Abstract: Objective: To investigate the molecular mechanism of 30 kPa hydrostatic pressure regulating the proliferation and apoptosis of condylar chondrocytes. Methods: Rat condylar chondrocytes were cultured in vitro. Cells divided into four groups: normal pressure group, 30 kPa pressure group, KN93 control group, and 30 kPa pressure+KN93 group. EdU labeling method was used to measure cell proliferation. Flow cytometry was used to detect the proportion of cell apoptosis. Fluorescence probe method was used to detect intracellular Ca²⁺ levels. Western blot was used to detect the expression of CaMK Ⅱ, p-c-Jun, c-Jun, p-ERK1/2, ERK1/2, p-p38, and p38 proteins in cells. Results: Compared with the normal pressure group, the cell proliferation rate in the 30 kPa pressure group decreased, the cell apoptosis rate increased significantly, the intracellular Ca²⁺ levels increased significantly, the expression of CaMK Ⅱ protein was upregulated, and the ratios of (p-c-Jun)/(c-Jun), (p-ERK1/2)/(ERK1/2), and (p-p38)/(p38) were all increased (P<0.01). Compared with the 30 kPa pressure group, the cell proliferation rate in the 30 kPa pressure+KN93 group was increased, the cell apoptosis rate decreased, the intracellular Ca²⁺ level decreases, the expression of CaMK Ⅱ protein was downregulated, and the ratios of (p-c-Jun)/(c-Jun), (p-ERK1/2)/(ERK1/2), and (p-p38)/(p38) were all reduced (P<0.01). Conclusion: The sustained effect of 30 kPa hydrostatic pressure can inhibit condylar chondrocytes proliferation, promote cell apoptosis, and increase intracellular Ca²⁺ levels. The mechanism of action may be that Ca²⁺ activates the MAPK signaling pathway through CaMK Ⅱ.

Key words: chondrocytes, hydrostatic pressure, proliferation, apoptosis, MAPK signaling pathway