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

Figure 7

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 allicin (10 μM) in combination with p38-MAPK activator Dehydrocorydaline chloride (Dc, 500 nM) for 2 h, then treated with AOPP (400 μg/ml) for 24 h. The cell proliferation was determined by EdU staining combined with DAPI staining for the nuclei under fluorescence microscope, with the EdU positive cells quantitated. Original magnification: ×200. (b) The cell apoptosis rate was detected by flow cytometry with Annexin V-FITC/PI dual staining. The proportion of apoptotic cells in the first and fourth quadrant was measured for analysis. (c) The intracellular ROS levels 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. Data were represented as . ^## versus the control group, and versus the AOPP alone treatment group, and ^& and ^&& versus the AOPP+allicin treatment group, .

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