灭活疫苗通过 NF-κB 通路促进心肌缺血再灌注损伤的保护。
Inactivated promotes protection against myocardial ischemia-reperfusion injury through NF-κB pathway.
机构信息
Gerontology Department, Affiliated Hospital of Yan'an University (Shanxi), No. 43 North Street, Yan'an, Shanxi Province 716000, P.R. China.
Intensive Care Unit, Affiliated Hospital of Yan'an University (Shanxi), No. 43 North Street, Yan'an, Shanxi Province 716000, P.R. China
出版信息
Biosci Rep. 2017 Nov 17;37(6). doi: 10.1042/BSR20171025. Print 2017 Dec 22.
Although restoration of blood flow to an ischemic organ is essential to prevent irreversible cellular injury, reperfusion may augment tissue injury in excess of that produced by ischemia alone. So this experiment was designed to study the protective effects and mechanism of inactivated (Lac) on myocardial ischemia-reperfusion (I-R) injury (MIRI). MIRI rat models were established by ligation of left anterior descending coronary artery for ~30 min and then, reperfusion for 120 min and divided into control group, model group, and Lac (10, 10, and 10 cfu/kg) groups. At the end of the test, the creatine kinase (CK) activity, lactate dehydrogenase (LDH) activity, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were assayed by corresponding kits. The heart was obtained from rats and the myocardial infarction area was determined by TTC staining and myocardial endothelial cell apoptosis rate was determined by Tunel kit. Besides, A20, IκB, nuclear factor (NF)-κB, and nitric oxide (NO) synthase (NOS) were also assayed by Western blot. When compared with model group, Lac obviously reduces MIRI in the rat by reducing myocardial infarction area and the apoptosis rate of endothelial cells; reduce the serum CK, LDH, and MDA content; increase the serum SOD activity; and suppress NF-κB signaling and NOS expression in the myocardial tissues. Lac pretreatment can inhibit lipid peroxidation and effectively improve MIRI caused by oxygen free radical through inhibiting NF-κB signaling.
虽然恢复缺血器官的血流对于防止细胞不可逆损伤至关重要，但再灌注可能会导致组织损伤超过单纯缺血所造成的损伤。因此，本实验旨在研究失活（Lac）对心肌缺血再灌注（I-R）损伤（MIRI）的保护作用及其机制。通过结扎左前降支冠状动脉约 30 分钟，然后再灌注 120 分钟，建立 MIRI 大鼠模型，并将其分为对照组、模型组和 Lac（10、10 和 10 cfu/kg）组。在测试结束时，通过相应的试剂盒测定肌酸激酶（CK）活性、乳酸脱氢酶（LDH）活性、超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量。从大鼠中取出心脏，通过 TTC 染色测定心肌梗死面积，通过 Tunel 试剂盒测定心肌内皮细胞凋亡率。此外，还通过 Western blot 测定 A20、IκB、核因子（NF）-κB 和一氧化氮（NO）合酶（NOS）。与模型组相比，Lac 通过降低心肌梗死面积和内皮细胞凋亡率、降低血清 CK、LDH 和 MDA 含量、增加血清 SOD 活性、抑制心肌组织中 NF-κB 信号通路和 NOS 表达，明显减轻大鼠的 MIRI。Lac 预处理可通过抑制 NF-κB 信号通路抑制氧自由基引起的脂质过氧化，有效改善 MIRI。
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