Baicalin enhances the thermotolerance of mouse blastocysts by activating the ERK1/2 signaling pathway and preventing mitochondrial dysfunction

Heat stress causes oxidative damage and induces excessive cell apoptosis and thus affects the development and/or even causes the death of preimplantation embryos. The effects of baicalin on the developmental competence of heat-stressed mouse embryos were investigated in this experiment. Two cell embryos were cultured in the presence of baicalin and subjected to heat stress (42 degrees C for 1 h) at their blastocyst stage followed by continuous culture at 37 degrees C until examination. The results showed that heat stress (H group) increased reactive oxygen species (ROS) production, apoptosis and even embryo death, along with reductions in both mitochondrial activity and membrane potential (DJm). Both heat stress (H group) and inhibition of the ERK1/2 signaling pathway (U group) led to significantly reduced expression levels of the genes c-fos, AP-1 and ERK2, and the phosphorylation of ERK1/2 and c-Fos, along with significantly increased c-Jun mRNA expression and phosphorylation levels. These negative effects of heat stress on the ERK1/2 signaling pathway were neutralized by baicalin treatment. To explore the signal transduction mechanism of baicalin in improving embryonic tolerance to heat stress, mitochondrial quality and apoptosis rate in the mouse blastocysts were also examined. Baicalin was found to up regulate the expression of mtDNA and TFAM mRNA, increased mitochondria activity and DJm, and improved the cellular mitochondria quality of mouse blastocysts undergoing heat stress. Moreover, baicalin decreased Bax transcript abundance in blastocyst, along with an increase in the blastocyst hatching rate, which were negatively affected by heat stress. Our findings suggest that baicalin improves the developmental capacity and quality of heat-stressed mouse embryos via a mechanism whereby mitochondrial quality is improved by activating the ERK1/2 signaling pathway and inducing anti-cellular apoptosis. (C) 2021 Published by Elsevier Inc.