The antioxidant transcription factor Nrf2 contributes to the protective effect of mild thermotolerance (40°C) against heat shock-induced apoptosis.

摘要: The exposure of cells to low doses stress induces adaptive survival responses that protect against subsequent toxic stress. ability resist following dose heat at 40°C is known as mild thermotolerance. Mild thermotolerance involves increased expression shock proteins and antioxidants, but the initiating factors in this response are not understood. This study aims understand role Nrf2 antioxidant pathway acquisition 40°C, secondly, whether could be involved protective effect heat-shock (42°C)-induced apoptosis. During cell preconditioning protein transcription factor after 15-60min. In addition, levels targets MnSOD, catalase, heme oxygenase-1, glutamate cysteine ligase Hsp70 40°C. Levels these were enhanced by activator oltipraz decreased shRNA targeting Nrf2. pro-oxidants 30-60min Pro-oxidant knockdown Increased catalase activity inhibited PEG-catalase p53 inhibitor pifithrin-α. These results suggest (40°C) increases cellular pro-oxidant levels, which turn activate its target genes. Moreover, contributes apoptosis, because activation thermotolerance, whereas partly reversed Improved knowledge about different mechanisms can crucial for potential use treat stress-related diseases.