EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response

Wang, Mian; Zhong, Hua; Zhang, Xian; Huang, Xin; Wang, Jing; Li, Zihao; Chen, Mengshi; Zhou, Xiao

doi:10.1038/s41598-021-90398-x

Cited by 50 publications

(39 citation statements)

References 54 publications

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“…IL-6 and TNF are common markers of inflammation. EGCG protects against LPS-induced lung injury by promoting PRCKA and inhibiting the expression of IL-6 and TNF ( Wang et al, 2021 ). EGCG protects the myocardium of streptozotocin-nicotinamide-induced diabetic rats through anti-inflammatory and anti-apoptotic pathways, mainly through diminishing the levels of IL-6, TNF-α and Caspase3 ( Othman et al, 2017a ).…”

Section: Discussionmentioning

confidence: 99%

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

Jiang

Wang

Xu³

et al. 2022

PeerJ

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Background Septic cardiomyopathy (SC) is a common complication of sepsis that leads to an increase in mortality. The pathogenesis of septic cardiomyopathy is unclear, and there is currently no effective treatment. EGCG (epigallocatechin gallate) is a polyphenol that has anti-inflammatory, antiapoptotic, and antioxidative stress effects. However, the role of EGCG in septic cardiomyopathy is unknown. Methods Network pharmacology was used to predict the potential targets and molecular mechanisms of EGCG in the treatment of septic cardiomyopathy, including the construction and analysis of protein-protein interaction (PPI) network, gene ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and molecular docking. The mouse model of septic cardiomyopathy was established after intraperitoneal injection of LPS (lipopolysaccharide). The myocardial protective effect of EGCG on septic mice is observed by cardiac ultrasound and HE staining. RT-PCR is used to verify the expression level of the EGCG target in the septic cardiomyopathy mouse model. Results A total of 128 anti-SC potential targets of EGCGareselected for analysis. The GO enrichment analysis and KEGG pathway analysis results indicated that the anti-SC targets of EGCG mainly participate in inflammatory and apoptosis processes. Molecular docking results suggest that EGCG has a high affinity for the crystal structure of six targets (IL-6 (interleukin-6), TNF (tumor necrosis factor), Caspase3, MAPK3 (Mitogen-activated protein kinase 3), AKT1, and VEGFA (vascular endothelial growth factor)), and the experimental verification result showed levated expression of these 6 hub targets in the LPS group, but there is an obvious decrease in expression in the LPS + EGCG group. The functional and morphological changes found by echocardiography and HE staining show that EGCG can effectively improve the cardiac function that is reduced by LPS. Conclusion Our results reveal that EGCG may be a potentially effective drug to improve septic cardiomyopathy. The potential mechanism by which EGCG improves myocardial injury in septic cardiomyopathy is through anti-inflammatory and anti-apoptotic effects. The anti-inflammatory and anti-apoptotic effects of EGCG occur not only through direct binding to six target proteins (IL-6,TNF-α, Caspase3, MAPK3, AKT1, and VEGFA) but also by reducing their expression.

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Section: Discussionmentioning

confidence: 99%

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

Jiang

Wang

Xu³

et al. 2022

PeerJ

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“…TRQ significantly decreased the number of inflammatory cells (neutrophils and macrophages) in lung and reduced MPO activity which was produced by neutrophils. The inflammatory mediators, including TNF-α, IL-1β, IL-6, and IFN-β, are closely associated with the exaggeration of ALI ( Wang M. et al, 2021 ). Our results showed that TRQ remarkably reduced TNF-α, IL-1β, IL-6, and IFN-β production in BALF of ALI mice and LPS-stimulated RAW 264.7 cells.…”

Section: Discussionmentioning

confidence: 99%

Tanreqing Inhibits LPS-Induced Acute Lung Injury In Vivo and In Vitro Through Downregulating STING Signaling Pathway

Zhou

Deng

et al. 2021

Front. Pharmacol.

