Abstract
Bone degradation is a serious complication of chronic inflammatory diseases such as septic arthritis, osteomyelitis, and infected orthopedic implant failure. Effective therapeutic treatments for bacteria-caused bone destruction are limited. In a previous study, we found that lipopolysaccharide (LPS) induced osteoblast apoptosis and inhibited early and late-stage differentiation of osteoblasts via activation of the C-Jun N-terminal kinase (JNK) pathway. This study aimed to investigate the effect of JNK inhibition by SP600125 on the apoptosis and differentiation of MC3T3-E1 osteoblasts suppressed by LPS. Following pretreatment with SP600125 for 2 h, MC3T3-E1 cells were treated LPS. Following this treatment, cell viability, activity of alkaline phosphatase (ALP) and caspase-3 were measured. mRNA and protein expression of osteoblast-specific genes, mitogen-activated protein kinases (MAPKs), Bax, Bcl-2 and caspase-3 were determined by quantitative polymerase chain reaction (qPCR) and western blot analysis. The results showed that SP600125 significantly restored LPS-inhibited cell metabolism and ALP activity and reduced the upregulated caspase-3 activity of MC3T3-E1 cells induced by LPS. SP600125 also significantly restored the LPS-s...Continue Reading
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