Exploring the molecular mechanism of notoginsenoside R1 in sepsis-induced cardiomyopathy based on network pharmacology and experiments validation

Abstract

Sepsis-induced cardiomyopathy (SIC) is an important manifestation of sepsis, and abnormal cardiac function affects the development of sepsis. Notoginsenoside R1 (NG-R1) is a unique bioactive component of Panax notoginseng with anti-inflammatory and antioxidant effects. However, the effects and possible mechanisms of NG-R1 on SIC are not clear. The purpose of this study was to identify the potential targets and regulatory mechanisms of the action of NG-R1 on SIC. To investigate the potential mechanism, we used network pharmacology, molecular docking, qRT-PCR, and immunofluorescence. The results showed that NG-R1 ameliorated myocardial fibrosis in septic mice. Validation of network pharmacology and molecular docking results revealed that NG-R1 reduced tumor necrosis factor-Alpha (TNF-α) expression in myocardial tissues and AC16 cardiomyocytes in mice, as well as inflammatory factor release in AC16 cells, so TNF-α may be a potential target of NG-R1 against SIC. The present study demonstrated that NG-R1 could protect against SIC and by regulating the expression of TNF-α inflammatory factors, providing a new idea for sepsis drug development.

Enhancing the inhibition of cell proliferation and induction of apoptosis in H22 hepatoma cells through biotransformation of notoginsenoside R1 by Lactiplantibacillus plantarum S165 into 20(S/R)-notoginsenoside R2

“…Notoginsenoside R1 is a bioactive compound that was isolated from Sanqi and has been extensively studied for its various therapeutic properties, including anti-inflammatory and anti-oxidative effects. 33 However, its clinical applications are limited owing to low bioavailability and poor solubility. Therefore, several studies have explored the transformation of notoginsenoside into its metabolites.…”

Research Progress on the Mechanism and Management of Septic Cardiomyopathy: A Comprehensive Review

“…Tumor necrosis factor (TNF)-α, as a major regulator of the infammatory response, has been proposed to be a key contributing factor in septic cardiomyopathy. It was reported that the early depression of contractility was largely due to LPS-induced TNF-α synthesis [33], and TNF-α was suggested to be the core target of anti-infammation in septic cardiomyopathy [34].…”