Sohrabi Farzaneh, Dianat Mahin, Badavi Mohammad, Radan Maryam, Mard Seyyed Ali
Department of Physiology, Physiology Research Center, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Iran J Basic Med Sci. 2020 Sep;23(9):1130-1138. doi: 10.22038/ijbms.2020.46427.10721.
Cardiovascular disease has an important role in mortality caused by lung injury. Emphysema is associated with impaired pulmonary gas exchange efficiency and airflow limitation associated with small airway inflammation. The aim was to evaluate the interactions between lung injury, inflammation, and cardiovascular disease. Since gallic acid has antioxidant and anti-inflammatory effects, we hypothesized that gallic acid protects the lung and the related heart dysfunction in elastase-induced lung injury.
Forty-eight Sprague-Dawley male rats were randomly divided into six groups: Control, Porcine pancreatic elastase (PPE) , PPE+GA, and 3 groups for different doses of gallic acid (GA 7.5, GA 15, GA 30 mg/kg). PPE was injected intra-tracheally on days 1 and 10 of the test. In each group, electrocardiography, hemodynamic parameters, oxidative stress, and bronchoalveolar lavage fluid were examined.
PPE administration showed a decrease in HR and QRS voltage of electrocardiogram parameters, as well as in hemodynamic parameters (<0.05, <0.01, and <0.001) and superoxide dismutase (SOD) (<0.05). Tumor Necrosis Factor α (TNF-α) (<0.001), interleukin 6 (IL-6) (<0.001), interleukin 6 (MDA) (<0.001), and the total number of white blood cells (<0.001) showed an increase in PPE groups. Gallic acid preserved the values of hemodynamic properties, oxidative stress, inflammation, and electrocardiogram parameters in comparison to the PPE group.
Briefly, this study showed the valuable effect of gallic acid in cardiac dysfunction related to elastase-induced lung injury. These findings suggested that gallic acid, as a natural antioxidant, has a potential therapeutic effect on preventing oxidative stress, inflammation, and subsequent cardiovascular disease.
心血管疾病在肺损伤导致的死亡中起重要作用。肺气肿与肺气体交换效率受损以及与小气道炎症相关的气流受限有关。本研究旨在评估肺损伤、炎症和心血管疾病之间的相互作用。由于没食子酸具有抗氧化和抗炎作用，我们假设没食子酸可保护肺及弹性蛋白酶诱导的肺损伤中相关的心脏功能障碍。
48只雄性Sprague-Dawley大鼠随机分为6组：对照组、猪胰弹性蛋白酶（PPE）组、PPE+GA组以及3个不同剂量没食子酸组（GA 7.5、GA 15、GA 30 mg/kg）。在试验的第1天和第10天经气管内注射PPE。对每组进行心电图、血流动力学参数、氧化应激和支气管肺泡灌洗等检查。
给予PPE后，心电图参数中的心率和QRS波电压降低，血流动力学参数（<0.05、<0.01和<0.001）以及超氧化物歧化酶（SOD）（<0.05）也降低。肿瘤坏死因子α（TNF-α）（<0.001）、白细胞介素6（IL-6）（<0.001）、丙二醛（MDA）（<0.001）以及白细胞总数（<0.001）在PPE组中升高。与PPE组相比，没食子酸可维持血流动力学特性、氧化应激、炎症和心电图参数的值。
简而言之，本研究显示了没食子酸在弹性蛋白酶诱导的肺损伤相关心脏功能障碍中的重要作用。这些发现表明，没食子酸作为一种天然抗氧化剂，在预防氧化应激、炎症及随后的心血管疾病方面具有潜在的治疗作用。
