题名 | Schisandrin B alleviates angiotensin II-induced cardiac inflammatory remodeling by inhibiting the recruitment of MyD88 to TLRs in mouse cardiomyocytes |
作者 | |
发表日期 | 2024-09-30 |
发表期刊 | International Immunopharmacology 影响因子和分区 |
语种 | 英语 |
原始文献类型 | Article |
关键词 | Schisandrin B Ang II Inflammation Cardiac inflammatory remodeling MyD88 TLRs |
其他关键词 | SIGNALING PATHWAY ; HYPERTROPHY ; RECOGNITION ; PRESSURE ; PROTEINS ; TRIF |
摘要 | Cardiac tissue remodeling is characterized by altered heart tissue architecture and dysfunction, leading to heart failure. Sustained activation of the renin-angiotensin-aldosterone system (RAAS) greatly promotes the development of myocardial remodeling. Angiotensin II (Ang II), which is the major component of RAAS, can directly lead to cardiac remodeling by inducing an inflammatory response. Schisandrin B (Sch B), the active component extracted from the fruit of Schisandra chinensis (Turcz.) Baill has been shown to exhibit anti-inflammatory activity through its ability to target TLR4 and its adaptor protein, MyD88. In this study, we explored whether Sch B alleviates Ang II-induced myocardial inflammation and remodeling via targeting MyD88. Sch B significantly suppressed Ang II-induced inflammation as well as increased the expression of several genes of tissue remodeling (beta-Mhc, Tgfb, Anp, alpha-Ska) both in vivo and in vitro. These protective effects of Sch B were due to the inhibition of recruitment of MyD88 to TLR2 and TLR4, suppressing the Ang II-induced NF-kappa B activation and reducing the following inflammatory responses. Moreover, the knockdown of Myd88 in cardiomyocytes abrogated the Ang IIinduced increases in the production of inflammatory cytokines and expression of remodeling genes. These findings provide new evidence that the mechanism of Sch B protection was attributed to selective inhibition of MyD88 signaling. This finding could pave the way for novel therapeutic strategies for myocardial inflammatory diseases. |
资助项目 | National Natural Science Foundation of China [82361138563]; Russian Science Foundation [24-45-00071] |
出版者 | ELSEVIER |
ISSN | 1567-5769 |
EISSN | 1878-1705 |
卷号 | 139 |
DOI | 10.1016/j.intimp.2024.112660 |
页数 | 10 |
WOS类目 | Immunology ; Pharmacology & Pharmacy |
WOS研究方向 | Immunology ; Pharmacology & Pharmacy |
WOS记录号 | WOS:001272062700001 |
收录类别 | SCIE ; SCOPUS ; PUBMED |
URL | 查看原文 |
PubMed ID | 39018688 |
SCOPUSEID | 2-s2.0-85198502864 |
通讯作者地址 | [Wang, Yi;Huang, Jianxiong]Wenzhou Med Univ, Joint Res Ctr Med, Affiliated Xiangshan Hosp, Ningbo 315700, Peoples R China. |
Scopus学科分类 | Immunology and Allergy;Immunology;Pharmacology |
SCOPUS_ID | SCOPUS_ID:85198502864 |
TOP期刊 | TOP期刊 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | https://kms.wmu.edu.cn/handle/3ETUA0LF/216750 |
专题 | 其他_附属象山医院(象山县第一人民医院) 口腔医学院、附属口腔医院 口腔医学院、附属口腔医院_口腔医学研究所 药学院(分析测试中心)_生物有机与药物化学研究中心 |
通讯作者 | Wang, Yi; Huang, Jianxiong |
作者单位 | 1.Wenzhou Med Univ, Joint Res Ctr Med, Affiliated Xiangshan Hosp, Ningbo 315700, Peoples R China; 2.Wenzhou Med Univ, Sch & Hosp Stomatol, Inst Stomatol, Wenzhou 325027, Peoples R China; 3.Hangzhou Normal Univ, Sch Pharm, Hangzhou 311121, Peoples R China; 4.Wenzhou Med Univ, Chem Biol Res Ctr, Sch Pharmaceut Sci, Wenzhou 325035, Peoples R China; 5.Bashkir State Med Univ, Dept Pharmacol, Ufa 450005, Russia |
第一作者单位 | 附属象山医院(象山县第一人民医院); 口腔医学院、附属口腔医院; 口腔医学研究所 |
通讯作者单位 | 附属象山医院(象山县第一人民医院) |
第一作者的第一单位 | 附属象山医院(象山县第一人民医院) |
推荐引用方式 GB/T 7714 | Xu, Sujing,Hu, Chenghong,Han, Jibo,et al. Schisandrin B alleviates angiotensin II-induced cardiac inflammatory remodeling by inhibiting the recruitment of MyD88 to TLRs in mouse cardiomyocytes[J]. International Immunopharmacology,2024,139. |
APA | Xu, Sujing., Hu, Chenghong., Han, Jibo., Luo, Wu., Huang, Lijiang., ... & Huang, Jianxiong. (2024). Schisandrin B alleviates angiotensin II-induced cardiac inflammatory remodeling by inhibiting the recruitment of MyD88 to TLRs in mouse cardiomyocytes. International Immunopharmacology, 139. |
MLA | Xu, Sujing,et al."Schisandrin B alleviates angiotensin II-induced cardiac inflammatory remodeling by inhibiting the recruitment of MyD88 to TLRs in mouse cardiomyocytes".International Immunopharmacology 139(2024). |
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