Abstract Title:

Ginsenoside Rg1 attenuates cardiomyocyte apoptosis and inflammation via the TLR4/NF-kB/NLRP3 pathway.

Abstract Source:

J Cell Biochem. 2019 Nov 11. Epub 2019 Nov 11. PMID: 31709615

Abstract Author(s):

Man Luo, Dongsheng Yan, Qingsong Sun, Jiali Tao, Liang Xu, Hong Sun, Hongmei Zhao

Article Affiliation:

Man Luo


Sepsis-induced myocardial dysfunction (SIMD) causes high mortality in seriously ill patients. Ginsenoside Rg1 has been proven to have effective anti-inflammatory and antiapoptotic properties. However, the specific role of Rg1 in SIMD and the molecular mechanism remain unclear. Hence, we aimed to investigate the latent effects of ginsenoside Rg1 against SIMD and explore its underlying mechanisms. Male C57BL/6J mice and neonatal rat cardiomyocytes (NRCMs) were used as in vivo and in vitro models, respectively. Western blot analysis was used to detect the level of protein expression, and reverse transcription polymerase chain reaction was conducted todetermine the messenger RNA expression of inflammatory factors. The terminal deoxynucleotidyl transferase-mediated nick end labeling assay and flow cytometry were used to determine the apoptosis rate. Echocardiography was performed to assess cardiac function. The results showed that Rg1 improved cardiac function and attenuated lipopolysaccharide (LPS)-induced apoptosis and inflammation in mice. In addition, in NRCMs, Rg1 downregulated the expression of LPS-induced inflammatory cytokines and reversed the increased expression of Toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB), and NOD-like receptor 3 (NLRP3). In addition, treatment with TLR4 small interfering RNA (siRNA), a p-NF-κB inhibitor, or NLRP3 siRNA suppressed LPS-induced apoptosis and inflammation. In conclusion, Rg1 can attenuate LPS-induced inflammation and apoptosis both in NRCMs and septic mice and restore impairedcardiac function. Moreover, Rg1 may exert its effect via blocking the TLR4/NF-κB/NLRP3 pathway.

Study Type : Animal Study, In Vitro Study

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