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Recently, we showed that <jats:italic>Terminalia bellirica<\/jats:italic> (Gaertn.) Roxb. extract (TBE) inhibits inflammatory response and reactive oxygen species (ROS) production in THP\u20101 macrophages. However, molecular mechanisms underlying anti\u2010inflammatory and antioxidant activities of TBE and its major polyphenolic compounds gallic acid (GA) and ellagic acid (EA) remain unclear. We found that TBE and GA attenuated LPS\u2010induced inflammatory mediator expression, ROS production, and activation of mitogen\u2010activated protein kinase (MAPK) and nuclear factor\u2010kappa B (NF\u2010<jats:italic>\u03ba<\/jats:italic>B) in RAW 264 macrophages. Furthermore, TBE and GA increased antioxidant enzyme expression along with upstream mediators nuclear factor erythroid\u20102\u2010related factor 2 (Nrf2), Akt, and AMP\u2010activated protein kinase (AMPK). Importantly, knockdown of Nrf2 by siRNA and specific inhibition of Akt and AMPK significantly reduced antioxidant enzyme expression induced by TBE and GA. Finally, <jats:italic>in vivo<\/jats:italic> effects on histopathology and gene expression were assessed in tissues collected after intraperitoneal injection of LPS with or without TBE treatment. TBE enhanced antioxidant enzyme expression and improved acute kidney injury in LPS\u2010shock model mice. In conclusion, TBE and GA exert protective effects against inflammation and oxidative stress by suppressing MAPK\/NF\u2010<jats:italic>\u03ba<\/jats:italic>B pathway and by activating Akt\/AMPK\/Nrf2 pathway. These results suggest that TBE and GA might be effective for the treatment of inflammation\u2010related diseases.<\/jats:p>","DOI":"10.1155\/2018\/9364364","type":"journal-article","created":{"date-parts":[[2018,11,8]],"date-time":"2018-11-08T23:34:02Z","timestamp":1541720042000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":140,"title":["<i>Terminalia bellirica<\/i> (Gaertn.) Roxb. 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