■炎症和氧化应激是心脏缺血(LISCI)引起的肺损伤的关键因素。大麻二酚(CBD)通过其抗氧化剂证明了组织保护特性,抗炎,和抗凋亡特性。本研究旨在评估CBD对LISCI的预防性(p-CBD)和治疗性(t-CBD)影响。
■将40只雄性Wistar白化病大鼠分为四组:对照组(CON),LISI,p-CBD,T-CBD结扎左冠状动脉前降支30分钟缺血,然后再灌注30分钟。然后提取肺组织进行组织病理学检查,免疫组织化学,遗传,和生化分析。
■组织病理学,明显的充血,间隔组织厚度增加,在LISCI组的肺组织中观察到炎症细胞浸润。分光光度法,总氧化剂状态和氧化应激指数水平升高,而总抗氧化剂状态水平下降。免疫组织化学,环氧合酶-1(COX1)的表达,粒细胞集落刺激因子(GCSF),白细胞介素-6(IL6)增加。在遗传分析中,PERK和CHOP表达增加,而核因子红系相关因子2(NRF2)和B细胞白血病/淋巴瘤2蛋白(BCL2)表达降低。通过预防性和治疗性CBD治疗方案缓解了这些参数。
■在LISI引起的损伤中,内质网和线粒体应激,以及氧化和炎症标志物,被触发,导致肺细胞损伤。然而,p-CBD和t-CBD治疗有效逆转了这些机制,使所有组织病理学正常化,生物化学,和PCR参数。
UNASSIGNED: Inflammation and oxidative stress are key players in lung injury stemming from cardiac ischemia (LISCI). Cannabidiol (CBD) demonstrates tissue-protective properties through its antioxidant, anti-inflammatory, and anti-apoptotic characteristics. This study aims to assess the preventive (p-CBD) and therapeutic (t-CBD) effects of CBD on LISCI.
UNASSIGNED: Forty male Wistar Albino rats were divided into four groups: control (CON), LISCI, p-CBD, and t-CBD. The left anterior descending coronary artery was ligated for 30 min of ischemia followed by 30 min of reperfusion. Lung tissues were then extracted for histopathological, immunohistochemical, genetic, and biochemical analyses.
UNASSIGNED: Histopathologically, marked hyperemia, increased septal tissue thickness, and inflammatory cell infiltrations were observed in the lung tissues of the LISCI group. Spectrophotometrically, total oxidant status and oxidative stress index levels were elevated, while total antioxidant status levels were decreased. Immunohistochemically, expressions of cyclooxygenase-1 (COX1), granulocyte colony-stimulating factor (GCSF), interleukin-6 (IL6) were increased. In genetic analyses, PERK and CHOP expressions were increased, whereas Nuclear factor erythroid 2-related factor 2 (NRF2) and B-cell leukemia/lymphoma 2 protein (BCL2) expressions were decreased. These parameters were alleviated by both prophylactic and therapeutic CBD treatment protocols.
UNASSIGNED: In LISCI-induced damage, both endoplasmic reticulum and mitochondrial stress, along with oxidative and inflammatory markers, were triggered, resulting in lung cell damage. However, both p-CBD and t-CBD treatments effectively reversed these mechanisms, normalizing all histopathological, biochemical, and PCR parameters.