Department of Anesthesiology, Cangzhou Central Hospital, No.16 Xinhua West Road, Yunhe District, Cangzhou, Hebei, China.
Department of Anesthesiology, Shanghai First People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Inflammation. 2018 Feb;41(1):114-121. doi: 10.1007/s10753-017-0669-3.
Artesunate (AS), a semi-synthetic derivative of Artemisia, has been shown to exert a wide range of pharmacological effects, such as anti-inflammatory and antioxidant functions. However, the protective functions of AS on renal ischemia reperfusion injury (RIR)-stimulated lung inflammation remain unclear. In this research, acute lung injury (ALI) was stimulated by renal ischemia reperfusion injury (RIR). AS (15 mg/kg) was intraperitoneal administrated to rat 1 h before RIR stimulation. Serum and pulmonary NO, MDA, IL-6, MIP-2, and PGE levels, arterial blood gas and biochemistry, lung wet/dry weight ratio and MPO activity, total cell number and protein concentration in BALF, tissue histology, and NF-κB expression were determined. The results indicated that serum and pulmonary NO, MDA, IL-6, MIP-2, and PGE levels, lung wet/dry weight ratio and MPO activity, total cell number, and protein concentration in BALF enhanced after RIR stimulation. These alterations were mitigated by AS. AS attenuated lung wet/dry weight ratio and MPO activity, total cell number, and protein concentration in BALF. AS attenuated RIR-stimulated pulmonary NF-κB phosphorylation. In addition, these previously mentioned actions of AS were antagonized by suppressing HO-1 pathway. However, RIR-stimulated arterial blood gas and biochemistry and lung histopathology were also attenuated by AS. In summary, AS inhibited RIR-stimulated lung inflammation by activating HO-1 pathway.
青蒿琥酯(AS)是青蒿的一种半合成衍生物,具有广泛的药理作用,如抗炎和抗氧化功能。然而,AS 对肾缺血再灌注损伤(RIR)刺激的肺炎症的保护作用尚不清楚。在这项研究中,通过肾缺血再灌注损伤(RIR)刺激急性肺损伤(ALI)。在 RIR 刺激前 1 小时,腹腔内给予大鼠 AS(15mg/kg)。测定血清和肺组织中 NO、MDA、IL-6、MIP-2 和 PGE 水平、动脉血气和生化、肺湿/干重比和 MPO 活性、BALF 中的总细胞数和蛋白浓度、组织学和 NF-κB 表达。结果表明,RIR 刺激后血清和肺组织中 NO、MDA、IL-6、MIP-2 和 PGE 水平、肺湿/干重比和 MPO 活性、BALF 中的总细胞数和蛋白浓度均升高。AS 减轻了这些变化。AS 减轻了肺湿/干重比和 MPO 活性、BALF 中的总细胞数和蛋白浓度。AS 减弱了 RIR 刺激的肺 NF-κB 磷酸化。此外,AS 还拮抗了 HO-1 通路,从而减弱了上述 AS 作用。然而,AS 也减轻了 RIR 刺激的动脉血气和生化以及肺组织病理学变化。总之,AS 通过激活 HO-1 通路抑制 RIR 刺激的肺炎症。