Allicin Attenuated Advanced Oxidation Protein Product-Induced Oxidative Stress and Mitochondrial Apoptosis in Human Nucleus Pulposus Cells

Figure 6

Allicin alleviated AOPP-induced oxidative stress and mitochondrial dysfunction via p38-MAPK pathway in human NP cells. (a) The human NP cells were pretreated with allicin (10 μM) or p38-MAPK inhibitor SB202190 (10 μM) for 2 h, then treated with AOPP (400 μg/ml) for 24 h. The cell proliferation was determined using EdU staining combined with DAPI staining for the nuclei under fluorescence microscope, with the EdU positive cells quantitated. Original magnification: ×200. (b) Representative images of immunofluorescence staining for cleaved caspase-3 in each group, with the relative fluorescence intensity quantified. Original magnification: ×400. (c) The intracellular ROS levels of the NP cells for each group were detected by ROS-specific fluorescent probe DHE and measured by subsequent flow cytometry analysis. (d) The mitochondrial membrane potential of human NP cells in each group was examined by JC-1 staining and measured by subsequent flow cytometry analysis. Representative scatter plots of flow cytometry and the quantitative analysis of red fluorescence to green fluorescence ratio were shown. Data were represented as . ^# and ^## versus the control group; and versus the AOPP alone treatment group, .

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