失血性休克（HS）是创伤患者死亡的主要原因。热射病后的炎症可导致心脏损伤。 Pachymic Acid (PA) 是一种从茯苓中提取的三萜类化合物，已被发现具有多种生物活性，包括抗炎和抗凋亡特性。我们的研究旨在探讨 PA 对 HS 引起的心脏损伤的保护作用及其潜在机制。雄性Sprague-Dawley大鼠每天腹腔注射PA（7.5或15[式：见正文]mg/kg），连续三天。随后，我们通过插入股动脉的导管抽血并进行复苏，创建了 HS 大鼠模型。结果表明，HS导致血流动力学、血清心肌酶水平和心脏结构异常，并诱导心脏细胞凋亡。然而，PA 预处理有效减轻了这些影响。 PA 预处理还抑制了心脏中白细胞介素 (IL)-1[公式：见正文]、IL-6 和肿瘤坏死因子 [公式：见正文] (TNF-[公式：见正文]) 的 mRNA 和蛋白质水平HS 大鼠的组织。此外，PA 预处理减少了 HS 大鼠心脏中的炎症细胞浸润和 M1 巨噬细胞极化，同时加剧了 M2 极化。研究观察到 M1 巨噬细胞（CD86[分子式：见正文]）及其标记物（iNOS）的表达比例下降，而 M2 巨噬细胞（CD206[分子式：见正文]）的表达比例增加，他们的标记（Arg-1）。值得注意的是，PA 预处理通过抑制 NF-[式：见文字]B p65 磷酸化及其核转位来抑制 NF-[式：见文字]B 通路激活。总之，PA 预处理可能通过抑制 NF-[式：见正文]B 通路改善 HS 引起的心脏损伤。因此，PA 治疗有望成为减轻 HS 心脏损伤的策略。

Hemorrhagic shock (HS) is the leading cause of death in trauma patients. Inflammation following HS can lead to cardiac damage. Pachymic acid (PA), a triterpenoid extracted from Poria cocos, has been found to possess various biological activities, including anti-inflammatory and anti-apoptotic properties. Our research aims to investigate the protective effects of PA against HS-induced heart damage and the underlying mechanisms involved. Male Sprague-Dawley rats were intraperitoneally injected with PA (7.5 or 15[Formula: see text]mg/kg) daily for three days. Subsequently, we created a rat model of HS by drawing blood through a catheter inserted into the femoral artery followed by resuscitation. The results revealed that HS led to abnormalities in hemodynamics, serum cardiac enzyme levels, and cardiac structure, as well as induced cardiac apoptosis. However, pretreatment with PA effectively alleviated these effects. PA-pretreatment also suppressed mRNA and protein levels of interleukin (IL)-1[Formula: see text], IL-6, and tumor necrosis factor [Formula: see text] (TNF-[Formula: see text]) in the heart tissues of HS rats. Additionally, PA-pretreatment reduced inflammatory cell infiltration and M1 macrophage polarization while exaggerating M2 polarization in HS rat hearts. The study observed a decreased proportion of the expression of of M1 macrophages (CD86[Formula: see text]) and their marker (iNOS), along with an increased proportion of the expression of M2 macrophages (CD206[Formula: see text]) and their marker (Arg-1). Notably, PA-pretreatment suppressed NF-[Formula: see text]B pathway activation via inhibiting NF-[Formula: see text]B p65 phosphorylation and its nuclear translocation. In conclusion, PA-pretreatment ameliorates HS-induced cardiac injury, potentially through its inhibition of the NF-[Formula: see text]B pathway. Therefore, PA treatment holds promise as a strategy for mitigating cardiac damage in HS.