PDF(Pubmed)
Abstract：
OBJECTIVE: The aim of this research was to examine how penehyclidine hydrochloride (PHC) impacts the occurrence of pyroptosis in lung tissue cells within a rat model of lung ischemia-reperfusion injury.
METHODS: Twenty-four Sprague Dawley (SD) rats, weighing 250 g to 270 g, were randomly distributed into three distinct groups as outlined below: a sham operation group (S group), a control group (C group), and a test group (PHC group). Rats in the PHC group received a preliminary intravenous injection of PHC at a dose of 3 mg/kg. At the conclusion of the experiment, lung tissue and blood samples were collected and properly stored for subsequent analysis. The levels of malondialdehyde, superoxide dismutase, and myeloperoxidase in the lung tissue, as well as IL-18 and IL-1β in the blood serum, were assessed using an Elisa kit. Pyroptosis-related proteins, including Caspase1 p20, GSDMD-N, and NLRP3, were detected through the western blot method. Additionally, the dry-to-wet ratio (D/W) of the lung tissue and the findings from the blood gas analysis were also documented.
RESULTS: In contrast to the control group, the PHC group showed enhancements in oxygenation metrics, reductions in oxidative stress and inflammatory reactions, and a decrease in lung injury. Additionally, the PHC group exhibited lowered levels of pyroptosis-associated proteins, including the N-terminal segment of gasdermin D (GSDMD-N), caspase-1p20, and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3).
CONCLUSIONS: Pre-administration of PHC has the potential to mitigate lung ischemia-reperfusion injuries by suppressing the pyroptosis of lung tissue cells, diminishing inflammatory reactions, and enhancing lung function. The primary mechanism behind anti-pyroptotic effect of PHC appears to involve the inhibition of oxidative stress.
METHODS: Twenty-four Sprague Dawley (SD) rats, weighing 250 g to 270 g, were randomly distributed into three distinct groups as outlined below: a sham operation group (S group), a control group (C group), and a test group (PHC group). Rats in the PHC group received a preliminary intravenous injection of PHC at a dose of 3 mg/kg. At the conclusion of the experiment, lung tissue and blood samples were collected and properly stored for subsequent analysis. The levels of malondialdehyde, superoxide dismutase, and myeloperoxidase in the lung tissue, as well as IL-18 and IL-1β in the blood serum, were assessed using an Elisa kit. Pyroptosis-related proteins, including Caspase1 p20, GSDMD-N, and NLRP3, were detected through the western blot method. Additionally, the dry-to-wet ratio (D/W) of the lung tissue and the findings from the blood gas analysis were also documented.
RESULTS: In contrast to the control group, the PHC group showed enhancements in oxygenation metrics, reductions in oxidative stress and inflammatory reactions, and a decrease in lung injury. Additionally, the PHC group exhibited lowered levels of pyroptosis-associated proteins, including the N-terminal segment of gasdermin D (GSDMD-N), caspase-1p20, and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3).
CONCLUSIONS: Pre-administration of PHC has the potential to mitigate lung ischemia-reperfusion injuries by suppressing the pyroptosis of lung tissue cells, diminishing inflammatory reactions, and enhancing lung function. The primary mechanism behind anti-pyroptotic effect of PHC appears to involve the inhibition of oxidative stress.
摘要：
目的：本研究的目的是研究盐酸戊乙奎醚（PHC）如何影响肺缺血再灌注损伤大鼠模型中肺组织细胞焦亡的发生。
方法：24只SD大鼠,重250克至270克，随机分为三个不同的组，如下所述：假手术组（S组），对照组（C组），和试验组(PHC组)。PHC组的大鼠接受3mg/kg剂量的PHC的初步静脉内注射。实验结束时,收集肺组织和血液样本并妥善储存用于后续分析.丙二醛的水平，超氧化物歧化酶,和肺组织中的髓过氧化物酶，以及血清中的IL-18和IL-1β，使用ELISA试剂盒进行评估。焦亡相关蛋白,包括Caspase1p20，GSDMD-N，和NLRP3，通过蛋白质印迹法检测。此外,还记录了肺组织的干湿比(D/W)和血气分析结果.
结果：与对照组相比，PHC组显示氧合指标增强，减少氧化应激和炎症反应，肺损伤减少。此外,PHC组表现出降低的焦亡相关蛋白水平，包括gasderminD(GSDMD-N)的N端节段，caspase-1p20和核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）。
结论：预先给药PHC有可能通过抑制肺组织细胞的焦亡来减轻肺缺血再灌注损伤，减少炎症反应，增强肺功能。PHC的抗热作用背后的主要机制似乎涉及氧化应激的抑制。
方法：24只SD大鼠,重250克至270克，随机分为三个不同的组，如下所述：假手术组（S组），对照组（C组），和试验组(PHC组)。PHC组的大鼠接受3mg/kg剂量的PHC的初步静脉内注射。实验结束时,收集肺组织和血液样本并妥善储存用于后续分析.丙二醛的水平，超氧化物歧化酶,和肺组织中的髓过氧化物酶，以及血清中的IL-18和IL-1β，使用ELISA试剂盒进行评估。焦亡相关蛋白,包括Caspase1p20，GSDMD-N，和NLRP3，通过蛋白质印迹法检测。此外,还记录了肺组织的干湿比(D/W)和血气分析结果.
结果：与对照组相比，PHC组显示氧合指标增强，减少氧化应激和炎症反应，肺损伤减少。此外,PHC组表现出降低的焦亡相关蛋白水平，包括gasderminD(GSDMD-N)的N端节段，caspase-1p20和核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）。
结论：预先给药PHC有可能通过抑制肺组织细胞的焦亡来减轻肺缺血再灌注损伤，减少炎症反应，增强肺功能。PHC的抗热作用背后的主要机制似乎涉及氧化应激的抑制。
