Chunhua Ma, Hongyan Long, Weina Zhu, Xiaoli He, Yajie Zhang, Jie Ruan
Central Laboratory, Nanjing Municipal Hospital of T.C.M, The Third Affiliated Hospital of Nanjing University of T.C.M, Nanjing 210001, China.
Central Laboratory, Nanjing Municipal Hospital of T.C.M, The Third Affiliated Hospital of Nanjing University of T.C.M, Nanjing 210001, China.
Biomed Pharmacother. 2017 Apr;88:617-624. doi: 10.1016/j.biopha.2017.01.079. Epub 2017 Feb 24.
Dang The present study was designed to investigate cardioprotective effects of Dang Gui Bu Xue Tang (DGBUT) on coronary artery ligation-induced myocardial ischemia. Myocardial ischemia (MI) model was induced in SD rats by surgical ligation of the left anterior descending coronary artery. ST segment elevation of Electrocardiograph (ECG) infarct size, levels of lactate dehydrogenase (LDH), creatine kinase (CK), glutathione (GSH) and catalase (CAT), catalase (SOD), malondialdehyde (MDA), and inflammatory cytokines and phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, p38, c-Jun NH2 terminal kinases (JNK), nuclear factor (NF)-κBp65, inhibitory kappa B (IκB) α, IκB kinase (IKK) α and IKKβ were evaluated in rats treated with or without DGBUT. DGBUT treatment significantly reduced the elevation of the ST segment of ECG, the myocardial infarct size of MI. The level of LDH, CK and MDA were suppressed, the contents of SOD, GSH and CAT were enhanced with DGBUT. The elevated concentration of inflammatory cytokines tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and IL-6 in MI rats were effectively reversed by the DGBUT administration. Also, highly expressed p-JNK, p-ERK, p-p38, p-NF-κBp65, p-IκBα, p-IKKα and p-IKKβ in MI rats were restored respectively by DGBUT treatment. The protective effect of DGBUT against MI injury might be associated with MAPK/NF-кB pathway.
当归补血汤对冠状动脉结扎诱导的心肌缺血的心脏保护作用
本研究旨在探讨当归补血汤（DGBUT）对冠状动脉结扎诱导的心肌缺血的心脏保护作用。通过手术结扎左冠状动脉前降支在SD大鼠中诱导心肌缺血（MI）模型。评估了在给予或未给予DGBUT的大鼠中，心电图（ECG）的ST段抬高、梗死面积、乳酸脱氢酶（LDH）、肌酸激酶（CK）、谷胱甘肽（GSH）和过氧化氢酶（CAT）水平、超氧化物歧化酶（SOD）、丙二醛（MDA）、炎性细胞因子以及细胞外信号调节激酶（ERK）1/2、p38、c-Jun氨基末端激酶（JNK）、核因子（NF）-κBp65、抑制性κB（IκB）α、IκB激酶（IKK）α和IKKβ的磷酸化情况。DGBUT治疗显著降低了ECG的ST段抬高以及MI的心肌梗死面积。DGBUT抑制了LDH、CK和MDA的水平，提高了SOD、GSH和CAT的含量。DGBUT给药有效逆转了MI大鼠中炎性细胞因子肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和IL-6浓度的升高。此外，DGBUT治疗分别恢复了MI大鼠中高表达的p-JNK、p-ERK、p-p38、p-NF-κBp65、p-IκBα、p-IKKα和p-IKKβ。DGBUT对MI损伤的保护作用可能与MAPK/NF-кB通路有关。
