Cardiovascular

Jingling Granules alleviate atherosclerosis through activating autophagy and inhibiting human umbilical vein endothelial cells apoptosis.

TL;DR

Jingling Granules decelerate atherosclerosis progression by inhibiting mTOR to enhance autophagy and suppress apoptosis, highlighting its therapeutic potential in early stage atherosclerosis.

Key Findings

JLG improved serum lipid profiles in high-fat diet-fed ApoE-/- mice.

  • The study used ApoE-/- mice fed a high-fat diet as an in vivo atherosclerosis model.
  • JLG treatment resulted in improved serum lipid profiles compared to untreated controls.
  • Specific lipid measurements (e.g., total cholesterol, LDL, triglycerides) were assessed but exact values are not reported in the abstract.

JLG moderately reduced atherosclerotic lesion area in ApoE-/- mice.

  • Atherosclerotic lesion area was quantified in high-fat diet-fed ApoE-/- mice.
  • The abstract characterizes the reduction as 'moderate', suggesting a partial but not complete attenuation of lesion development.
  • The authors highlight therapeutic potential specifically in 'early stage atherosclerosis'.

JLG suppressed systemic inflammation in the atherosclerosis mouse model.

  • Systemic inflammation was assessed in high-fat diet-fed ApoE-/- mice treated with JLG.
  • JLG treatment led to suppression of systemic inflammatory markers compared to controls.
  • Specific inflammatory markers and their measured values are not detailed in the abstract.

JLG enhanced autophagic flux in vivo in atherosclerotic mice.

  • Autophagic flux was evaluated in the ApoE-/- high-fat diet mouse model.
  • JLG treatment enhanced autophagic flux compared to untreated atherosclerotic mice.
  • Enhanced autophagy was associated with attenuation of endothelial cell apoptosis.

JLG attenuated endothelial cell apoptosis in atherosclerotic mice.

  • Endothelial cell apoptosis was measured in high-fat diet-fed ApoE-/- mice.
  • JLG treatment reduced apoptosis of endothelial cells in the atherosclerotic context.
  • Reduced apoptosis occurred alongside enhanced autophagic flux.

JLG downregulated phosphorylated mTOR (p-mTOR), indicating inhibition of the mTOR signaling pathway.

  • Mechanistic analysis was performed measuring phosphorylated mTOR (p-mTOR) levels.
  • JLG treatment resulted in downregulation of p-mTOR, indicating mTOR pathway inhibition.
  • mTOR pathway inhibition was identified as the mechanistic basis for JLG's effects on autophagy and apoptosis.

In palmitic acid-challenged HUVECs, JLG promoted autophagy and reduced apoptosis through mTOR inhibition.

  • Human umbilical vein endothelial cells (HUVECs) were challenged with palmitic acid to model lipotoxic endothelial injury in vitro.
  • JLG treatment promoted autophagy and reduced apoptosis in this cell model.
  • The mTOR activator MHY1485 abolished the protective effects of JLG on both autophagy and apoptosis, confirming mTOR dependence.
  • This pharmacological rescue experiment provides mechanistic confirmation that JLG's effects are mediated via mTOR signaling.

What This Means

This research suggests that a traditional Chinese medicine formulation called Jingling Granules (JLG) can slow the progression of atherosclerosis — the buildup of plaques in arteries that is a major cause of heart disease — by activating a cellular 'self-cleaning' process called autophagy and reducing the death of cells lining blood vessels. The researchers tested JLG in mice genetically prone to atherosclerosis and fed a high-fat diet, finding that JLG improved blood fat levels, modestly reduced plaque size, and lowered whole-body inflammation. They also found that JLG activated autophagy and reduced programmed cell death (apoptosis) in vascular endothelial cells. To understand how JLG works at a molecular level, the researchers examined a key signaling protein called mTOR, which normally suppresses autophagy. JLG was found to reduce the active (phosphorylated) form of mTOR, suggesting it works by 'putting the brakes' on this suppressor, thereby allowing cells to clean up damaged components and survive longer. When this mechanism was tested in lab-grown human blood vessel cells stressed with a fatty acid (palmitic acid), JLG's protective effects were completely blocked when an mTOR-activating drug was added, confirming that mTOR inhibition is central to JLG's action. This research suggests that JLG may have potential as a complementary therapy for early-stage atherosclerosis by targeting the mTOR pathway to simultaneously promote cellular housekeeping and reduce cell death in blood vessels. The findings provide a scientific mechanism to explain the vascular protective effects of this clinically used formulation and may support further investigation into mTOR-targeting strategies for cardiovascular disease.

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Citation

Wang Y, Liu Y, Niu D, Liu C, Wu Q, Cao L, et al.. (2026). Jingling Granules alleviate atherosclerosis through activating autophagy and inhibiting human umbilical vein endothelial cells apoptosis.. Scientific reports. https://doi.org/10.1038/s41598-026-63278-5