Millimeter Wave Treatment Inhibits Apoptosis of Chondrocytes via Regulation Dynamic Equilibrium of Intracellular Free Ca²⁺

Abstract

The molecular mechanisms of TNF-α-induced apoptosis of chondrocyte and the role of Ca2+ mediating the effects of MW on TNF-α-induced apoptosis of chondrocytes remained unclear. In this study, we investigated the molecular mechanism underlying inhibiting TNF-α-induced chondrocytes apoptosis of MW. MTT assay, DAPI, and flow cytometry demonstrated that MW significantly increased cell activity and inhibited chromatin condensation accompanying the loss of plasma membrane asymmetry and the collapse of mitochondrial membrane potential. Our results also indicated that MW reduced the elevation of [Ca2+]i in chondrocytes by LSCM. Moreover, MW suppressed the protein levels of calpain, Bax, cytochrome c, and caspase-3, while the expressions of Bcl-2, collagen II, and aggrecan were increased. Our evidences indicated that MW treatment inhibited the apoptosis of chondrocytes through depression of [Ca2+]i. It also inhibited calpain activation, which mediated Bax cleavage and cytochrome c release and initiated the apoptotic execution phase. In addition, MW treatment increased the expression of collagen II and aggrecan of chondrocytes.

Icariin Activates Autophagy via Down-Regulation of the NF-κB Signaling-Mediated Apoptosis in Chondrocytes

“…The present study results consistent with previous studies which showed that TNF-α induced chondrocyte apoptosis via upregulated expression level of ROS and NO. In addition, previous studies, as well as the current study, have demonstrated that TNF-α induced the pro-apoptotic protein Bax production and reduced the anti-apoptotic protein Bcl-2 production, leading to hypercatabolism in chondrocytes ( Ye et al, 2015 ). It should be noted that there are other proinflammatory cytokines contribute to the autophagy suppression and apoptosis induction in OA ( Goldring and Otero, 2011 ).…”

Cibotium barometz polysaccharides stimulate chondrocyte proliferation in vitro by promoting G1/S cell cycle transition

“…Considering that chondrocytes are responsible for secreting extracellular matrix, and the maintenance of cartilage homeostasis is involved in the pathological characteristics of OA, promoting chondrocyte proliferation may be a prospective and potential method for the treatment of OA (19–21). …”

“…The incidence of osteoarthritis (OA) still poses a major public health challenge throughout the world, and, currently there is no thoroughly effective therapy available. Considering that chondrocytes are responsible for secreting extracellular matrix, and the maintenance of cartilage homeostasis is involved in the pathological characteristics of OA, promoting chondrocyte proliferation may be a prospective and potential method for the treatment of OA ( 19 – 21 ).…”