Publications by authors named "Sai-Bo Cheng"

Ethnopharmacological Relevance: Dingxin Recipe Ⅲ (DXR Ⅲ) is a traditional Chinese medicine compound used for hyperlipidemia treatment in clinical practice. However, its curative effects and pharmacological mechanisms in hyperlipidemia have not been clarified to date.

Aim Of The Study: Studies have demonstrated that gut barrier was strongly implicated in lipid deposition.

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This study was designed to explore the effect and mechanism of Gegen Qinlian Decoction(GQD) on cardiac function of diabetic mice with damp-heat syndrome. The db/db diabetic mice were exposed to the damp-heat environment test chamber for inducing the damp-heat syndrome. Forty-eight six-week-old db/db mice were randomly divided into six groups, namely the db/db diabetic model group, db/db diabetic mouse with damp-heat syndrome(db/db-dh) group, db/db diabetic mouse with damp-heat syndrome treated with low-dose GQD(db/db-dh+GQD-L) group, db/db-dh+GQD-M(medium-dose) group, db/db-dh+GQD-H(high-dose) group, and db/db-dh+lipro(liprostatin-1, the inhibitor of ferroptosis) group, with eight six-week-old db/m mice classified into the control group.

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Article Synopsis
  • Macrophage autophagy defects are linked to the worsening of atherosclerosis and are influenced by the TREM2 receptor, which also plays a role in Alzheimer's disease.
  • Although geniposide (GP) can slow atherosclerosis and boost macrophage autophagy, the specific mechanisms of how it works are not yet fully understood.
  • Research showed that high-fat diets increase TREM2 and inhibit autophagy in macrophages; however, GP can reduce TREM2 levels and enhance autophagy, potentially helping to combat atherosclerosis.
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The LOX-1/p38 mitogen-activated protein kinase (MAPK) pathway has been proved to participate in the endothelial dysfunction in atherosclerosis. Trichosanatineis is an active compound isolated from the peel of . This study aims to determine whether trichosanatine prevents the oxidized low-density lipoprotein (ox-LDL)-induced insult through inhibition of the LOX-1/p38 MAPK pathway in HUVECs.

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