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  3. SIRT3 mediates Tubeimoside I's inhibition on pulmonary artery smooth muscle cell proliferation and oxidative stress in pulmonary arterial hypertension

SIRT3 mediates Tubeimoside I's inhibition on pulmonary artery smooth muscle cell proliferation and oxidative stress in pulmonary arterial hypertension

  • Eur J Pharmacol. 2025 Oct 5:1004:177938. doi: 10.1016/j.ejphar.2025.177938.
Yan Li 1,  Yumin Zhang 1,  Yunwei Chen 2,  Zhuo Qiao 1,  Dongrong Wang 3,  Yunjing Yang 1,  Wei Huang 4,  Jianghong Yan 5
Affiliations

Affiliations

  • 1 Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
  • 2 Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China; Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China.
  • 3 Department of Biochemistry and Molecular Biology, College of Basic Medicine, Chongqing Medical University, Chongqing, 400016, China.
  • 4 Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China. Electronic address: 202728@hospital.cqmu.edu.cn.
  • 5 Department of Biochemistry and Molecular Biology, College of Basic Medicine, Chongqing Medical University, Chongqing, 400016, China; Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, China. Electronic address: yanjianghong@cqmu.edu.cn.
PMID: 40685102 DOI: 10.1016/j.ejphar.2025.177938
Abstract

Pulmonary arterial hypertension (PAH) is defined as a mean pulmonary arterial pressure (mPAP) ≥ 20 mmHg. None of the approved therapies involve persistent vessel injury or vascular remodelling. Tubeimoside I (TBM) is a triterpenoid saponin purified from the traditional Chinese medicine tubeimu. In this study, we detected a favourable effect of TBM in ameliorating right cardiac function, haemodynamics and pulmonary arteriole remodelling. To elucidate the mechanism by which TBM exerts its effects, we examined the effects of TBM on oxidative stress and the proliferation of pulmonary artery smooth muscle cells (PASMCs) both in vivo and in vitro. Notably, Sirtuin 3 (SIRT3) expression was decreased in the lung tissue and PASMCs in the PAH model, whereas TBM treatment reversed the decrease in SIRT3 expression. To clarify how SIRT3 functions in the antiproliferative and antioxidative effects of TBM, we generated a knockdown of SIRT3 via small interfering RNA (siRNA) before TBM treatment. We demonstrated that the antiproliferative and antioxidative effects of TBM were largely abolished by eliciting the knockdown of SIRT3 with siRNA. These findings suggest that SIRT3 plays an essential role in the antiproliferative and antioxidative effects of TBM and that TBM may be a potential drug candidate for treating PAH.

Keywords

Proliferation; Pulmonary arterial hypertension; Pulmonary artery smooth muscle cell; Sirt3; Tubeimoside I.

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