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In hepatic fibrosis, curcumin downregulates beta-catenin protein expression and activity in hepatic stellate cells (HSCs), accelerates HSC senescence via PPARgamma/P53 signaling, inhibits HSC activation and migration by suppressing the CXCL12/CXCR4 bioaxis and RhoA/ROCK signaling, targets the p38MAPK pathway to downregulate methionine adenosyltransferase 2B, reduces Gr1hi monocyte recruitment by downregulating MCP-1 expression, upregulates IL-10 to downregulate TNF-alpha, IL-6, and TGF-beta, decreases oxidative stress by downregulating Rac1-guanosine triphosphate, Rho-related C3 botulinum toxin substrate, and NOX1, and attenuates liver injury by inhibiting pro-angiogenic factors like HIF-1alpha, VEGFR-1, placental growth factor, and COX-2
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This process is mediated by protein arginine methyltransferases (PRMTs), which catalyze methylation to modify the guanidino nitrogens of the arginine residue by adding one or two methyl groups 95
Possible role of the gut microbiotabrain axis in the antidepressant effects of (R)-ketamine in a social defeat stress model
