Caspase 3 expression and plasma level of Fas ligand as apoptosis biomarkers in inflammatory endotoxemic lung injury

Vol. 57 No. 3, 2016

ROMANIAN JOURNAL of MORPHOLOGY and EMBRYOLOGY

Raluca-Stefania Fodor, Anca-Meda Georgescu, Bianca-Liana Grigorescu, Adrian-Dan Cioc, Mihaly Veres, Ovidiu-Simion Cotoi, Pal Fodor, Sanda-Maria Copotoiu, Leonard Azamfirei

Objective: The objective of this study is to evaluate if the immunohistochemical expression of a pulmonary apoptosis marker and plasma level of Fas ligand (FasL) correlates with the dose- and time-dependent severity of lung injury, induced by the administration of lipo-polysaccharide (LPS) in an endotoxemic rat model. Materials and Methods: Our study included 30 male Wistar rats, randomly divided into three groups: one control group (n=6) and two experimental groups (n=12/group), in whom we induced endotoxemia by intraperitoneal injection of progressively increasing doses of LPS (5, 10 mg/kg). We measured FasL plasma levels of the rats at different time points and analyzed the relationships with markers of lung injury. To investigate the level of caspase 3-protein expression, the immunohistochemistry of the lung tissue was assessed. Results: The median percentage of caspase 3-stained cells for the 5 mg/kg LPS dose was 0.36%, for the 10 mg/kg LPS dose was 0.4% and for the control group was 0.03% (p<0.0001). The elevated expression levels of caspase 3 were consistent with the altered lung morphologies observed (rs=0.88). LPS administration in rats resulted in a significant dose-dependent increase in the levels of plasma FasL (p<0.0001). These levels correlated with markers of lung injury: degree of hypoxemia (rs=-0.42), histological measured lung injury score (rs=0.72), the density of the caspase 3 staining cells in the immunohistochemistry assessment of apoptosis (rs=0.81) and with the plasma RAGE (receptor for advanced glycated end-products) values (rs=0.70). Conclusions: Apoptosis is increased in edotoxemia induced lung injury and is likely to contribute to alveolar injury.

Corresponding author: Anca-Meda Georgescu, Associate Professor, MD, PhD; e-mail: ancameda.georgescu@umftgm.ro

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