Epigallocatechin‑3‑gallate ameliorates LPS‑induced inflammation by inhibiting the phosphorylation of Akt and ERK signaling molecules in rat H9c2 cells

Abstract

T he inf lam mator y response has been implicated in various cardiac and systemic diseases. Epigallocatechin-3-gallate (EGCG), the major polyphenol extracted from green tea, has various biological and pharmacological properties, such as anti-inflammation, anti-oxidative and anti-tumorigenesis. To some extent, the mechanism of EGCG in the inflammatory response that characterizes myocardial dysfunction is not fully understood. The present study aimed to investigate the inhibiting effect of EGCG on lipopolysaccharide (LPS)-induced inflammation in vitro. Treatment with LPS affected rat H9c2 cardiomyocytes and induced an inflammatory response. However, the LPS-induced effects were attenuated after treatment with EGCG. The present results demonstrated that EGCG treatment repressed several inflammatory mediators, such as vascular endothelial growth factor, chemokine ligand 5, chemokine ligand 2, intercellular adhesion molecule-1, matrix metalloproteinase-2, tumor necrosis factor-α and nitric oxide (induced by LPS), and the repressing effect of EGCG on inflammatory response was dose-dependent in the range of 6.25-100 µM. EGCG inhibited these marked inflammatory key signaling molecules by reducing the expression of phospho-nuclear factor-κB p65,-Akt,-ERK and-MAPK p38 while the total protein level of these signal proteins were not affected. In conclusion, the present findings suggested that EGCG possesses cardiomyocyte-protective action in reducing the LPS-induced inflammatory response due to the inhibition of the phosphorylation of Akt and ERK signaling molecules.

Epigallocatechin-3-Gallate Attenuates Myocardial Dysfunction via Inhibition of Endothelial-to-Mesenchymal Transition

“…In addition, EGCG can significantly inhibit the late EndMT markers MMP-2 and MMP-9 in vivo. Similar to this study, in which EGCG was treated, MMP-2 was reduced to control LPS-induced inflammation in rat H9c2 cells [50], and the effect of reducing MMP-9 was also confirmed in a study targeting myocardial reperfusion [51]. These results suggest that EGCG not only has a cardioprotective effect through antioxidant activity, but also has a direct effect on EndMT, which regulates endothelial cell functions and effectively controls MF, thereby playing a key role in the treatment of cardiovascular disease.…”

Analysis of the role and mechanism of EGCG in septic cardiomyopathy based on network pharmacology

“…In previous studies, EGCG improved intestinal injury ( Ma et al, 2021 ), cerebral nervous system injury ( Cheng et al, 2021 ), lung injury ( Wang, Fan & Zhang, 2019 ) and endothelial injury ( Baek et al, 2019 ) in LPS-induced sepsis in mice. Li et al (2020b) found that EGCG can inhibit AKT phosphorylation and the ERK signaling pathway to improve LPS-induced H9C2 cell injury. As shown in Fig.…”

Biochanin A inhibits endothelial dysfunction induced by IL‑6‑stimulated endothelial microparticles in Perthes disease via the NFκB pathway

“…BCA can inhibit the phosphorylation level of prostaglandin E-2, NOS-2, NFκB and cyclooxygenase-2 to protect rat chondrocytes from IL-induced inflammation ( 54 ). Notably, there are other Chinese traditional medicine extracts or prescriptions that can resist inflammation and improve endothelial dysfunction, such as hederagenin ( 55 ), cycloastragenol ( 56 ), epigallocatechin-3-gallate ( 57 ), He xue ming mu tablet ( 58 ), glycyrrhizic acid ( 59 ), tanshinone IIA sodium sulfonate ( 60 ) and quercetin ( 61 ), but some of them exhibit clinical toxicity and side effects, such as nausea, insomnia and hepatotoxicity. At present, there is no relevant research comparing BCA with the aforementioned drugs in terms of anti-inflammatory activity and improving endothelial dysfunction, therefore it is not possible to identify a clear advantage of BCA over the aforementioned drugs.…”