Tannic acid protects against experimental acute lung injury through downregulation of TLR4 and MAPK. Issue 5 (24th September 2018)

• Record Type: Journal Article
• Authors: Sivanantham, Ayyanar; Pattarayan, Dhamotharan; Bethunaickan, Ramalingam; Kar, Amrita; Mahapatra, Santanu Kar; Thimmulappa, Rajesh K.; Palanichamy, Rajaguru; Rajasekaran, Subbiah
• Is Part Of: Journal of cellular physiology. Volume 234:Issue 5(2019:May)
• Page Start: 6463
• Page End: 6476
• Publication Date: 2018-09-24
• Subjects: ALI -- cytokines -- LPS -- MAPK -- tannic acid -- TLR4; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.27383
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: Acute lung injury (ALI) and its severe form acute respiratory distress syndrome (ARDS) remain a major cause of morbidity and mortality in critically ill patients, and no specific therapies are still available to control the mortality rate. Thus, we explored the preventive and therapeutic effects of tannic acid (TA), a natural polyphenol in the context of ALI. We used in vivo and in vitro models, respectively, using lipopolysaccharide (LPS) to induce ALI in mice and exposing J774 and BEAS‐2B cells to LPS. In both preventive and therapeutic approaches, TA attenuated LPS‐induced histopathological alterations, lipid peroxidation, lung permeability, infiltration of inflammatory cells, and the expression of proinflammatory mediators. In addition, in‐vitro study showed that TA treatment could reduce the expression of proinflammatory mediators. Further studies revealed that TA‐dampened inflammatory responses by downregulating the LPS‐induced toll‐like receptor 4 (TLR4) expression and inhibiting extracellular‐signal‐regulated kinase (ERK)1/2 and p38 mitogen‐activated protein kinase (MAPK) activation. Furthermore, cells treated with the inhibitors of ERK1/2 (PD98059) and p38 (SB203580) mitigated the expression of cytokines induced by LPS, thus suggesting that ERK1/2 and p38 activity are required for the inflammatory response. In conclusion, TA could attenuate LPS‐induced inflammation and may be a potential therapeutic agent for ALI‐associated inflammation in clinical settings. Abstract : Acute lung injury and its severe form acute respiratory distress syndrome remain a major cause of morbidity and mortality in critically ill patients, and no specific therapies are still available to control the mortality rate. In this study, our results demonstrated that tannic acid, a natural polyphenol treatment attenuated lipopolysaccharide‐induced inflammatory response and oxidative stress by blocking toll‐like receptor 4 expression and mitogen‐activated protein kinase activation