Jianpi Qutan Formula attenuates vulnerable plaques by regulating IGFBP3.

Area of Science:

• Integrative Medicine
• Cardiovascular Research
• Molecular Biology

Background:

• Spleen deficiency phlegm-turbidity syndrome (SD-PTS) is a key pattern in unstable angina (UAP), characterized by impaired spleen function leading to phlegm-turbidity obstruction.
• Jianpi Qutan Formula (JPQT), a traditional Chinese medicine, is used for coronary heart disease, but its mechanism in stabilizing vulnerable plaques is unclear.

Purpose of the Study:

• Investigate IGF-1/IGFBP3 axis expression in UAP patients with SD-PTS.
• Explore JPQT's mechanism in stabilizing atherosclerotic plaques via the IGF-1/IGFBP3 axis and endothelial-mesenchymal transition (EndMT).

Main Methods:

• Quantitative proteomic analysis of plasma from UAP patients and controls.
• Established a mouse model of atherosclerotic vulnerable plaques with SD-PTS.
• Assessed plaque characteristics, IGF-1/IGFBP3 levels, and EndMT markers in mice treated with JPQT or atorvastatin.

Main Results:

• Plasma IGFBP3 was upregulated in UAP patients with SD-PTS, identified as a core target.
• Mouse models showed reduced IGF-1, elevated IGFBP3, activated EndMT, and increased plaque vulnerability.
• JPQT intervention reversed these changes, improving plaque stability.

Conclusions:

• IGF-1/IGFBP3 axis imbalance and EndMT activation are key in UAP with SD-PTS.
• JPQT stabilizes vulnerable plaques by regulating the IGF-1/IGFBP3 axis and inhibiting EndMT.
• Provides a scientific basis for JPQT's clinical use in UAP.