The effect of captopril on brain apoptosis after burn injury in rats

Abstract

AIm: The purpose of this study was to determine the possible protective effects of captopril treatment against apoptosis in the brain induced by burn injury. mAterIAl and methOds: Under ether anaesthesia, Wistar albino rats (200-250 g) were exposed to a 900C (burn) or 250C (sham) water bath for 10 s. The ACE group was treated with i.p. 10 mg/kg captopril immediately after burn injury and this treatment was repeated twice daily. At the end of the 24 hours, brain samples were taken. Apoptotic brain cells marked by terminal deoxynucleotidyl transferase-mediated d-UTPnick end labeling (TUNEL) were evaluated in the cerebellum and midbrain of rats.results: Apoptotic cells in the cerebellum were significantly decreased after captopril treatment and found to be lower when compared to the burn group (p<0.001). In the midbrain of rats, the numbers of TUNEL-positive cells and apoptotic bodies were significantly increased in the burn group when compared to the control group (p<0.001). The burn-induced changes were reduced in the captopril-treated burn group (p<0.01).COnClusIOn: Captopril has beneficial effects in burn injury and should be assessed as a therapeutic agent in the management of this condition.

Pathological changes in the brain after peripheral burns

“…Peripheral burn injury can lead to neuronal apoptosis. In burn-injured animal models, neurons underwent this orchestrated form of cell death characterized by the swelling of cell bodies, axons and mitochondria, as well as a decrease or disappearance of Nissl bodies, concentration of axoplasm, and expansion or vacuolation of the Golgi complex [ 42 , 65 , 66 ]. Sometimes, neurons are shrunken with condensed nuclei during the early stage of apoptosis [ 65 ].…”

“…Thus, estrogens suppress neuroinflammation and apoptosis following severe burn injury and may provide a novel clinical strategy for burn-induced brain injury. Other promising molecular targets, such as sphingosine 1-phosphate, pentoxifylline, gelsolin and captopril, have been reported in different animal studies to maintain BBB integrity, suppress inflammation, reduce apoptotic signaling and alter neuronal nitricoxide synthase (nNOS) expression [ 65 , 66 , 151–153 ].…”