A new study has found that Tanreqing injection (TRQ) may help attenuate the remodeling of pulmonary artery smooth muscle cells (PASMCs) in hypoxia-induced pulmonary arterial hypertension (HPAH).

The study, published in Oxidative Medicine and Cellular Longevity, suggests that TRQ might achieve these effects by inhibiting reactive oxygen species (ROS) and the TRPC1/CX3CL1 signaling pathway.

HPAH occurs due to vascular endothelial cell damage and increased pulmonary vascular tension caused by hypoxia and oxidative stress. Its etiology is complicated, but one primary pathological change in HPAH involves the migration and proliferation of PASMCs. The researchers attempted to simulate the environment of PASMCs in HPAH and assess the effect of TRQ on these cells.

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In addition, calcium channels are known to initiate cell proliferation signal transduction, leading to pulmonary vasoconstriction. Thus, another area the team explored was the effect of TRQ on calcium changes in PASMCs undergoing hypoxia.

Read more about PAH etiology

“Tanreqing injection is a new traditional Chinese medicine with good antibacterial, antiviral, antipyretic, and anticonvulsion effects and developed in the treatment of acute upper respiratory tract infection and acute pneumonia,” the research team explained. “In the present study, we explored the effect of TRQ on human pulmonary artery smooth muscle cells undergoing hypoxia and feasible molecular mechanisms.”

Their results revealed that TRQ inhibited hypoxia-induced increases in cell adhesion, ROS, calcium, hydroxyl free radicals, and CX3CR1, among other aspects affected by hypoxia, perhaps by inhibiting ROS and the TRPC1/CX3CL1 signaling pathway. However, the experiments were conducted in vitro, so firm conclusions cannot yet be drawn from the findings. The research team plans to explore the effect of TRQ on HPAH in a rat model in a future study.


Xiang Y, Zheng F, Zhang Q, et al. Tanreqing injection regulates cell function of hypoxia-induced human pulmonary artery smooth muscle cells (HPASMCs) through TRPC1/CX3CL1 signaling pathway. Oxid Med Cell Longev. 2022;2022:3235102. doi:10.1155/2022/3235102