Rastegar-Moghaddam Seyed Hamidreza, Amirahmadi Sabiheh, Akbarian Mahsan, Sharizina Matin, Beheshti Farimah, Rajabian Arezoo, Eshaghi Ghalibaf Mohammad Hosein, Azimi Mohaddeseh, Mahmoudabady Maryam, Hosseini Mahmoud
Department of Anatomy and Cell Biology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
J Cardiovasc Thorac Res. 2024;16(2):120-128. doi: 10.34172/jcvtr.33112. Epub 2024 Jun 25.
Evidence declared lipopolysaccharide (LPS) initiates inflammatory responses by stimulating the abandon of cytokines, which may perturb organ function. On the other side, it has been suggested Cedrol has potential properties, including anti-inflammatory and anti-oxidative activities. Herein, this study was done to assess the protective effect of Cedrol against LPS-associated heart damage.
Thirty-five rats (200-250 g) were sorted into five groups, including control, LPS, LPS-Cedrol 7.5 mg/kg, LPS-Cedrol 15 mg/kg, and LPS-Cedrol 30 mg/kg groups. Cedrol was administrated through injected intra-peritoneally for two weeks. The heart tissues were removed and malondialdehyde (MDA) as a lipid peroxidation marker, superoxide dismutase (SOD), and catalase (CAT) as antioxidant markers were assessed. Furthermore, the interleukin (IL)-6 level in cardiac tissue was measured and Masson's trichrome methods were employed to appraise cardiac inflammation and fibrosis, respectively.
Inflammation induced by LPS was significantly accompanied by myocardial fibrosis which was shown by Masson's trichrome staining (<0.001). In addition, LPS administration enhanced the MDA level while it diminished the activity of anti-oxidant markers such as CAT and SOD (<0.001 for all cases). In the histological results, Cedrol improved LPS-induced inflammation and cardiac fibrosis (<0.01 to <0.001). Cedrol also enhanced CAT and SOD activities, whereas declined MDA level in the cardiac tissue (<0.01 to <0.001).
The current findings proposed that the administration of Cedrol exerted a protective role in LPS-associated heart damage by reducing inflammation, cardiac fibrosis, and oxidative stress.
有证据表明脂多糖（LPS）通过刺激细胞因子的释放引发炎症反应，这可能会扰乱器官功能。另一方面，有研究表明雪松醇具有潜在特性，包括抗炎和抗氧化活性。因此，本研究旨在评估雪松醇对脂多糖相关心脏损伤的保护作用。
将35只体重200 - 250克的大鼠分为五组，包括对照组、脂多糖组、7.5毫克/千克雪松醇 + 脂多糖组、15毫克/千克雪松醇 + 脂多糖组和30毫克/千克雪松醇 + 脂多糖组。通过腹腔注射给予雪松醇，持续两周。取出心脏组织，评估作为脂质过氧化标志物的丙二醛（MDA）、作为抗氧化标志物的超氧化物歧化酶（SOD）和过氧化氢酶（CAT）。此外，测量心脏组织中的白细胞介素（IL）-6水平，并分别采用Masson三色染色法评估心脏炎症和纤维化。
脂多糖诱导的炎症显著伴有心肌纤维化，Masson三色染色显示了这一点（<0.001）。此外，给予脂多糖会提高MDA水平，同时降低抗氧化标志物如CAT和SOD的活性（所有情况均<0.001）。在组织学结果中，雪松醇改善了脂多糖诱导的炎症和心脏纤维化（<0.01至<0.001）。雪松醇还增强了CAT和SOD的活性，同时降低了心脏组织中的MDA水平（<0.01至<0.001）。
目前的研究结果表明，给予雪松醇通过减轻炎症、心脏纤维化和氧化应激，对脂多糖相关的心脏损伤发挥了保护作用。
