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Fig. 2 | Journal of Orthopaedic Surgery and Research

Fig. 2

From: MiR-4303 relieves chondrocyte inflammation by targeting ASPN in osteoarthritis

Fig. 2

MiR-4303 overexpression rescues LPS-inhibited chondrocyte viability, proliferation and cell cycle and alleviates LPS-induced chondrocyte apoptosis. Chondrocytes were randomly divided into four groups, control group; chondrocytes were untreated; LPS group, 1 × 105 chondrocytes were treated with 10 μL LPS (100 ng/mL); NC mimic + LPS group, 1 × 105 chondrocytes were treated with 10 μL LPS (100 ng/mL) and 100 nM NC mimics; miR-4303 mimic + LPS group, 1 × 105 chondrocytes were treated with 10 μL LPS (100 ng/mL) and 100 nM miR-4303 mimics. Untreated chondrocytes served as the negative control for LPS-treated chondrocytes; NC mimics served as the negative control for miR-4303 mimics. A RT-qPCR was performed to assess the levels of miR-4303. B CCK-8 assay was conducted to evaluate cell viability. C EdU assay was carried to measure cell proliferation. D Western blot was conducted to measure the levels of proliferation-related proteins, including PCNA and Ki-67. E FACs were performed to evaluate the distribution of chondrocytes in each cell cycle. F Western blot was conducted to measure the levels of cell cycle-related proteins, including CyclinA1, CyclinB1, CyclinD2 and p27. G FACs were conducted to assess chondrocytes apoptosis. H Western blot was performed to detect the levels of apoptosis-related proteins, including Bax, Bcl-2, Cleaved-casapase3 and Cleaved-casapase9. Tukey post-test was used for comparison between multiple groups. *P < 0.05, **P < 0.01 versus control group; #P < 0.05, ##P < 0.01 versus NC mimic + LPS group. Error bars represented SD. Data represented three independent experiments

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