Lysophosphatidic acid (LPA), a ubiquitous phospholipid, plays a crucial role in the pathogenesis and pathophysiological process of neurological diseases, which constitute the pathological course after cerebral ischemia. Nevertheless, the molecular mechanisms associated with the pathogenic roles of LPA remain elusive. In this study, we evaluated the expression of the liver X receptor (LXR) and nuclear factor kappa B (NFκB) by Western blotting, quantified the levels of IL-1β, IL-6, TNF-α, and LPA by ELISA, and evaluated apoptosis and infarct by TUNEL (terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling) and TTC (triphenyltetrazolium chloride) staining respectively in Sprague-Dawley (SD) rats after middle cerebral artery occlusion (MCAO). The levels of LPA, an extracellular signaling molecule, increased after ischemia and caused neurological injury effect, decreased the expression level of LXR, and increased the expression level of inflammatory factors (IL-1β, IL-6, and TNF-α) via the NFκB signaling pathway. This elevated LPA-induced pathological process is one of the pathological reactions associated with ischemic brain injury. We present a direct or indirect connection between LPA and LXR in the pathophysiological process. In conclusion, we speculate that the inhibition of LPA generation and administration of LXR agonist may be explored as potential cerebral infarction treatment strategies.

中文翻译：

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脑缺血再灌注损伤：溶血磷脂酸通过降低肝脏X受体的表达介导炎症。

溶血磷脂酸（LPA）是一种普遍存在的磷脂，在神经疾病的发病机理和病理生理过程中起着至关重要的作用，这些疾病构成了脑缺血后的病理过程。然而，与LPA的致病作用有关的分子机制仍然难以捉摸。在这项研究中，我们通过Western印迹评估了肝X受体（LXR）和核因子κB（NFκB）的表达，通过ELISA定量了IL-1β，IL-6，TNF-α和LPA的水平，并在大脑中动脉闭塞（MCAO）后，通过TUNEL（末端脱氧核苷酸转移酶（TdT）dUTP缺口末端标记）和TTC（氯化三苯基四唑鎓）染色分别评估了凋亡和梗死。LPA（一种细胞外信号分子）的水平 通过NFκB信号通路增加缺血后增加并引起神经损伤作用，降低LXR的表达水平，并增加炎性因子（IL-1β，IL-6和TNF-α）的表达水平。这种升高的LPA诱导的病理过程是与缺血性脑损伤相关的病理反应之一。我们提出了在病理生理过程中LPA和LXR之间的直接或间接连接。总之，我们推测对LPA的抑制和LXR激动剂的给药可能被探讨为潜在的脑梗塞治疗策略。这种升高的LPA诱导的病理过程是与缺血性脑损伤相关的病理反应之一。我们提出了在病理生理过程中LPA和LXR之间的直接或间接连接。总之，我们推测对LPA的抑制和LXR激动剂的给药可能被探讨为潜在的脑梗塞治疗策略。这种升高的LPA诱导的病理过程是与缺血性脑损伤相关的病理反应之一。我们提出了在病理生理过程中LPA和LXR之间的直接或间接连接。总之，我们推测对LPA的抑制和LXR激动剂的给药可能被探讨为潜在的脑梗塞治疗策略。