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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Apoptosis, Apoptosis Regulatory Proteins, Autophagy, Beclin-1, Caspase 3, Caspase 9, Cell Line, Cytochromes c, Diterpenes, Endothelial Cells, Glutathione, Humans, JNK Mitogen-Activated Protein Kinases, Kidney Tubules, Proximal, Membrane Potential, Mitochondrial, Membrane Proteins, Proto-Oncogene Proteins c-bcl-2, Reactive Oxygen Species, Sulfates, Superoxide Dismutase, bcl-2-Associated X Protein.
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Is andrographolide sodium bisulfate-induced apoptosis and autophagy in human proximal tubular endothelial cells a ROS-mediated pathway? Context: The nephrotoxic mechanisms of andrographolide sodium bisulfate (ASB) remain largely unknown. This study attempted to explore the mechanism of ASB-induced nephrotoxicity using human proximal tubular endothelial cells (HK-2). For this study HK-2 cells were treated with rising concentrations of ASB. Their survival rate was detected using MTT assay and ultrastructure was observed with electron microscopy. L-Lactate dehydrogenase (LDH) assay was followed by examination of mitochondrial membrane potential (MMP). Reactive oxygen species (ROS) was detected using different methods and apoptosis/autophage related proteins were detected using immunoblotting. We found that ASB inhibited HK-2 cell proliferation and decreased cell survival rate in a time and dose-dependent manner (P<0.05, P<0.01, respectively). With increasing ASB concentration, cell structure was variably damaged and evidence of apoptosis and autophagy were observed. MMP gradually decreased and ROS was induced. The expression of JNK and Beclin-1 increased and activation of the JNK signaling pathway were seen. Apoptosis was induced via the mitochondrial-dependent caspase-3 and caspase-9 pathway, and autophagy related protein Beclin-1 was enhanced by ASB.
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The data show that ASB induces high levels of ROS generation in HK-2 cells and activates JNK signaling. Furthermore, ASB induces cell apoptosis via the caspase-dependent mitochondrial pathway, and induces cellular autophagy, in part by enhancing Beclin-1 protein expression. Final Decision: yes