Tripterine enhances regulatory effect of TNF-a on Caspase-3 and induces apoptosis of lung cancer cell

Lung cancer is a common malignancy of the respiratory system with a high morbidity and mortality. We intended to identify the apoptosis-promoting role of tripterine in lung cancer. Lung cancer SPC-A-1 cells were exposed to low, moderate, and high dosage of tripterine (2, 5 and 10 mu mol/L) with the model group not being intervened. After treatment, the role of tripterine in SPC-A-1 cell apoptosis was observed. In addiIP: 203 8 10920 On: Tue 12 Sep 2023 02:31:34 tion, lung cancer cells were transfectedCopyr gh:with TNF-a American mimic Scientific (pc-TNF-a Publishers group) and TNF-a inhibitor (si-TNF-a group). Tripterine +pc-TNF-a group was set up to determinthe interaction between tripterine and TNF-a. Delive ed by Inge nta The cell survival rate, TNF-a and Caspase-3 expression levels then were detected by MTT and flow cytometry. Tripteryglide treatment dose-dependently decreased lung cancer cell viability and induced cell apoptosis, resulting in an increase of TNF-a expression. However, when TNF-a expression was inhibited upon transfection, SPC-A-1 cell apoptosis was suppressed. TNF-a mimics activated apoptosis and up-regulated Caspase-3 expression. Combination of tripteryglide and TNF-a mimics more significantly elevated apoptotic rate of lung cancer cells when elevating the content of Caspase-3. SPC-A-1 cells are highly sensitive to TNF-a and TNF-a significantly increases the activity and expression of Caspase-3. Tripteryglide can up-regulate TNF-a expression to facilitate lung cancer cell apoptosis and increase Caspase-3 expression.