Apoptosis is a basic biological phenomenon of cells, which plays an important role in the evolution of biology, the stability of the internal environment and the development of multiple systems. K + is the main cation in the cell, and K + outflow will occur during apoptosis. Preventing the loss of K + can effectively inhibit the development of apoptosis. In 2009, scientists in Mexico and Australia used "non-damaging micro-measurement technology" and patch clamp to study apoptosis, and found that 1μM STS (cross-sporine) will quickly cause K + outflow, peaking in about 15 minutes, and then weakened. At the same time, it was recorded that the current of the Kbg channel increased, accompanied by a sharp decrease in membrane depolarization. The current of Kv1.3 is not affected by STS, but this inactive channel is converted to more positive potential. The contribution of Kbg and Kv1.3 channels to STS-induced K + outflow has a chronological relationship. Bupivacaine (bupivacaine) mainly inhibits Kbg current, and margatoxin (margaret toxin) is a specific inhibitor of Kv1.3. The channel regulates the K + outflow to cause the contraction of the cell, activating the cysteine ​​protease (apoptosis protease), so that the cell changes from a normal physiological state to an apoptotic physiological state, and then to a non-physiological state. The environment inside the cell changes rapidly, such as cell size, membrane potential, pH, and Ca2 + concentration, and the mechanism of K + regulation is crucial in the change of the cell environment. The Kbg channel regulates the early K + outflow. The Kv1.3 channel plays a major role in the later period. After the K + outflow is inhibited, it completely stops, and the activity of caspase-3 also changes. This research provides new evidence for understanding the internal mechanism of apoptosis. This real-time and easy-to-operate research method is expected to diagnose or detect apoptotic cells in clinical and other practical applications. Keywords: staurosporine (STS, staurosporine), Jurkat cells (T cells), Kbg and Kv1.3 channels References: Valencia-Cruz G, et al. Am J Physiol Cell Physiol, 2009, 297: C1544–C1553
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