Why the study?
Atrial fibrosis induced by Ang II plays a crucial role in the development of AF, but the involvement of salidroside in AF, AF vulnerability, and Ang II-induced inflammatory atrial fibrosis was unknown.
Does salidroside reduce atrial fibrosis and atrial fibrillation vulnerability in an angiotensin II-induced mouse model?
Does salidroside reduce atrial fibrosis and atrial fibrillation vulnerability in an angiotensin II-induced mouse model?
Salidroside attenuates angiotensin II-induced atrial fibrosis and AF vulnerability in mice by suppressing the LOXL2-TGF-β1-Smad2/3 pathway.
May attenuate Ang II-induced AF in animals; leaves open any role in human AF prevention.
Aims and objectives Salidroside (SAL), an active component isolated from the Chinese plant Rose Rhodiola, has anti-inflammatory, antioxidant, anti-cancer, neuroprotective, and renal protective properties. Atrial fibrosis developed due to angiotensin II (Ang II) plays a crucial function in developing atrial fibrillation (AF). This research investigates the involvement of SAL in AF, its vulnerability to AF, and Ang II-induced inflammatory atrial fibrosis. Methods Ang II (2 mg/kg/day) was infused underneath the skin into male C57BL/6 mice (8–10 weeks old, n = 40) for four weeks to create the AF model. SAL (50 mg/kg/day) was given intraperitoneally once per day for 28 days. Analyses of morphology, histology, and biochemical were carried out. Transesophageal burst pacing was used in vivo to induce AF. Results Ang II injection increased mice's heart rate and systolic blood pressure (SBP), whereas SAL treatment was significantly reduced. Ang II infusion increased left atrial diameter (LAD) in mice, which was attenuated after SAL treatment. SAL alone did not affect AF inducibility, but SAL therapy markedly decreased Ang II-induced AF inducibility. Additionally, the expression levels of interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were inhibited with SAL therapy in mice. Compared to the Ang II group, Ang II infusion raised malondialdehyde (MDA) levels and reduced superoxide dismutase (SOD) and catalase (CAT) activity, but SAL therapy altered all of these effects. SAL treatment significantly reduced LOXL2, TGF-β1, p -Smad2 and p -Smad3 protein expression than the Ang II group mice. Conclusion SAL inhibits atrial fibrosis and potentially attenuates increased susceptibility to AF by suppressing the LOXL2-TGF-β1-Smad2/3 pathway.
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内海 et al. (2023) studied this question.
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