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新橙皮苷通过抑制 JNK 和 NF-κB p65 的活性缓解大鼠心肌缺血再灌注损伤的病理损伤和免疫失衡。

Neohesperidin alleviated pathological damage and immunological imbalance in rat myocardial ischemia-reperfusion injury via inactivation of JNK and NF-κB p65.

机构信息

Internal Medicine-Cardiovascular Department, Affiliated Hospital of Yangzhou University, Yangzhou, Jiangsu Province, China.

出版信息

Biosci Biotechnol Biochem. 2021 Feb 18;85(2):251-261. doi: 10.1093/bbb/zbaa064.

DOI:10.1093/bbb/zbaa064
PMID:33604646
Abstract

Neohesperidin (NEO) exerts antiviral, antioxidant, anti-inflammation, and antitumor effects in some diseases. The purpose of this study was to investigate the effect and mechanism of NEO on myocardial ischemia-reperfusion (I/R) injury. Results indicated that NEO suppressed the levels of serum inflammatory cytokines, myocardial damage markers, and oxidative stress markers, and increased the levels of antioxidant in myocardial I/R rats. NEO also inhibited cell apoptosis. Besides, NEO also inhibited the phosphorylation of c-Jun N-terminal kinases (JNK) and nuclear factor kappa B (NF-κB) p65. Furthermore, the protective effects of NEO on myocardial tissue damage, inflammatory cytokines, myocardial injury markers, oxidative stress markers, cell apoptosis, spleen, thymus and liver indices, and phagocytic indices were reversed by JNK activator and NF-κB activator, respectively. In conclusion, NEO alleviates myocardial damage, oxidative stress, cell apoptosis, and immunological imbalance in I/R injury via the inactivation of JNK and NF-κB, making NEO a potential agent for myocardial I/R therapy.

摘要

新橙皮苷(NEO)在一些疾病中具有抗病毒、抗氧化、抗炎和抗肿瘤作用。本研究旨在探讨 NEO 对心肌缺血再灌注(I/R)损伤的作用及其机制。结果表明,NEO 可抑制心肌 I/R 大鼠血清炎症细胞因子、心肌损伤标志物和氧化应激标志物的水平,提高抗氧化水平。NEO 还抑制细胞凋亡。此外,NEO 还抑制 c-Jun N 末端激酶(JNK)和核因子 kappa B(NF-κB)p65 的磷酸化。进一步研究发现,JNK 激活剂和 NF-κB 激活剂可分别逆转 NEO 对心肌组织损伤、炎症细胞因子、心肌损伤标志物、氧化应激标志物、细胞凋亡、脾、胸腺和肝指数以及吞噬指数的保护作用。综上所述,NEO 通过抑制 JNK 和 NF-κB 的活化,减轻 I/R 损伤引起的心肌损伤、氧化应激、细胞凋亡和免疫失衡,使 NEO 成为心肌 I/R 治疗的潜在药物。

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