Remote Ischemic Postconditioning Inhibits Hippocampal Neuronal Apoptosis and Mitophagy After Cardiopulmonary Resuscitation in Rats was written by Xie, Biao;Gao, XuHui;Huang, Yang;Zhang, Yu;Zhu, Shuibo. And the article was included in Shock in 2021.Electric Literature of C16H19BrN2OS The following contents are mentioned in the article:
Studies have shown that remote ischemic post-conditioning can improve brain damage caused by ischemia and hypoxia. However, the specific mechanism underlying this phenomenon is still unclear. The purpose of this study was to investigate the effects of remote ischemic post-conditioning on neuronal apoptosis and mitophagy after cardiopulmonary resuscitation (CPR) in rats. Male Sprague-Dawley rats were used to establish an asphyxia cardiac arrest model by clamping the tracheal duct. First, the expression levels of P53, Cytochrome c (Cytc), and Parkin in the cytoplasm and mitochondria were observed at 3, 6, 24, and 72h after the restoration of spontaneous circulation (ROSC). Then neurol. deficit scores, hippocampal neuron apoptosis, mitochondrial P53 and Parkin, cytoplasmic Cytc, and neuron ultrastructure were evaluated 24h after ROSC. P53 and Parkin can translocate from the cytoplasm to the mitochondria, promoting the translocation of cytoplasmic Cytc to mitochondria after CPR, reaching a peak at 24h after the ROSC. The P53 inhibitor Pifithrin-μ reduced apoptosis induced by P53 mitochondrial translocation. Apoptosis was induced after cardiac arrest and attenuated by remote ischemic postconditioning via inhibiting P53 mitochondrial translocation and the release of Cytc to the cytoplasm. In addition, remote ischemic postconditioning could inhibit Parkin-mediated mitophagy. Taken together, our results show that remote ischemic post-conditioning improves neural function after CPR by inhibiting P53 mitochondrial translocation-induced apoptosis and Parkin-mediated mitophagy. This study involved multiple reactions and reactants, such as 2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2Electric Literature of C16H19BrN2OS).
2-(2-Imino-4,5,6,7-tetrahydrobenzothiazol-3-yl)-1-p-tolylethanone Hydrobromide (cas: 63208-82-2) belongs to thiazole derivatives. Thiazoles in peptides or their ability to bind proteins, DNA and RNA has led to many synthetic studies and new applications. There are numerous natural products that possess a thiazole ring with broad pharmacological activities. Thiamine, also known as vitamin B1, possesses a thiazole ring linked with 2-methylpyrimidine-4-amine as hydrochloride salt.Electric Literature of C16H19BrN2OS
Referemce:
Thiazole | C3H3NS – PubChem,
Thiazole | chemical compound | Britannica