Na 3 V 2 (PO 4 ) 3 represents a well-known NASICON-structured SIB cathode. It possesses a theoretical capacity of 117 mAh g −1 with a discharge plateau at ≈3.4 V.

Background/Objectives: The polyphenol resveratrol (Rev) has been found to exhibit various beneficial effects including prevention of pulmonary arterial hypertension (PAH). The present study was designed to investigate the action and potential mechanism of Rev on PAH, focusing on the role of SIRT1 (Silent Information Regulator 1) in apoptosis of pulmonary artery smooth muscle cells (PASMCs). Methods: PAH rats were established by exposure to hypoxia for 21 days. Rev and SRT1720 (a selective SIRT1 activator) were used to reverse PAH by gavaging rats. PASMCs were confronted with hypoxia for 24 h or 48 h and were then treated with Rev or SRT1720 in vitro. Western blot was performed to detect the protein expression of SIRT1. CCK-8 and scratch wound experiments were carried out to verify cell proliferation. In addition, the TUNEL positive assay and flow cytometry assay were used to measure PASMC apoptosis. Mitochondrial permeability transition (mPT) was identified by confocal microscopy. Right ventricular systolic pressure (RVSP) was determined with a Gould pressure transducer, and right ventricular hypertrophy (RVH) was determined by weighing the cardiac muscle. Results: We demonstrated that Rev could reverse the remodelling of the pulmonary vasculature, thus contributing to alleviating the severity of PAH. Down-regulation of SIRT1 was observed in PAH, but administration of Rev had no obvious effect on the protein expression of SIRT1. In addition, Rev could induce mitochondrial swelling and nuclear pyknosis, leading to small, dense, and dysmorphic mitochondria in rats exposed to hypoxia alone. Rev treatment inhibited PASMC proliferation in a dose-dependent manner in vitro. Incubation with SRT1720, a specific activator of SIRT1, significantly retarded PASMC proliferation and promoted PASMC apoptosis in vitro. The mechanism could be associated with inducing mPT damage in PASMCs. Rev and SRT1720 treatment mitigated RVSP and reduced RVH. Conclusion: Rev produced a beneficial effect partially by enhancing the activation of SIRT1, thus improving RVSP and reducing RVH. SIRT1 activation increased PASMC apoptosis by inducing mPT dysfunction, which might be a novel future strategy for the treatment of PAH.

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Stromal cell-derived factor 1 (CXCL12) and its receptor CXC chemokine receptor 4 (CXCR4) are known to modulate hypoxia-induced pulmonary hypertension (PH) and vascular remodeling by mobilization and recruitment of progenitor cells to the pulmonary vasculature. However, little is known about CXCL12/CXCR4 regulating proliferation and cell cycle progression of pulmonary arterial smooth muscle cells (PASMCs). To determine whether CXCL12/CXCR4 regulates PASMC proliferation and the cell cycle, immunohistochemistry, Western blot, bromodeoxyuridine incorporation and cell cycle analysis were preformed in this study. Our results showed that CXCR4 was induced by hypoxia in pulmonary arteries and PASMCs of rats. Hypoxia-increased cell viability, DNA synthesis and proliferating cell nuclear antigen expression were blocked by administration of CXCR4 antagonist AMD3100, silencing CXCR4 or CXCL12. Furthermore, inhibition of CXCL12/CXCR4 suppressed cell cycle progression, decreased the number of cells in S+G2/M phase and attenuated the expression of proteins that regulate the cell cycle progression at these phases. In addition, PI3K/Akt signaling mediated CXCL12/CXCR4 regulating proliferation and cell cycle progression in PASMCs. Thus, these results indicate that blockade of CXCL12/CXCR4 inhibited PASMC proliferation and cell cycle progression in hypoxia-induced PH via PI3K/Akt signaling pathway.