Claudia Espinosa-Garcia

TL;DR: Treatment with progesterone significantly attenuated stress-induced microglial priming by modulating polarized microglia and the inflammatory environment in the hippocampus, the area most vulnerable to ischemic injury.

TL;DR: It is shown that stress and global ischemia exert a synergistic effect in HMGB1 release, resulting in exacerbation of NLRP3 inflammasome activation and autophagy impairment in the hippocampus of ischemic animals, suggesting that modulation of microglial priming is one of the molecular mechanisms by which PROG ameliorates isChemic brain injury under stressful conditions.

TL;DR: Performance of P₄ or ALLO treated rats in learning and memory tests suggests that these steroids promoted neural conditions accounting for adequate functioning long after ischemia, in spite of the loss of hippocampal pyramidal neurons.

TL;DR: The reduction of neurite growth inhibitory molecules Nogo-A, Ng-R, and Rho-A is suggested to be a part of the restorative effects of progesterone possibly allowing the plastic phenomena to occur, able to support the functional preservation of the hippocampus following global cerebral ischemia.

TL;DR: Progesterone inhibits the modulators of glycolytic metabolism and induces premature senescence in GBM cells and this can help to reduce/slow tumor progression.