Zhao Hongyu, Zhao Min, Wang Yu, Li Fengchun, Zhang Zhigang
Department of Emergency Medicine, Shengjing Hospital of China Medical University, 36 Sanhao Street, Shenyang 110004, China.
Evid Based Complement Alternat Med. 2016;2016:8219287. doi: 10.1155/2016/8219287. Epub 2016 Jan 24.
Glycyrrhizic acid (GA) is a major active ingredient in licorice. In our study, the effects of GA on acute kidney injury (AKI) in rats and its underlying molecular mechanisms were investigated. The sepsis model was produced by caecal ligation and puncture (CLP) in rats. The molecular and histological experiments were performed in the kidney tissues and serum samples of rats. According to the results obtained, GA alleviated sepsis-induced AKI by improving the pathological changes, decreasing the levels of blood urea nitrogen (BUN), creatinine (Cre), and increasing the survival rate of rats with AKI significantly. The production of inflammatory cytokines, such as TNF-α, IL-1β, and IL-6, was markedly inhibited by GA. Moreover, treatment with GA inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) and expression levels of induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in kidney tissues. Furtherly, the apoptosis in kidney tissue induced by AKI was suppressed by GA. Finally, GA could inhibit the activation of NF-κB signaling pathway. Our study suggests that GA alleviates sepsis-induced AKI by inhibiting the NF-κB signaling pathway, which provides a strong evidence for a new approach for treating sepsis-induced AKI.
甘草酸（GA）是甘草中的主要活性成分。在我们的研究中，研究了GA对大鼠急性肾损伤（AKI）的影响及其潜在的分子机制。通过大鼠盲肠结扎和穿刺（CLP）建立脓毒症模型。在大鼠的肾脏组织和血清样本中进行分子和组织学实验。根据所得结果，GA通过改善病理变化、降低血尿素氮（BUN）、肌酐（Cre）水平，并显著提高AKI大鼠的存活率，从而减轻脓毒症诱导的AKI。GA显著抑制了炎症细胞因子如TNF-α、IL-1β和IL-6的产生。此外，GA处理抑制了肾脏组织中一氧化氮（NO）和前列腺素E2（PGE2）的产生以及诱导型一氧化氮合酶（iNOS）和环氧化酶-2（COX-2）的表达水平。此外，GA抑制了AKI诱导的肾脏组织细胞凋亡。最后，GA可以抑制NF-κB信号通路的激活。我们的研究表明，GA通过抑制NF-κB信号通路减轻脓毒症诱导的AKI，这为治疗脓毒症诱导的AKI的新方法提供了有力证据。
