Department of Critical Care Medicine, Beijing Tsinghua Changgung Hospital, Beijing 102218, P.R. China.
Department of Applied Chemistry, Peking University, Beijing 100871, P.R. China.
Mol Med Rep. 2018 May;17(5):7142-7148. doi: 10.3892/mmr.2018.8767. Epub 2018 Mar 16.
Ursolic acid (UA) as a multiple bioactive native compound has recently been demonstrated to treat sepsis in animal models. However, the beneficial effects of UA in sepsis‑induced acute kidney injury (AKI) are not completely understood. In the present study, the effect of UA on sepsis‑induced AKI in cecal ligation and puncture (CLP) surgery mice was investigated. Renal histomorphological analysis was performed by hematoxylin and eosin staining. The expression of inflammatory markers in the kidney of septic mice was measured by reverse transcription‑quantitative polymerase chain reaction and western blotting. The results demonstrated that UA administration improved survival in septic mice induced by CLP surgery. The treatment with UA revealed protection against AKI induced by CLP surgery, including the alleviation of glomerular damage and vacuolization in the proximal tubules. In addition, the effects of UA on oxidative stress and inflammation in septic mice were determined. The findings suggested that UA may protect against sepsis‑induced AKI by inhibiting reactive oxygen species and inflammatory cytokines, including tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6, in the kidney from septic mice. Finally, UA inhibited CLP‑induced activation of nuclear factor‑κB signaling in the kidney from septic mice. The findings of the present study demonstrated that UA may be used as a potential therapeutic agent for complications of sepsis, especially for sepsis-induced AKI.
熊果酸(UA)作为一种具有多种生物活性的天然化合物,最近已被证明可在动物模型中治疗脓毒症。然而,UA 在脓毒症引起的急性肾损伤(AKI)中的有益作用尚不完全清楚。在本研究中,研究了 UA 对盲肠结扎和穿刺(CLP)手术小鼠脓毒症诱导的 AKI 的影响。通过苏木精和伊红染色进行肾组织形态学分析。通过逆转录-定量聚合酶链反应和蛋白质印迹法测量脓毒症小鼠肾脏中炎症标志物的表达。结果表明,UA 给药可提高 CLP 手术诱导的脓毒症小鼠的存活率。UA 治疗对 CLP 手术诱导的 AKI 具有保护作用,包括减轻肾小球损伤和近端肾小管空泡化。此外,还确定了 UA 对脓毒症小鼠氧化应激和炎症的影响。研究结果表明,UA 可能通过抑制活性氧物质和炎症细胞因子(包括肿瘤坏死因子-α、白细胞介素(IL)-1β 和 IL-6)来保护脓毒症小鼠的肾脏免受脓毒症诱导的 AKI。最后,UA 抑制了脓毒症小鼠肾脏中核因子-κB 信号的 CLP 诱导激活。本研究的结果表明,UA 可作为治疗脓毒症并发症的潜在治疗剂,特别是用于治疗脓毒症引起的 AKI。