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. 2023 Sep 23;14(1):1–19. doi: 10.1016/j.apsb.2023.09.014

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© 2024 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

Diagram of the mechanism of GB on independent risk factors for atherosclerosis. Trimethylamine N-oxide (TMAO) levels in the blood can be utilized as a predictor of early atherosclerosis. Trimellitic anhydride (TMA) is derived from digested and absorbed foods containing choline or trimethylamine ingredients and then oxidized to TMAO by flavin monooxygenases (FMOs) secreted by the liver. This process could be inhibited by regulating the intestinal flora after GB treatment. In addition, a high-fat diet (HFD) resulted in higher levels of TG, TC, and LDL-C in serum, which were positively correlated with atherosclerosis. GB significantly attenuated the abnormal lipid and cholesterol metabolism induced by HFD. On the other hand, GB can improve resistance to ferroptosis through the Nrf2/HO-1 signaling pathway, thereby improving the pathological process of atherosclerosis. In addition to ameliorating HFD-induced atherosclerosis, GB also reduces endothelial dysfunction after high glucose treatment by inhibiting PAF-R and TLR4 binding, and it can treat diabetes mellitus by protecting β cells.