Department of Cardiology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.
Department of Traumatic Orthopaedics, The Third Affiliated Hospital of Shandong First Medical University (Affiliated Hospital of Shandong Academy of Medical Sciences), Jinan, Shandong, China.
J Cardiovasc Pharmacol. 2022 Jan 1;79(1):e116-e121. doi: 10.1097/FJC.0000000000001148.
Catalpol is an iridoid glycoside obtained from Rehmannia glutinosa, which in previous studies showed various pharmacological properties, including anti-inflammatory, antioxidant, antidiabetic, antitumor, and dopaminergic neurons protecting effects. Here, we examined the effect of catalpol on renal injury induced by angiotensin II (Ang II) and further to explore its latent molecular mechanisms. We used an in vivo model of Ang II-induced renal injury mice; catalpol (25, 50, and 100 mg/kg) was administered for 28 days. Mouse glomerular mesangial cells (SV40 MES 13), rat kidney interstitial fibroblasts cells (NRK-49F), and human proximal tubular epithelial cells (HK-2) were induced by Ang II (10 µM) in the presence or absence of catalpol (1, 5, and 10 µM) and incubated for 48 hours in vitro. In our study, periodic acid-Schiff and Masson staining of renal tissue showed that catalpol reduced Ang II-induced renal injury in a concentration-dependent manner. The positive expressions of collagen IV and TGF-β1 were observed to decrease sharply after catalpol treatment. In renal tissue, the levels of pro-inflammatory cytokines tumor necrosis factor α and interleukin 6 were evidently decreased after catalpol intervention. Catalpol can relieve Ang II-induced renal injury by inactivating NF-κB and TGF-β1/Smads signaling pathways. Therefore, catalpol may act as a potential drug to treat Ang II-induced renal injury.
梓醇是从地黄中提取的环烯醚萜苷，先前的研究表明其具有多种药理活性，包括抗炎、抗氧化、抗糖尿病、抗肿瘤和保护多巴胺能神经元作用。在这里，我们研究了梓醇对血管紧张素 II（Ang II）诱导的肾损伤的作用，并进一步探讨了其潜在的分子机制。我们使用 Ang II 诱导的肾损伤小鼠的体内模型；梓醇（25、50 和 100mg/kg）给药 28 天。在存在或不存在梓醇（1、5 和 10µM）的情况下，用 Ang II（10µM）诱导小鼠肾小球系膜细胞（SV40 MES 13）、大鼠肾间质成纤维细胞（NRK-49F）和人近端肾小管上皮细胞（HK-2）48 小时进行体外孵育。在我们的研究中，对肾组织进行过碘酸-Schiff 和 Masson 染色显示，梓醇以浓度依赖的方式减轻 Ang II 诱导的肾损伤。胶原 IV 和 TGF-β1 的阳性表达在梓醇处理后明显减少。在肾组织中，肿瘤坏死因子 α 和白细胞介素 6 等促炎细胞因子的水平在梓醇干预后明显降低。梓醇通过抑制 NF-κB 和 TGF-β1/Smads 信号通路来缓解 Ang II 诱导的肾损伤。因此，梓醇可能作为一种治疗 Ang II 诱导的肾损伤的潜在药物。
