Abstract：
The study aimed to assess 𝛾-Terpinene\'s (𝛾-TER) neuroprotective potential in acute cerebral ischemia, characterized by reduced cerebral blood flow in rats. Middle cerebral artery occlusion (MCAO), a standard method for inducing cerebral ischemia, was employed in male Wistar rats. 𝛾-TER at varying doses (5, 10, and 15 mg/kg) were intraperitoneally administered during reperfusion onset. Neurological outcomes, cerebral infarct size, edema, and enzymatic activities (SOD, GPx, and catalase) in the brain were evaluated using diverse techniques. The study examined gene expression and pathways associated with neuroinflammation and apoptosis using Cytoscape software, identifying the top 10 genes involved. Pro-inflammatory and pro-apoptotic factors were assessed through real-time PCR and ELISA, while apoptotic cell rates were measured using the TUNEL and Flow cytometry assay. Immunohistochemistry assessed apoptosis-related proteins like Bax and bcl-2 in the ischemic area. 𝛾-TER, particularly at doses of 10 and 15 mg/kg, significantly reduced neurological deficits and cerebral infarction size. The 15 mg/kg dose mitigated TNF-α, IL-1β, Bax, and caspase-3 gene and protein levels in the cortex, hippocampus, and striatum compared to controls. Furthermore, Bcl-2 levels increased in these regions. 𝛾-TER show cased neuroprotective effects by suppressing inflammation, apoptosis, and oxidation. In conclusion, 𝛾-TER, possessing natural anti-inflammatory and anti-apoptotic properties, shields the brain against ischemic damage by reducing infarction, edema, oxidative stress, and inflammation. It modulates the expression of crucial genes and proteins associated with apoptosis in diverse brain regions. These findings position 𝛾-TER as a potential therapeutic agent for ischemic stroke.
摘要：
该研究旨在评估急性脑缺血的β-萜品烯（β-TER）神经保护潜能，以大鼠脑血流量减少为特征。大脑中动脉闭塞(MCAO),诱发脑缺血的标准方法，被用于雄性Wistar大鼠。在再灌注发作期间，腹膜内施用不同剂量（5、10和15mg/kg）的？-TER。神经系统的结果，脑梗塞大小,水肿,和酶活性(SOD，GPx,和过氧化氢酶）在大脑中使用不同的技术进行评估。该研究使用Cytoscape软件检查了与神经炎症和细胞凋亡相关的基因表达和通路，确定涉及的前10个基因。通过实时PCR和ELISA评估促炎和促凋亡因子，而凋亡细胞率使用TUNEL和流式细胞术测定。免疫组织化学评估缺血区域的凋亡相关蛋白如Bax和bcl-2。?-TER,特别是在10和15mg/kg的剂量下，显着减少神经功能缺损和脑梗死的大小。15mg/kg剂量减轻TNF-α，IL-1β,Bax,皮质中的caspase-3基因和蛋白质水平，海马体,和纹状体与对照组相比。此外，Bcl-2水平在这些区域增加。？-TER通过抑制炎症表现出神经保护作用，凋亡，和氧化。总之,?-TER,具有天然的抗炎和抗凋亡特性，通过减少梗塞保护大脑免受缺血性损伤，水肿,氧化应激，和炎症。它调节与不同脑区凋亡相关的关键基因和蛋白质的表达。这些发现将?-TER定位为缺血性卒中的潜在治疗剂。
