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Metformin Delays The Aging Process Of Chondrocytes And Promotes The Secretion Of Cartilage Matrix By Chondrocytes

Posted on:2020-10-11Degree:MasterType:Thesis
Country:ChinaCandidate:K TangFull Text:PDF
GTID:2404330605974801Subject:Surgery
Abstract/Summary:PDF Full Text Request
Objective:Cartilage is a tissue composed of chondrocytes and interstitial cells.The matrix in the cartilage is in a gel state and has strong toughness.In patients with osteoarthritis(OA),the joints and surrounding tissues gradually degenerate,and the articular cartilage and joints also degenerate.When the balance between joint tissue repair and tissue destruction is interrupted,the articular cartilage will appear to fall off,the subchondral bone will gradually reshape,and the osteophyte will form eventually;thus,the ligaments around the joints will be loosened and the muscles around the joints will be weakened.When the above irreversible damage continues to develop,OA will eventually form.Metformin can exert systemic anti-inflammatory effects,reduce inflammatory factor levels,and increase anti-inflammatory factor levels.It also reduces inflammatory factor-mediated cartilage breakdown,maintains cartilage homeostasis,and protects cartilage.This study was designed to investigate whether metformin can promote the secretion of extracellular matrix in chondrocytes in vitro and whether metformin can delay the process of chondrocyte senescence.Methods:Primary rabbit chondrocytes were obtained from the knee joint of New Zealand white rabbits.Primary cells were digested and passaged to obtain P1 generation of rabbit chondrocytes,and P1 rabbit chondrocytes were cultured into cell pellet and cultured.Different concentrations of metformin(1,10,100,1000?mol/L)were added during the process.After 14 days of culture,safranin O staining and immunohistochemical staining were performed to observe whether metformin could promote the expression of extracellular matrix of the rabbit chondrocytes.Then,CCK-8 experiment and RT-PCR experiment were carried out to observe the morphology of chondrocytes,and to detect whether different concentrations of metformin have an effect on the proliferation ability of chondrocytes.Finally,different concentrations of H2O2 were induced topremature senility of rabbit chondrocytes.After determining the optimal premature aging concentration,different concentrations of metformin were added to premature senescent cells,and?-galactosidase staining and DAPI staining were used to detect cells.The ratio of positive senescent cells was calculated by calculating the number of positive cells.To study and observe whether metformin has an effect on the aging process of chondrocytes.Results:Through Safranin O staining and immunohistochemical staining,we found that metformin can promote the secretion of extracellular matrix by rabbit chondrocytes to a certain extent.It can be seen from CCK-8 that metformin can promote the proliferation of rabbit chondrocytes to some extent.Through H2O2 induced rabbit chondrocyte premature aging experiment,we can conclude that the biological activity of premature aging rabbit chondrocytes can be manifested by adding different concentrations of metformin.It can be seen that metformin has a certain ability to delay the aging process of premature senility chondrocyte.Conclusion:Metformin can delay the aging process of premature senile chondrocyte and promote chondrocyte to secrete extracellular matrix such as collagen II.
Keywords/Search Tags:Chondrocytes, metformin, osteoarthritis, premature aging, type ? collagen
PDF Full Text Request
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