动物造模,急性重症一氧化碳 z-bio 2022-03-18 606

　　Objective To explore the mechanism of piceatannol on brain injury in rats with acute severe carbon monoxide poisoning by regulating MAPK/ERK signaling pathway.

　　Methods 100 SPF male SD rats were randomly divided into four groups, three of which were infused in a CO gas treatment box for 1 h to prepare an acute CO poisoning model. Immediately after leaving the box, HbCO%, PIC The group received 2 mL of 200 mg/kg PIC for intragastric administration, the PIC + ERK group received 2 mL of 200 mg/kg PIC and 0. 2 mg/kg ERK inhibitor P-4313 for co-treatment, and the CO and NC groups were given equal volume of physiological Saline gavage treatment. After 1, 7, 14, 21, and 28 days, the water maze experiment was performed. After the experiment, the brain tissue of the four groups of rats was collected for HE staining observation, TUNEL staining to detect cell apoptosis, observation of neuronal ultrastructure in brain tissue, and observation of brain tissue. The mitochondrial membrane potential of nerve cells, the oxidative stress damage index of brain tissue cells, and the expression of Nrf-2 and Bcl-2 proteins were detected by Western blot.

　　Results Compared with the NC group, in the CO group and PIC + ERK group, the performance of learning and memory in the water maze test decreased, the morphology of brain tissue cells changed, the ultrastructure of nerve cells was damaged, and the number of apoptotic cells was higher (P< 0. 001), the MFI value decreased significantly (P < 0. 001), and the ROS content increased (P < 0. 001); compared with the CO group, the rats in the PIC group behaved normally in behavioral experiments, and the brain tissue cell morphology did not occur. The ultrastructure of nerve cells was intact, the number of apoptotic cells was less (P<0.001), the MFI value and ROS content were lower (P<0.001), and the protein expressions of Nrf-2 and Bcl-2 were slightly increased.

　　Conclusion Piceatannol may increase the expression of Nrf-2 and Bcl-2 proteins by regulating the MAPK/ERK signaling pathway, and play a protective effect on brain injury caused by acute CO poisoning.