Xin-Ji-Er-Kang Alleviates Isoproterenol-Induced Myocardial Hypertrophy in Mice through the Nrf2/HO-1 Signaling Pathway
Yu, Ting-Ting3; Sun, Li-Jun4; Chen, Chen4; Wang, Zi-Jian1; Liu, Xue-Sheng5; Zhu, Feng-Qin2; Gao, Shan4
刊名EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
2022-08-22
卷号2022
ISSN号1741-427X
DOI10.1155/2022/7229080
通讯作者Gao, Shan(gaoshan@ahmu.edu.cn)
英文摘要Xin-Ji-Er-Kang (XJEK) inhibited cardiovascular remodeling in hypertensive mice in our previous studies. We hypothesized that XJEK may prevent isoproterenol (ISO)-induced myocardial hypertrophy (MH) in mice by ameliorating oxidative stress (OS) through a mechanism that may be related to the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1(HO-1) pathways. Forty SPF male Kunming mice were randomized into 5 groups (n = 8 mice per group): control group, MH group, MH+ diTerent doses of XJEK (7.5 g/kg/day and 10 g/kg/day), and MH+ metoprolol (60 mg/kg/day). On the eighth day after drug treatment, electrocardiogram (ECG) and echocardiography were performed, the mice were sacrioced, and blood and heart tissues were collected for further analysis. XJEK administration markedly ameliorated cardiovascular remodeling (CR), as manifested by a decreased HW/BW ratio and CSA and less collagen deposition after MH. XJEK administration also improved MH, as evidenced by decreased atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and.-myosin heavy chain (beta-MHC) levels. XJEK also suppressed the decreased superoxide dismutase (SOD) and catalase (CAT) activities and increased malondialdehyde (MDA) levels in serum of mice with MH. XJEK-induced oxidative stress may be related to potentiating Nrf2 nuclear translocation and HO-1 expression compared with the MH groups. XJEK ameliorates MH by activating the Nrf2/HO-1 signaling pathway, suggesting that XJEK is a potential treatment for MH.
资助项目National Natural Science Foundation of China[818731226] ; Special Professor of Wanjiang Scholars (2019) ; Anhui Provincial Institute of Translational Medicine Research Fund[2021zhyx-C20] ; Basic and clinical cooperation research promotion plan from Anhui Medical University[2021xkjT020]
WOS关键词TRANSCRIPTION FACTOR NRF2 ; OXIDATIVE STRESS ; CARDIAC-HYPERTROPHY ; DISEASES
WOS研究方向Integrative & Complementary Medicine
语种英语
出版者HINDAWI LTD
WOS记录号WOS:000884006500012
资助机构National Natural Science Foundation of China ; Special Professor of Wanjiang Scholars (2019) ; Anhui Provincial Institute of Translational Medicine Research Fund ; Basic and clinical cooperation research promotion plan from Anhui Medical University
内容类型期刊论文
源URL[http://ir.hfcas.ac.cn:8080/handle/334002/130297]  
专题中国科学院合肥物质科学研究院
通讯作者Gao, Shan
作者单位1.Anhui Med Univ, Med Clin, Sch Med, Hefei 230032, Anhui, Peoples R China
2.Chinese Acad Sci, Canc Hosp, Hefei 230032, Anhui, Peoples R China
3.Wannan Med Coll, Dept Funct Expt Training Ctr, Basic Med Coll, Wuhu 241002, Peoples R China
4.Anhui Med Univ, Dept Pharmacol, Basic Med Coll, Hefei 230032, Anhui, Peoples R China
5.Anhui Med Univ, Affiliated Hosp 1, Dept Anesthesiol, Hefei 230032, Anhui, Peoples R China
推荐引用方式
GB/T 7714
Yu, Ting-Ting,Sun, Li-Jun,Chen, Chen,et al. Xin-Ji-Er-Kang Alleviates Isoproterenol-Induced Myocardial Hypertrophy in Mice through the Nrf2/HO-1 Signaling Pathway[J]. EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE,2022,2022.
APA Yu, Ting-Ting.,Sun, Li-Jun.,Chen, Chen.,Wang, Zi-Jian.,Liu, Xue-Sheng.,...&Gao, Shan.(2022).Xin-Ji-Er-Kang Alleviates Isoproterenol-Induced Myocardial Hypertrophy in Mice through the Nrf2/HO-1 Signaling Pathway.EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE,2022.
MLA Yu, Ting-Ting,et al."Xin-Ji-Er-Kang Alleviates Isoproterenol-Induced Myocardial Hypertrophy in Mice through the Nrf2/HO-1 Signaling Pathway".EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE 2022(2022).
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