Summary
Green tea, particularly its active ingredient (-)-epigallocatechin-3-<i>O</i>-gallate (EGCG), reduces the risk of cancer, liver disease and obesity, however, the precise mechanisms underlying these effects remain unclear. Herein, we examined the role of the myeloid cell 67-kDa laminin receptor (67LR) in mediating its physiological effects and demonstrated that the therapeutic effects of EGCG on liver fibrosis and obesity were attenuated in myeloid cell-specific 67LR knockout (67LR<sup>ΔLysM</sup>) mice. EGCG treatment ameliorated liver fibrosis in the control 67LR<sup>fl/fl</sup> male mice but not in the 67LR<sup>ΔLysM</sup> male mice. Next-generation sequencing revealed that EGCG regulates miRNA expression in macrophages through the 67LR. Our results elucidated the anti-inflammatory mecha
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