According to a recent study published in the Journal of Molecular and Cellular Cardiology, an herb called Salidroside can reduce chronic hypoxia-induced Pulmonary arterial hypertension by promoting PASMCs apoptosis via an A2aR related mitochondria dependent pathway.
Pulmonary arterial hypertension (PAH) is a subset of pulmonary hypertensive syndromes and characterized by pulmonary arterial remodeling, leading to increased pulmonary vascular resistance and increased pulmonary arterial pressure. PAH is a debilitating disease and results ultimately in right ventricular failure and death. It is reported that PAH is diagnosed in approximately 12–50 adult people per million.
Chronic hypoxia-induced PAH is a common type of PAH, mainly secondary to disorders of the respiratory system. Pulmonary arterial remodeling is mainly due to the abnormal growth, excess cellular proliferation, and apoptosis resistance of smooth muscle cells. Therefore, inhibition of the cell proliferation or induction of the cell apoptosis may be an efficient therapeutic strategy for PAH.
Salidroside is an active ingredient isolated from Rhodiola rosea, a member of Crassulaceae and a well-known herb used to relieve high altitude sickness and acute exacerbation of PAH. Several experimental and clinical studies of salidroside have provided evidence of its multiple pharmacological activities including anti-inflammation, anti-oxidation, anti-stress, anti-cancer, and enhancing immune effects.
In the study tiled “Salidroside attenuates chronic hypoxia-induced pulmonary hypertension via adenosine A2a receptor related mitochondria-dependent apoptosis pathway,” Xiaoying Huang and colleagues from the Division of Pulmonary Medicine First Affiliated Hospital of Wenzhou Medical University in China examined the effects of salidroside on PAH and pulmonary arterial remodeling with a mouse model of chronic hypoxia-induced PAH and examined whether salidroside affects hypoxia-induced cell apoptosis resistance both in vivo and in vitro.
The researchers gave the mice an increasing concentration of salidroside (0, 16 mg/kg, 32 mg/kg, and 64 mg/kg), with results revealing that following salidroside treatment, the chronic hypoxia-induced right ventricular hypertrophy and pulmonary arterial remodeling were reduced, indicating a protective role played by salidroside in PAH.
The researchers concluded that salidroside is an effective agent that is able to inhibit chronic hypoxia-induced PAH and pulmonary arterial remodeling partially via the mechanism of enhancing A2aR related mitochondria-dependent apoptosis. Findings from this study can provide an insight into the protective effects of salidroside in patients with PAH. In addition, the findings provide new scientific knowledge regarding the underlying mechanisms of the use of salidroside in the management of clinical hypoxic pulmonary hypertension.
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