Mechanisms of palmitate-induced cell death in human osteoblasts

Mechanisms of palmitate-induced cell death in human osteoblasts

Lipotoxicity is an overload of lipids in non-adipose tissues that affects function and induces cell death. Lipotoxicity has been demonstrated in bone cells in vitro using osteoblasts and adipocytes in coculture. In this condition, lipotoxicity was induced by high levels of saturated fatty acids (mostly palmitate) secreted by cultured adipocytes acting in a paracrine manner. In the present study...

Dexmedetomidine attenuates H2O2-induced cell death in human osteoblasts

BACKGROUND Reactive oxygen species play critical roles in homeostasis and cell signaling. Dexmedetomidine, a specific agonist of the α2-adrenoceptor, has been commonly used for sedation, and it has been reported to have a protective effect against oxidative stress. In this study, we investigated whether dexmedetomidine has a protective effect against H2O2-induced oxidative stress and the mechan...

Cell Death in Chondrocytes, Osteoblasts, and Osteocytes

Cell death in skeletal component cells, including chondrocytes, osteoblasts, and osteocytes, plays roles in skeletal development, maintenance, and repair as well as in the pathogenesis of osteoarthritis and osteoporosis. Chondrocyte proliferation, differentiation, and apoptosis are important steps for endochondral ossification. Although the inactivation of P53 and RB is involved in the pathogen...

Neuroprotective effect of topiramate against 6-hydroxydopamine-induced cell death in Parkinson's disease cell mode

Introduction: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by progressive neuronal dysfunction. Growing evidence has shown that oxidative stress plays a crucial role in the pathogenesis of Parkinson's disease. Correspondingly, the current study evaluated the protective effect of topiramate in 6-hydroxydopamine induced oxidative stress and apoptosis in PC12 cells...

Neuronal death and survival - targeting glutamate-induced cell death mechanisms