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Acute lung injury (ALI) is a common life-threatening lung disease, which is mostly associated with severe inflammatory responses and oxidative stress. Tanreqing injection (TRQ), a Chinese patent medicine, is clinically used for respiratory-related diseases. However, the effects and action mechanism of TRQ on ALI are still unclear. Recently, STING as a cytoplasmic DNA sensor has been found to be related to the progress of ALI. Here, we showed that TRQ significantly inhibited LPS-induced lung histological change, lung edema, and inflammatory cell infiltration. Moreover, TRQ markedly reduced inflammatory mediators release (TNF-α, IL-6, IL-1β, and IFN-β). Furthermore, TRQ also alleviated oxidative stress, manifested by increased SOD and GSH activities and decreased 4-HNE, MDA, LDH, and ROS activities. In addition, we further found that TRQ significantly prevented cGAS, STING, P-TBK, P-P65, P-IRF3, and P-IκBα expression in ALI mice. And we also confirmed that TRQ could inhibit mtDNA release and suppress signaling pathway mediated by STING in vitro. Importantly, the addition of STING agonist DMXAA dramatically abolished the protective effects of TRQ. Taken together, this study indicated that TRQ alleviated LPS-induced ALI and inhibited inflammatory responses and oxidative stress through STING signaling pathway.

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“…As a bioactive dietary component, EG owns a great many pharmacological actions including antioxidation, anti-inflammation, antifibrosis, and inhibiting endoplasmic reticulum stress [ 16 – 18 ]. In acute lung injury induced by sepsis, acute pancreatitis, paraquat, and hip fracture, EG treatment could exert vital protective roles by different mechanisms [ 19 – 22 ]. In transverse aortic constriction-induced cardiac fibrosis, EG treatment significantly decreased collagen deposition and cardiomyocyte hypertrophy by blocking AKT/mTOR pathway [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin Gallate Relieved PM2.5-Induced Lung Fibrosis by Inhibiting Oxidative Damage and Epithelial-Mesenchymal Transition through AKT/mTOR Pathway

Zhongyin

Wang

Juan

et al. 2022

Oxidative Medicine and Cellular Longevity

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Oxidative damage and epithelial-mesenchymal transition (EMT) are main pathological processes leading to the development of PM2.5-induced lung fibrosis. Epigallocatechin gallate (EG), a natural polyphenol extracted from green tea, possesses the ability to combat oxidative stress and inflammation. However, the potential roles of EG in PM2.5-induced lung fibrosis have not been reported yet. In the present study, we investigated whether EG could relieve PM2.5-induced lung injury and fibrosis in vivo and in vitro. To mimic PM2.5-induced lung fibrosis, C57/BL6 mice were intranasally instilled with PM2.5 suspension, and MLE-12 lung epithelial cells were stimulated with PM2.5 (100 μg/mL) in vitro. The results showed that intragastric administration of EG (20 mg/kg/d or 80 mg/kg/d for 8 weeks) significantly prevented lung injury, inflammation, and oxidative stress in PM2.5-induced mice, apart from inhibiting collagen deposition. Additionally, EG treatment also suppressed the activation of AKT/mTOR signaling pathway in lung tissues challenged with PM2.5. In vitro experiments further demonstrated that EG treatment could enhance cell viability in a concentration-dependent manner in PM2.5-treated MLE-12 lung epithelial cells. Also, the overexpression of constitutively active AKT could offset the inhibitory effects of EG on EMT and oxidative stress in PM2.5-treated MLE-12 lung epithelial cells. Finally, AKT overexpression also blocked the inhibitory effect of EG on the phosphorylation of mTOR in PM2.5-treated MLE-12 lung epithelial cells. In conclusion, EG could improve PM2.5-induced lung fibrosis by decreasing oxidative damage and EMT through AKT/mTOR pathway, which might be a potential candidate for the treatment of PM2.5-induced lung fibrosis.

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EGCG promotes PRKCA expression to alleviate LPS-induced acute lung injury and inflammatory response

Cited by 50 publications

References 54 publications

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

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

Tanreqing Inhibits LPS-Induced Acute Lung Injury In Vivo and In Vitro Through Downregulating STING Signaling Pathway

Epigallocatechin Gallate Relieved PM2.5-Induced Lung Fibrosis by Inhibiting Oxidative Damage and Epithelial-Mesenchymal Transition through AKT/mTOR Pathway

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