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. 2021 Dec 15;12:767333. doi: 10.3389/fphar.2021.767333

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Copyright © 2021 Gao, Yan, Zhou, Wang, Sai, Fu, Liu and Ding.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Puerarin protected against HFD/CUMS-induced depression via the TLR4/cPLA2/COX-2 pathway. HFD/CUMS stimulation induced depression-like behavior via increasing inflammatory damages. Inflammatory response is related to TLR4 activation, inducing the changes of structure and function in the brain and small intestine tissues. Puerarin treatment alleviated the depressive phenotype by suppressing TLR4 activation and cytokine over-production, restoring lipid metabolites, inhibiting enzyme activities of cPLA2 and COX-2, and decreasing downstream PGE₂ production. HFD: high-fat diet; CUMS: chronic unpredictable mild stress; TLR4: Toll-like receptor 4; LOX: lipoxygenase; cPLA2: calcium-dependent cytosolic phospholipases A2; COX-2: cyclooxygenase-2; PGE₂: prostaglandin E₂; HETEs: hydroxyeicosatetraenoic acids.