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Schematic presentation indicating the suggested mechanisms by which inhibit NF-κB-induced SKM-1 cell apoptosis by ATO combined with TL. The combined effect of TL and ATO inhibits the NF-κB signaling pathway, promotes the expression of p65, further inhibits the expression of IkBα, p52, and RelB, further upregulates the expression of Caspase-3, Caspase-8, PARP, downregulates the expression of Bcl-2, Bcl-XL, and cIAP1, and ultimately promotes SKM-1 cell apoptosis.

Journal: Medicine

Article Title: Triptolide combined with arsenic trioxide induces apoptosis of myelodysplastic syndrome cells by inhibiting the NF-κB signaling pathway

doi: 10.1097/MD.0000000000046206

Figure Lengend Snippet: Schematic presentation indicating the suggested mechanisms by which inhibit NF-κB-induced SKM-1 cell apoptosis by ATO combined with TL. The combined effect of TL and ATO inhibits the NF-κB signaling pathway, promotes the expression of p65, further inhibits the expression of IkBα, p52, and RelB, further upregulates the expression of Caspase-3, Caspase-8, PARP, downregulates the expression of Bcl-2, Bcl-XL, and cIAP1, and ultimately promotes SKM-1 cell apoptosis.

Article Snippet: Western blot, qPCR, and BCA protein assay kits were obtained from Nanjing Vazyme Biotech Co., Ltd. Antibodies targeting apoptosis proteins like Bcl-2, Bcl-XL, cIAP1, Caspase-3, Caspase-8, and poly ADP-ribose polymerase (PARP), as well as those for NF-κB pathway proteins including IkBα, p65, p52, and RelB, were obtained from Proteintech Group, Inc.

Techniques: Expressing