Department of Cardiovascular Surgery, Medical School of Harran University, Şanliurfa, Turkey.
Departmant of Medicinal Biochemistry, Medical School of Harran University, Şanliurfa, Turkey.
Braz J Cardiovasc Surg. 2023 Jul 4;38(4):e20220251. doi: 10.21470/1678-9741-2022-0251.
Fuziline is one of the many antioxidants currently being tested to treat cardiac damage. In our study, histopathological and biochemical effects of fuziline were investigated in mice with dobutamine-induced heart damage in vitro.
Thirty-two adult male BALB/c mice, average weight of 18-20 g, were randomly divided into four groups - Group 1 (sham, n=8), Group 2 (control, dobutamine, n=8), Group 3 (treatment 1, dobutamine + fuziline, n=8), and Group 4 (treatment 2, fuziline, n=8). Biochemical parameters and total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) values were measured. Interleukin 1 beta (IL-1β), NLR family, pyrin domain containing protein 3 (NLRP3), 8-hydroxy-deoxyguanosine (8-OHDG), gasdermin D (GSDMD), and galectin 3 (GAL-3) levels were analyzed by enzyme-linked immunosorbent assay method, and histopathological examination of heart tissues was performed.
When dobutamine + fuziline and fuziline groups were compared, troponin-I (P<0.05), NLRP3 (P<0.001), GSDMD (P<0.001), 8-OHDG (P<0.001), IL-1β (P<0.001), and GAL-3 (P<0.05) were found to be statistically significant. TOS level was the highest in the dobutamine group (P<0.001) and TAS level was the highest in the fuziline group (P<0.001). OSI level was statistically significant between the groups (P<0.001). In histopathological examination, focal necrosis areas were smaller in the dobutamine + fuziline group than in the dobutamine group, and cardiac myocytes were better preserved.
Fuziline markedly reduced cardiac damage and pyroptosis in mice with dobutamine-induced heart damage by lowering the levels of GSDMD, 8-OHDG, IL-1β, and GAL-3. It also prevented necrosis of cardiac myocytes in histopathological evaluation.
福齐林是目前正在测试的众多抗氧化剂之一，用于治疗心脏损伤。在我们的研究中，我们研究了福齐林在体外多巴酚丁胺诱导的心肌损伤的小鼠中的组织病理学和生化作用。
32 只成年雄性 BALB/c 小鼠，平均体重 18-20 克，随机分为四组-第 1 组（假手术，n=8）、第 2 组（对照组，多巴酚丁胺，n=8）、第 3 组（治疗 1 组，多巴酚丁胺+福齐林，n=8）和第 4 组（治疗 2 组，福齐林，n=8）。测量生化参数和总抗氧化状态（TAS）、总氧化状态（TOS）和氧化应激指数（OSI）值。通过酶联免疫吸附试验法分析白细胞介素 1β（IL-1β）、NLR 家族、含吡咯烷域蛋白 3（NLRP3）、8-羟基脱氧鸟苷（8-OHDG）、gasdermin D（GSDMD）和半乳糖凝集素 3（GAL-3）水平，并进行心脏组织的组织病理学检查。
当多巴酚丁胺+福齐林和福齐林组进行比较时，肌钙蛋白 I（P<0.05）、NLRP3（P<0.001）、GSDMD（P<0.001）、8-OHDG（P<0.001）、IL-1β（P<0.001）和 GAL-3（P<0.05）差异具有统计学意义。TOS 水平在多巴酚丁胺组最高（P<0.001），TAS 水平在福齐林组最高（P<0.001）。OSI 水平在各组之间差异具有统计学意义（P<0.001）。在组织病理学检查中，与多巴酚丁胺组相比，多巴酚丁胺+福齐林组的局灶性坏死面积较小，心肌细胞保存较好。
福齐林通过降低 GSDMD、8-OHDG、IL-1β 和 GAL-3 的水平，显著减轻了多巴酚丁胺诱导的心脏损伤小鼠的心脏损伤和细胞焦亡，并在组织病理学评估中防止了心肌细胞坏死。
