2021年 · 第44卷第05期

The focus of this issue is the diagnosis and treatment of tuberculosis. Three articles have been published in the special written talks and treatises columns, so stay tuned.

Background and PurposeChangshanone (HF) is a derivative of changshanine isolated from the traditional Chinese medicine Changshan, which has anti-hypertrophy, anti-fibrosis and anti-proliferation effects. We sought to investigate whether HF can cause pulmonary vasodilation and alleviate pulmonary arterial hypertension (HPH) due to chronic hypoxia. Methods Voltage-dependent Ca in pulmonary artery smooth muscle cells (PASMC) was detected by patch-clamp assay²⁺Activity of channel H (VDCC). Detection of intracellular Ca in PASMC by digital fluorescence microscopy²⁺Concentration. Pulmonary artery pressure was measured with isolated perfused and ventilated mouse lungs. Hypoxia in mice (10% O₂) 4 weeks in vivo experiments were performed for the HPH model. Results HF increases the voltage gating K in PASMC⁺(Kv) current, and HEK cells transfected with the KCNA5 gene K through the KCNA5 channel⁺Current increases. HF (0.03~1 μ mol/L) inhibited receptor-manipulated Ca in HEK cells transfected with calcium-sensitive receptor genes²⁺channel (ROCE), blocking the storage-manipulated Ca in the PASMC²⁺Channel (SOCE). Acute (3-5 min) intrapulmonary perfusion of HF significantly and reversibly inhibited alveolar hypoxia-induced pulmonary vasoconstriction in a dose-dependent manner (0.1-10 μ mol/L). Intraperitoneal injection of HF (0.3 mg/kg for 2 weeks) can partially reverse the formation of PH in mice. Conclusion HF is an effective pulmonary vasodilator by activating Kv channels and blocking voltage-gated, receptor-manipulated, and storage-manipulated Ca in PASMC²⁺The channel works. The therapeutic effect of HF on experimental HPH may be the result of a combination of vasodilatation by inhibition of E-C coupling and antiproliferation by inhibition of PI3K/AKT/mTOR signaling pathway.