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 AngII-induced renal injury induced by angiotensin II (AngII), and further to explore its latent molecular mechanisms. We used an in vivo model of AngII-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 AngII (10 µM) in the presence or absence of catalpol (1, 5, and 10 µM) and incubated for 48 h in vitro. In our study, PAS and masson staining of renal tissue showed that catalpol reduced AngII-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 TNF-α and IL-6 were evidently decreased after catalpol intervention. Catalpol can relieve AngII-induced renal injury by inactivating NF/κB and TGF-β1/Smads signaling pathways. Therefore, catalpol may act as a potential drug to treat AngII-induced renal injury.

中文翻译：

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梓醇通过 NF/κB 通路和 TGF-β1/Smads 通路减轻 Ang II 诱导的肾损伤。

梓醇是一种从地黄中提取的环烯醚萜苷，在以前的研究中显示出多种药理特性，包括抗炎、抗氧化、抗糖尿病、抗肿瘤和多巴胺能神经元保护作用。在这里，我们研究了梓醇对血管紧张素 II (AngII) 诱导的 AngII 肾损伤的影响，并进一步探索其潜在的分子机制。我们使用 AngII 诱导的肾损伤小鼠的体内模型，给予梓醇（25、50 和 100 mg/kg）28 天。AngII (10 µM) 在存在或不存在梓醇 (1, 5 和 10 μM）并在体外孵育 48 小时。在我们的研究中，肾组织的PAS和masson染色显示梓醇以浓度依赖性方式减少AngII诱导的肾损伤。在梓醇处理后观察到胶原蛋白IV和TGF-β1的阳性表达急剧下降。梓醇干预后肾组织中促炎细胞因子TNF-α和IL-6水平明显降低。Catalpol 可以通过灭活 NF/κB 和 TGF-β1/Smads 信号通路来缓解 AngII 诱导的肾损伤。因此，梓醇可作为治疗 AngII 引起的肾损伤的潜在药物。梓醇干预后促炎细胞因子TNF-α和IL-6水平明显下降。Catalpol 可以通过灭活 NF/κB 和 TGF-β1/Smads 信号通路来缓解 AngII 诱导的肾损伤。因此，梓醇可作为治疗 AngII 引起的肾损伤的潜在药物。梓醇干预后促炎细胞因子TNF-α和IL-6水平明显下降。Catalpol 可以通过灭活 NF/κB 和 TGF-β1/Smads 信号通路来缓解 AngII 诱导的肾损伤。因此，梓醇可作为治疗 AngII 引起的肾损伤的潜在药物。