Wogonoside preserves against ischemia/reperfusion-induced myocardial injury by suppression of apoptosis, inflammation, and fibrosis via modulating Nrf2/HO-1 pathway

心肌保护 标记法 细胞凋亡 缺血 再灌注损伤 医学 药理学 纤维化 炎症 p38丝裂原活化蛋白激酶 信号转导 化学 心脏病学 内科学 生物化学 MAPK/ERK通路
作者
Bingshan Zhang,Di Xu
出处
期刊:Immunopharmacology and Immunotoxicology [Taylor & Francis]
卷期号:44 (6): 877-885 被引量:1
标识
DOI:10.1080/08923973.2022.2090955
摘要

Myocardial ischemia/reperfusion (I/R) injury occurs after restoring blood supply, which brings about extra damage to heart tissue. Thus, exploring protection measures and underlying mechanisms appear to be particularly important. In this study, we investigated the cardioprotection of wogonoside against I/R injury in mice and further uncovered its mechanism.Mice model of myocardial I/R injury was established by left anterior descending coronary artery (LAD). Before modeling, mice were administered the wogonoside (10, 20, and 40 mg/kg) for 7 d. To evaluate the effect of wogonoside through nuclear factor E2-associated factor 2/heme oxygenase-1 (Nrf2/HO-1) pathway, sh-Nrf2 was transfected into wogonoside-treated I/R mice. Subsequently, echocardiography detection, HE staining, western blotting, ELISA, TUNEL assay, and MASSON assay were utilized to evaluate the degree of myocardial injury.In I/R group, mice had severe myocardial injury, however, pretreatment of wogonoside at doses of 20 and 40 mg/kg ameliorated the cardiac function, as evidenced by improving hemodynamic parameters. Besides, wogonoside could relieved the abnormality of cardiomyocytes structure, inflammatory reaction, apoptosis, and myocardial fibrosis. Importantly, wogonoside activated the Nrf2/HO-1 pathway, as demonstrated by increasing Nrf2 expression in nucleus and its downstream genes including HO-1 and NADPH quinone oxidoreductase-1 (NQO1). However, effects of wogonoside on cardioprotection were abolished by sh-Nrf2.Wogonoside exerted the protective role against I/R-induced myocardial injury by suppression of apoptosis, inflammation, and fibrosis via activating Nrf2/HO-1 pathway.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
guozizi应助科研通管家采纳,获得200
刚刚
深情安青应助科研通管家采纳,获得10
刚刚
CR7应助科研通管家采纳,获得20
1秒前
chx2256120完成签到,获得积分10
1秒前
大个应助科研通管家采纳,获得10
1秒前
1秒前
怎么说应助科研通管家采纳,获得10
1秒前
好运来应助科研通管家采纳,获得10
1秒前
1秒前
皮皮应助科研通管家采纳,获得10
1秒前
萧水白应助科研通管家采纳,获得10
1秒前
简化为完成签到,获得积分10
1秒前
1秒前
1秒前
2秒前
2秒前
iNk应助科研通管家采纳,获得10
2秒前
2秒前
2秒前
iNk应助科研通管家采纳,获得10
2秒前
李健应助科研通管家采纳,获得10
2秒前
上好佳发布了新的文献求助10
2秒前
2秒前
晶晶完成签到,获得积分10
2秒前
Young发布了新的文献求助10
2秒前
stinkyfish完成签到,获得积分20
2秒前
无花果应助科研民工采纳,获得10
2秒前
朴素的松鼠完成签到,获得积分10
2秒前
爆米花应助耍酷的醉蓝采纳,获得10
3秒前
天天天才完成签到,获得积分10
3秒前
ZHQ完成签到,获得积分10
3秒前
zp应助kento采纳,获得100
3秒前
luanfeng发布了新的文献求助10
3秒前
ZoeyD完成签到 ,获得积分10
3秒前
伶俐妙海应助LLY采纳,获得20
4秒前
4秒前
left_right完成签到,获得积分10
4秒前
jim_hacker发布了新的文献求助10
5秒前
5秒前
5秒前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
Cognitive Neuroscience: The Biology of the Mind 1000
Technical Brochure TB 814: LPIT applications in HV gas insulated switchgear 1000
Immigrant Incorporation in East Asian Democracies 600
Nucleophilic substitution in azasydnone-modified dinitroanisoles 500
不知道标题是什么 500
A Preliminary Study on Correlation Between Independent Components of Facial Thermal Images and Subjective Assessment of Chronic Stress 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 3968771
求助须知:如何正确求助?哪些是违规求助? 3513729
关于积分的说明 11169450
捐赠科研通 3249084
什么是DOI,文献DOI怎么找? 1794592
邀请新用户注册赠送积分活动 875258
科研通“疑难数据库(出版商)”最低求助积分说明 804740