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Here's a breakdown of what the study found, how the protocol worked, and why this data matters

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Mcl-1 inhibits apoptosis through the inhibition of Bax

Red - loading control ab8245 (Mouse anti-GAPDH antibody [6C5]) observed at 37 kDa

The targeting construct was then transfected into embryonic stem cells

However, unlike previous findings, shikonin, icariin, and other drugs induce mitochondrial dysfunction by increasing ROS levels, decreasing mitochondrial membrane potential, and elevating the release of cytochrome C and pro-apoptotic proteins, such as caspase-3 and caspase-9, to induce apoptosis in FLSs to suppress inflammatory response (265, 266)