AI Article Synopsis

  • The study explored how l-cystathionine affects the death of human macrophages triggered by oxidized low-density lipoprotein (ox-LDL).
  • It involved differentiating THP-1 cells into macrophages and examining changes in superoxide anion levels, apoptosis, and mitochondrial functions after treatment with ox-LDL.
  • Results showed that l-cystathionine significantly reduced harmful effects like superoxide production and apoptosis, indicating its potential protective role against macrophage death caused by ox-LDL.

Article Abstract

This study was designed to investigate the regulatory role of l-cystathionine in human macrophage apoptosis induced by oxidized low density lipoprotein (ox-LDL) and its possible mechanisms. THP-1 cells were induced with phorbol 12-myristate 13-acetate (PMA) and differentiated into macrophages. Macrophages were incubated with ox-LDL after pretreatment with l-cystathionine. Superoxide anion, apoptosis, mitochondrial membrane potential, and mitochondrial permeability transition pore (MPTP) opening were examined. Caspase-9 activities and expression of cleaved caspase-3 were measured. The results showed that compared with control group, ox-LDL treatment significantly promoted superoxide anion generation, release of cytochrome c (cytc) from mitochondrion into cytoplasm, caspase-9 activities, cleavage of caspase-3, and cell apoptosis, in addition to reduced mitochondrial membrane potential as well as increased MPTP opening. However, 0.3 and 1.0 mmol/L l-cystathionine significantly reduced superoxide anion generation, increased mitochondrial membrane potential, and markedly decreased MPTP opening in ox-LDL + l-cystathionine macrophages. Moreover, compared to ox-LDL treated-cells, release of cytc from mitochondrion into cytoplasm, caspase-9 activities, cleavage of caspase-3, and apoptosis levels in l-cystathionine pretreated cells were profoundly attenuated. Taken together, our results suggested that l-cystathionine could antagonize mitochondria-mediated human macrophage apoptosis induced by ox-LDL via inhibition of cytc release and caspase activation.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4284754PMC
http://dx.doi.org/10.3390/ijms151223059DOI Listing

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