Stroke is an acute central nervous system disease with high morbidity and mortality rate. Cerebral ischemia reperfusion (I/R) injury is easily induced during the development or treatment of stroke and subsequently leads to more serious brain damage. Prostaglandin E₂ (PGE₂) is one of the most important inflammatory mediators in the brain and contributes to both physiological and pathophysiological functions. It may be upregulated and subsequently plays a key role in cerebral ischemia reperfusion injury. The synthesis and degradation of PGE₂ is an extremely complex process, with multiple key stages and molecules. However, there are few comprehensive and systematic studies conducted to investigate the synthesis and degradation of PGE₂ during cerebral I/R injury, which is what we want to demonstrate. In this study, qRT-PCR and immunoblotting demonstrated that the key enzymes in PGE₂ synthesis, including COX-1, COX-2, mPGES-1 and mPGES-2, were upregulated during cerebral I/R injury, but 15-PGDH, the main PGE₂ degradation enzyme, was downregulated. In addition, two of PGE₂ receptors, EP3 and EP4, were also increased. Meanwhile, immunohistochemistry demonstrated the localization of these molecules in ischemic areas, including cortex, striatum and hippocampus, and reflected their expression patterns in different regions. Combining the results of PCR, Western blotting and immunohistochemistry, we can determine where the increase or decrease of these molecules occurs. Overall, these results further indicate a possible pathway that mediates enhanced production of PGE₂, and thus that may impact production of inflammatory cytokines including IL-1β and TNF-α during cerebral I/R injury.

脑卒中是一种急性中枢神经系统疾病，发病率和死亡率较高。在中风的发生或治疗过程中很容易诱发脑缺血再灌注（I/R）损伤，从而导致更严重的脑损伤。前列腺素E ₂ (PGE ₂ ) 是大脑中最重要的炎症介质之一，有助于生理和病理生理功能。它可能被上调并随后在脑缺血再灌注损伤中发挥关键作用。 PGE ₂的合成和降解是一个极其复杂的过程，具有多个关键阶段和分子。然而，目前对于脑I/R损伤过程中PGE ₂的合成和降解的全面、系统的研究还很少，而这正是我们想要证明的。在本研究中，qRT-PCR和免疫印迹表明，PGE ₂合成的关键酶，包括COX-1、COX-2、mPGES-1和mPGES-2，在脑I/R损伤期间上调，但15-PGDH、主要的 PGE ₂降解酶下调。此外，两种PGE ₂受体EP3和EP4也增加。同时，免疫组织化学证明了这些分子在缺血区域的定位，包括皮质、纹状体和海马，并反映了它们在不同区域的表达模式。结合PCR、蛋白质印迹和免疫组织化学的结果，我们可以确定这些分子的增加或减少发生在哪里。 总体而言，这些结果进一步表明介导PGE ₂产生增强的可能途径，因此可能影响脑I/R损伤期间炎性细胞因子（包括IL-1β和TNF-α）的产生。