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. 2021 Aug 28;27:96. doi: 10.1186/s10020-021-00360-w

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Activation of GPER reduces the apoptosis of chondrocytes induced by mechanical stress. a Cell viabilities for chondrocytes treated with mechanical stress, 8 μM estrogen, and 8 μM G15 (n = 3). b Protein expression of Bax and Bcl-2 for chondrocytes treated with mechanical stress, 8 μM estrogen, and 8 μM G15 (n = 3). c Cell viabilities for chondrocytes with GPER or scrambled siRNA after treatment with mechanical stress, and estrogen (n = 3). d Protein expression of Bax and Bcl-2 for chondrocytes with GPER or scrambled siRNA after treatment with mechanical stress, and estrogen (n = 3). e Cell viabilities for chondrocytes treated with mechanical stress, 10 μM G-1, and 8 μM G15. f Protein expression of Bax and Bcl-2 for chondrocytes treated with mechanical stress, 10 μM G-1, and 8 μM G15. g Cell viabilities for chondrocytes with GPER or scrambled siRNA after treatment with mechanical stress, and G-1 (n = 3). h Protein expression of Bax and Bcl-2 for chondrocytes with GPER or scrambled siRNA after treatment with mechanical stress, and G-1 (n = 3). All data are presented in mean ± SD (n = 3). *P < 0.05, compared with DMSO group. **P < 0.01, compared with DMSO group. ^#P < 0.05, compared with mechanical stress + DMSO group. ^##P < 0.01, compared with mechanical stress + DMSO group

Fig. 3 — Activation of GPER reduces the apoptosis of chondrocytes induced by mechanical stress. a Cell viabilities for chondrocytes treated with mechanical stress, 8 μM estrogen, and 8 μM G15 (n = 3). b Protein expression of Bax and Bcl-2 for chondrocytes treated with mechanical stress, 8 μM estrogen, and 8 μM G15 (n = 3). c Cell viabilities for chondrocytes with GPER or scrambled siRNA after treatment with mechanical stress, and estrogen (n = 3). d Protein expression of Bax and Bcl-2 for chondrocytes with GPER or scrambled siRNA after treatment with mechanical stress, and estrogen (n = 3). e Cell viabilities for chondrocytes treated with mechanical stress, 10 μM G-1, and 8 μM G15. f Protein expression of Bax and Bcl-2 for chondrocytes treated with mechanical stress, 10 μM G-1, and 8 μM G15. g Cell viabilities for chondrocytes with GPER or scrambled siRNA after treatment with mechanical stress, and G-1 (n = 3). h Protein expression of Bax and Bcl-2 for chondrocytes with GPER or scrambled siRNA after treatment with mechanical stress, and G-1 (n = 3). All data are presented in mean ± SD (n = 3). *P < 0.05, compared with DMSO group. **P < 0.01, compared with DMSO group. ^#P < 0.05, compared with mechanical stress + DMSO group. ^##P < 0.01, compared with mechanical stress + DMSO group