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Background <p>Cardiac hypertrophy can induce cardiac dysfunction and is an independent risk factor for heart failure. The occurrence of cardiac hypertrophic response is closely associated with cellular mechanisms such as apoptosis and autophagy. Stigmasterol (ST) is a natural steroid and involved in the regulation of many cellular processes. In this study, we aimed to clarify the ST’s cardioprotective role against cardiac hypertrophy and the molecular mechanisms underlying it.</p> Methods <p>The hypertrophy rat model was established by abdominal aortic constriction (AAC). H&amp;E staining evaluated cardiomyocyte size in heart tissues. RT-qPCR assessed the expression of hypertrophic markers ANP and BNP. H9c2 cell injury model was established by angiotensin-II (Ang II) stimulation. The measurement of cell size was conducted by F-actin staining. TUNEL staining was used to evaluate cell apoptosis. The autophagic flux was detected using RFP‐GFP‐LC3. Western blotting was used to measure the levels of apoptosis, autophagy, and signaling-related proteins.</p> Results <p>ST reduced the heart weight to body weight ratio (HW/BW) and the left ventricle weight to body weight ratio (LVW/BW) in AAC-induced rats. ST reduced cell size and downregulated ANP and BNP expression in rat heart and in Ang II-stimulated H9c2 cells. ST inhibited Ang II-induced H9c2 cell apoptosis and excessive autophagy in a concentration-dependent manner. ST treatment reduced p-AMPK levels and increased p-mTOR and p-P70S6K levels in Ang II-stimulated H9c2 cells to inhibit the activation of AMPK/mTOR/p70S6K signaling.</p> Conclusion <p>Overall, ST protects against cardiac hypertrophy by inhibiting cardiomyocyte apoptosis and autophagy through the inactivation of AMPK/mTOR/p70S6K signaling.</p>

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Stigmasterol protects H9c2 cells from angiotensin-II induced hypertrophy by regulating apoptosis and autophagy

  • 期刊论文

  • 发表日期：

    2025年5月13日

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  • Mingming Chang,
  • Jinjin Meng,
  • Ge Liu,
  • Chao Shi

摘要

Background

Cardiac hypertrophy can induce cardiac dysfunction and is an independent risk factor for heart failure. The occurrence of cardiac hypertrophic response is closely associated with cellular mechanisms such as apoptosis and autophagy. Stigmasterol (ST) is a natural steroid and involved in the regulation of many cellular processes. In this study, we aimed to clarify the ST’s cardioprotective role against cardiac hypertrophy and the molecular mechanisms underlying it.

Methods

The hypertrophy rat model was established by abdominal aortic constriction (AAC). H&E staining evaluated cardiomyocyte size in heart tissues. RT-qPCR assessed the expression of hypertrophic markers ANP and BNP. H9c2 cell injury model was established by angiotensin-II (Ang II) stimulation. The measurement of cell size was conducted by F-actin staining. TUNEL staining was used to evaluate cell apoptosis. The autophagic flux was detected using RFP‐GFP‐LC3. Western blotting was used to measure the levels of apoptosis, autophagy, and signaling-related proteins.

Results

ST reduced the heart weight to body weight ratio (HW/BW) and the left ventricle weight to body weight ratio (LVW/BW) in AAC-induced rats. ST reduced cell size and downregulated ANP and BNP expression in rat heart and in Ang II-stimulated H9c2 cells. ST inhibited Ang II-induced H9c2 cell apoptosis and excessive autophagy in a concentration-dependent manner. ST treatment reduced p-AMPK levels and increased p-mTOR and p-P70S6K levels in Ang II-stimulated H9c2 cells to inhibit the activation of AMPK/mTOR/p70S6K signaling.

Conclusion

Overall, ST protects against cardiac hypertrophy by inhibiting cardiomyocyte apoptosis and autophagy through the inactivation of AMPK/mTOR/p70S6K signaling.