| Backgroud:Ion channels are all kinds of inorganic ions of passive transport across a cell membrane. The passways of inorganic ions across the membrane have passive transport (along the ion concentration gradient) and active transport (inverse ion concentration gradient). Passive transport pathway was called ion channels, active transport vehicle was called ion pump of ions. Biological membrane permeability of ions with various activities was closely related to the life process.Cell ion channels, the structure and function of normal is to maintain life process. Genetic mutations and dysfunction of the ion channels is related to many diseases. Ion channels have some main types:potassium, sodium, calcium, chloride, and the nonselectivity cationic ion channels, and every channel have certain subtypes. The main functions of ion channels are:improving cell calcium concentration, triggering the physiological effect, determining the cell excitability, refractoriness and conductivity, adjusting vascular of smooth muscle vasomotion activities, participating in synaptic transmission, maintaining the normal cell volume. The main research methods of ion channels are:certain block, patch clamp technique, molecular biology technology, fluorescence probe calcium image analysis technology.Ion channel disease refers to the structure or function of ion channel abnormalities. Changes of ion channel in disease is due to some disease or drug-induced one or a few number of ion channels functional or structural changes, leading to the occurrence or the body to correct some of pathological changes. From the perspective of the relationship between ion channels and disease strengthening of molecular biology, biophysics, genetics, pharmacology and many other interdisciplinary in-depth study, for in-depth to explore the pathophysiology of certain diseases, early diagnosis and discovery of drugs or specific treatment Measures have great theoretical and practical significance.A large number of studies have found variety of different ion channels the same in other excitable cells on the membrane of articular cartilage. These ion channels and cartilage cells are closed related to life activities of Chondrocytes. Ion channels themselves and their blockers on cartilage cell proliferation, Apoptosis and metabolism also have significant impact. These evidents from the other side show ion channels and cartilage-related diseases are closely linked. By ion channel blockers on the metabolism of cartilage cells researching could explore the effects of ion channels in the cartilage-related diseases such as osteoarthritis in the pathogenesis and the process. These could provide the seed cells for cartilage tissue engineering in a new cultured way. The method can also in-depth study of ion channels in the cartilage cells in the mechanism of life activities and provide a theoretical basis for clinical treatment of articular cartilage-related diseases and provide a theoretical basis for drug development, but also for the clinical application of ion-channel blocker drug delivery application of the guidance.Objectives:Block rabbit articular cartilage cells sodium ion channels with 0.2mmol/L lidocaine. Observe the impact on cartilage cell apoptosis in vitro culture, specific metabolites Glycosaminoglycan (GAG) and Collagen typeⅡ. From the perspective of ion channel clarify the physiology of the sodium ion channels activity in the cartilage cells, in order to further clarify its effect on articular cartilage-related diseases such as osteoarthritis, to explore the pathogenesis of OA with a view from this area.Methods:Chondrocytes were isolated from the knee joints of five two-month New Zealand White Rabbit knees with sterile operation. Divide into control group and 0.2mmol/L lidocaine group, Cell density of 2×106/ml, vitro culture. Detect the apoptosis of chondrocytes at 24h and 48h. The GAG and Collagen typeⅡconcentrations of supernatants were measured at 3,6,9 day.Results:0.2mmol/L Lidocaine has no effect on apoptosis of chondrocytes (p>0.05). The secretion of GAG was inhibited by Lidocaine at the 3th day(p<0.05) but was accelerated at the 9th day(p<0.05); Compared with the control groupe, the secretion of Collagen typeⅡof Lidocaine group has reduce trend but no Statistical differences(p>0.05).Conclusions:0.2mmol/L Lidocaine has no effect on apoptosis of chondrocytes.The secretion of GAG was inhibited by Lidocaine at Short-term culture,but accelerated at long-term culture; Lidocaine also has no effect on the secretion of Collagen type II. |
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