杜松子粗萃物對失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 Protects Against Hemorrhagic Shock-Induced Acute Kidney Injury in Conscious mice

Ta-Chin Lin1, 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:

Understanding the host response to severe hemorrhage has been discussed, and hemorrhagic shock (HS) is a form of hypovolemic shock that blood loss causes inadequate oxygen delivery. Several inflammatory mediators such as tumor necrosis factor α (TNF-α), interleukin 10 (IL-10), and reactive oxygen species (ROS) can be produced by HS and lead to acute kidney injury and multiple organ dysfunction. 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) treatment after HS in conscious mice.

Materials and Methods:

Male C57BL/6 mice were received femoral artery catheterization at 8-week-old. By withdrawing 40% of total blood volume from a femoral arterialcatheter (6 ml/100 g body weight [BW]) for more than 10 min, HS was induced. The mean arterial pressure (MAP) and heart rate (HR) were monitored continuously for 48 hr after the start of blood withdrawal. Levels of biochemical parameters, including glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN), creatinine (Cre), and lactic dehydrogenase (LDH), were measured at 48 hour after HS. The kidneys were removed for pathology assessment of H&E stain and immunohistochemical staining.

Results:

HS significantly increased blood GOT, GPT, BUN, LDH, CPK, TNF-α, and IL-10 levels in conscious mice. JCo improved the survival, and decreased blood BUN, Cre levels in serum. JCo also decreased markers of kidney injury (KIM-1) after HS in immunohistochemical staining.

Conclusions:

Juniperus communis extract attenuated HS induced AKI in mice by reducing KIM-1 expression. Moreover, E-cadherin staining is much more intense in the JCO group than that in the HS group. Posttreatment propofol suppressed the release of pro-inflammatory TNF-α production and increased anti-inflammatory IL-10 production after HS and decreased the levels of markers of kidney injury associated with HS in conscious mice. Juniperus communis extract may have protective effects against HS.