20(S)-ginsenoside Rh2 inhibits angiotensin-2 mediated cardiac remodeling and inflammation associated with suppression of the JNK/AP-1 pathway

• Published in: Biomedicine & pharmacotherapy Vol. 169; p. 115880
• Main Authors: Yu, Tianxiang, Xu, Jiachen, Wang, Qinyan, Han, Xue, Tu, Yu, Wang, Yi, Luo, Wu, Wang, Mengyang, Liang, Guang
• Format: Journal Article
• Language: English
• Published: Elsevier Masson SAS 31.12.2023; Elsevier
• Subjects: 20(S)-ginsenoside Rh2; Angiotensin II; C-Jun N-terminal kinase; Hypertensive heart failure; Inflammation; 20(S)-ginsenoside Rh2; Inflammation; Angiotensin II; C-Jun N-terminal kinase; Hypertensive heart failure
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2023.115880

Enhanced levels of angiotensin-2 (Ang-II) causes hypertensive heart failure (HHF) through non-hemodynamical and hemodynamical alterations. 20(S)-ginsenoside Rh2 (20(S)-Rh2) is a natural ginseng compound with numerous cardiovascular benefits. This investigation elucidates the influence of 20(S)-Rh2 on Ang-II-induced heart failure and cardiac alterations. Ang-II was administered in C57BL/6 mice for 4 weeks to induce HHF. In the last 2 weeks of treatment, 20(S)-Rh2 was orally administered in mice to assess the potential 20(S)-Rh2 mechanism. Subsequently, RNA sequencing was carried out. It was indicated that 20(S)-Rh2 suppresses myocardial fibrosis, hypertrophy, and inflammation, thereby inhibiting cardiac disruption in Ang-II-challenged mice without affecting blood pressure. According to the RNA sequencing data, this cardio-protective effect was linked with the (JNK)/AP 1 pathway. 20(S)-Rh2 alleviated heart tissue and cardiomyocytes inflammation by inhibiting the Ang-II-mediated JNK/AP-1 pathway. Within cardiomyocytes, JNK or AP-1 absence abolished the anti-inflammatory effects of 20(S)-Rh2. This study investigation indicated that 20(S)-Rh2 prevents cardiovascular dysfunction induced by Ang-II induced by decreasing JNK-regulated inflammatory responses, providing evidence for its use as an efficient regimen for HHF. [Display omitted]