杜松子粗萃物對敗血性休克引起急性腎損傷的保護作用
林大欽1、徐邦治2、李崇仁3
1三軍總醫院澎湖分院泌尿科；2花蓮慈濟醫院腎臟科；3慈濟科技大學護理系
Juniperus Communis Extract Ameliorates Lipopolysaccharide-Induced Acute Kidney Injury
Ta Chin Lin 1, Bang-Gee Hsu2, Chung-Jen Lee3
1Divisions of Urology, Tri-Service General Hospital; 2Division of Nephrology, Hualien Tzu Chi Hospital; 3Department of Nursing, Tzu Chi University of Science and Technology
Purpose: Lpopolysaccharide induced endotoxin shock can induce the production of several inflammatory mediators that leading to acute kidney injury (AKI). Juniperus communis extract had shown great improvement on anti-inflammatory effect. We investigated the pleiotropic effects of Juniperus communis extract (JCo, 1 mg/kg, intravenous administration) on lipopolysaccharide (LPS) induced AKI rat.
Materials and Methods : Male SD rats were received femoral artery and vein catheterization, then induced endotoxin shock by intravenous injected 20 mg/kg LPS at 8-week-old. A total 32 animals were randomly divided to three groups (Control, JCO, LPS, LPS+JCo ; each n = 8) and were observed for 48 hour after sepsis. Mean artery pressure (MAP) and biochemical parameters, including blood urea nitrogen (BUN), creatinine (Cre) were measured at 1, 3, 6, 9, 12, 24 hour after sepsis. The kidneys were removed for pathology assessment of H&E stain and Immunohistochemical staining 48 hour later. NRK-52E cells were treated JCo (10 μg/ml) with or without LPS (10 μg/ml) and real-time polymerase chain reaction, western blot analysis were performed.
Results: Endotoxin shock significantly decreased MAP and increased bood BUN, Cre in sepsis rat. JCo improved the survival, and decreased blood BUN, Cre levels, decreased markers of kidney injury (KIM-1) after sepsis. JCo attenuated the inflammation by activating the AMP-activated protein kinase pathway and restored nuclear factor erythroid-2- related factor (Nrf2) and heme oxygenase 1 (HO-1) protein and decreased NF-κB, TNF-α, and IL-1β in NRK-52E cells after sepsis.
Conclusions: Juniperus communis extract attenuated LPS induced AKI in rats by reducing inflammation via activating the AMP kinase pathway and decreasing pro-inflammatory cytokines production.