Salidroside attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II through inhibition of LOXL2-TGF-β1-Smad2/3 pathway
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 developin...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-11-01
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| Series: | Heliyon |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405844023084281 |
| _version_ | 1797429897871753216 |
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| author | Zhen Hai Yingbiao Wu Zhongping Ning |
| author_facet | Zhen Hai Yingbiao Wu Zhongping Ning |
| author_sort | Zhen Hai |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-09T09:19:32Z |
| format | Article |
| id | doaj.art-31a619e3ac714184a77bcae11f2cddb1 |
| institution | Directory Open Access Journal |
| issn | 2405-8440 |
| language | English |
| last_indexed | 2024-03-09T09:19:32Z |
| publishDate | 2023-11-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Heliyon |
| spelling | doaj.art-31a619e3ac714184a77bcae11f2cddb12023-12-02T07:01:31ZengElsevierHeliyon2405-84402023-11-01911e21220Salidroside attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II through inhibition of LOXL2-TGF-β1-Smad2/3 pathwayZhen Hai0Yingbiao Wu1Zhongping Ning2Department of Cardiology, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road Zhangjiang Hi-Tech Park, Pudong New Area, Shanghai, 201203, ChinaDepartment of Cardiology, Shanghai Pudong New Area Zhoupu Hospital (Zhoupu Hospital affiliated to Shanghai Medical College of Health), No.1500 Zhouyuan Road, Pudong New District, Shanghai 201318, ChinaDepartment of Cardiology, Shanghai Pudong New Area Zhoupu Hospital (Zhoupu Hospital affiliated to Shanghai Medical College of Health), No.1500 Zhouyuan Road, Pudong New District, Shanghai 201318, China; Corresponding author.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.http://www.sciencedirect.com/science/article/pii/S2405844023084281SalidrosideAtrial fibrillationAtrial fibrosisAngiotensin IILysyl oxidase-like 2 |
| spellingShingle | Zhen Hai Yingbiao Wu Zhongping Ning Salidroside attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II through inhibition of LOXL2-TGF-β1-Smad2/3 pathway Heliyon Salidroside Atrial fibrillation Atrial fibrosis Angiotensin II Lysyl oxidase-like 2 |
| title | Salidroside attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II through inhibition of LOXL2-TGF-β1-Smad2/3 pathway |
| title_full | Salidroside attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II through inhibition of LOXL2-TGF-β1-Smad2/3 pathway |
| title_fullStr | Salidroside attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II through inhibition of LOXL2-TGF-β1-Smad2/3 pathway |
| title_full_unstemmed | Salidroside attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II through inhibition of LOXL2-TGF-β1-Smad2/3 pathway |
| title_short | Salidroside attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin-II through inhibition of LOXL2-TGF-β1-Smad2/3 pathway |
| title_sort | salidroside attenuates atrial fibrosis and atrial fibrillation vulnerability induced by angiotensin ii through inhibition of loxl2 tgf β1 smad2 3 pathway |
| topic | Salidroside Atrial fibrillation Atrial fibrosis Angiotensin II Lysyl oxidase-like 2 |
| url | http://www.sciencedirect.com/science/article/pii/S2405844023084281 |
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