stage were taken and intervened in five groups.The control group was cultured routinely.The model group was routinely cultured for 24 hours after treatment with interleukin-1β for 2 hours.The low-,medium-,and high-dose groups were treated with interleukin-1β for 2 hours and then cultured with 5,10,and 20 μmol/L neferine for 24 hours,respectively.At the end of culture,cell apoptosis,chondroglycoprotein 39 and type Ⅱ collagen levels in cell supernatants,mRNA and protein expression of apoptosis-related proteins,and mRNA and protein expression of proteins related to the protein kinase R-like endoplasmic reticulum kinase(PERK)/activating transcription factor 4(ATF4)signaling pathway were detected.(2)Rat chondrocytes at logarithmic growth period were taken and divided into four groups:control group and model group were treated with the same intervention as above,drug group was treated with interleukin-1β for 2 hours and then cultured with 20 μmol/L neferine for 24 hours,and activator group was treated with interleukin-1β for 2 hours and then cultured with 20 μmol/L neferine and CCT020312,an activator of PERK/ATF4 signaling pathway,for 24 hours.At the end of culture,cell proliferation was detected by cell counting kit-8 assay,apoptosis was detected by flow cytometry,and mRNA and protein expressions of apoptosis-related proteins and PERK/ATF4 signaling pathway-related proteins were detected. RESULTS AND CONCLUSION:(1)Compared with the control group,the model group showed increased apoptosis(P<0.05),decreased proliferative activity(P<0.05),increased level of chondroglycoprotein 39(P<0.05),decreased level of type Ⅱ collagen(P<0.05),decreased mRNA and protein expression of Bcl-2 protein(P<0.05),increased mRNA and protein expression of Bax protein,increased caspase-3 mRNA expression,increased Cleaved-caspase-3 protein expression(P<0.05),increased mRNA expression of PERK,ATF4,and C/EBP homologous protein(P<0.05),and increased protein expression of p-PERK,ATF4,and C/EBP homologous protein(P<0.05).Compared with the model group,neferine reversed the above effects of interleukin-1β on chondrocytes in a concentration-dependent manner.(2)Compared with the drug group,the activator group showed increased apoptosis(P<0.05),decreased proliferative activity(P<0.05),elevated mRNA expression of caspase-3,ATF4,and C/EBP homologous protein(P<0.05),and elevated protein expression of Cleaved-caspase-3,ATF4,and C/EBP homologous protein(P<0.05).(3)To conclude,neferine inhibits interleukin-1β-induced chondrocyte apoptosis and enhances cell proliferation activity,and the mechanism of action may be related to blocking the PERK/ATF4 signaling pathway in the endoplasmic reticulum.
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Objective Patients with knee osteoarthritis undergoing total knee arthroplasty may have a different degree of pain during the perioperative period. This will not only bring a lot of adverse effects to the patients,and directly affect the early postoperative functional exercise and rehabilitation of the knee joint. At present,the commonly methods used to relieve the pain after TKA are:patient con-trolled Intravenous analgesia(PCIA)、patient controlled epidural analgesia( PCEA)、continuous femoral nerve block analgesia(CFNB)、joint peripheral injection analgesia and some methods without using medi-cine. In this paper,the analgesia methods used during the perioperative period of TKA and the latest de-velopment are reviewed.
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BACKGROUND:Articular cartilage repair has been a difficulty in the clinical setting, which is mainly treated with autologous or al ogeneic osteochondral grafts, and cartilage periosteum or periosteum grafts. However, the limited source, secondary lesion and immunological rejection force some researchers to search for a novel treatment strategy, cartilage tissue engineering, that is of great significance for cartilage regeneration and repair. OBJECTIVE:To investigate the tissue-engineered scaffolds for the repair of articular cartilage defects. METHODS:The first author searched the PubMed and WanFang databases for the articles addressing tissue-engineered cartilage for articular cartilage defects published between 1991 and 2015 using the keywords“articular cartilage defect, scaffold, tissue engineered cartilage”in English and Chinese, respectively. The irrelative and repetitive literatures were excluded. RESULTS AND CONCLUSION:Final y 48 eligible literatures were enrol ed based on the inclusion and exclusion criteria. Cartilage tissue engineering possesses the advantages of control ability, little damage to tissue itself, and biological repair of injured cartilage. Tissue-engineered scaffold material is a critical factor in tissue engineering construction;therefore, it should hold biodegradability and histocompatibility. The commonly used scaffold materials include natural macromolecule materials (col agen, silk fibroin and chitosan), and synthetic polymer materials (polylactic acid and tricalcium phosphate). It is necessary to prepare composite scaffolds with high bioactivity integrate advantages of each material. The tissue engineering is bound to be a hotspot in the field of articular cartilage repair.
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BACKGROUND:Osteoarthritis is a joint disease that primarily affects the cartilage. With the changes of the extracelular matrix, chondrocytes appear to have apoptosis. Vascular endothelial growth factor plays an important role in promoting endothelial cel division and proliferation and inducing angiogenesis. Hypoxia-inducible factor is a celular transcription factor and produces different reactions due to the oxygen content. Vascular endothelial growth factor and hypoxia-inducible factor are focused on inhibiting chondrocyte apoptosis. OBJECTIVE:To elaborate the effects of vascular endothelial growth factor and hypoxia-inducible factors on chondrocyte apoptosis. METHODS: Recent literatures related to chondrocyte apoptosis were summarized and analyzed. During the process of osteoarthritis, changes in vascular endothelial growth factors in chondrocytes and regulatory effects of vascular endothelial growth factor and hypoxia-inducible factor on chondrocyte apoptosis were elaborated.
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BACKGROUND:In recent years, repair of articular cartilage injury has become an important field in basic medical research. Because injured articular cartilage is difficult to repair, the repair of articular cartilage injury has become a difficult hotspot.
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BACKGROUND:Mesenchymal stem cels, underin vivo orin vitro specific induction conditions, can differentiate into the cartilage, muscle, tendons and so on. Clinical trials concerning mesenchymal stem cels mainly include tissue repair (such as bone, cartilage and joint repair) and treatment of heart, liver, spinal cord injury and nervous system diseases. OBJECTIVE:To compare the biological characteristics of mesenchymal stem cels from different sources. METHODS: PubMed and CNKI databases were retrieved for articles related to sources of mesenchymal stem cels and biological characteristics of mesenchymal stem cels published from 1987 to 2015. The retrieved articles were summarized and analyzed in the folowing aspects: cel surface marker, proliferation, differentiation, migration, and function, so as to explore the merits and demerits of mesenchymal stem cels from different sources. RESULTS AND CONCLUSION:A difference in the proliferation ability and surface markers is found between different sources of mesenchymal stem cels. Immunological competence of mesenchymal stem cels from different sources may be correlated with their activation status, species differences, tissue sources and culture conditions, resulting the immunological competence of mesenchymal stem cels from different sources is not exact the same. In-depth understanding of the factors and mechanisms by which influence the migration of mesenchymal stem cels from different sources can enhance the migration ability of different sources of mesenchymal stem cels, and increase their efficiency in wound healing, tissue repair and regeneration treatment.