ABSTRACT
OBJECTIVE: The present study aims to investigate the therapeutic effects of resveratrol (RES) on isoproterenol (ISO) induced myocardial injury rat model. METHODS: Catecholamine-induced heart damage was induced by ISO treatment for 30 days. The rats were divided into four groups as follows: the control group received saline, the ISO group received 5.0 mg/kg ISO, the RES group received 10 mg/kg RES, and the ISO-RES group received 10 mg/kg RES and 5 mg/kg ISO treatments for 30 days. Following echocardiographic measurements and body weight recorded, the rats were decapitated. Plasma and cardiac tissue samples obtained by decapitation were analyzed using biochemical, histopathological, molecular and immunohistochemical methods. RESULTS: In the ISO group, Na+/K+ ATPase activity and ATP content, GSH, and caveolin-3 levels were low. LDH, CK and lysosomal enzyme activities, MDA level, and MPO activity were found to be high. It was determined that GSH and MDA levels and MPO, Na+/K+ ATPase activity, ATP content caveolin-3 levels changes that arose from ISO treatment were suppressed by RES treatment. CONCLUSION: RES treatment has ameliorated all the functional and biochemical parameters. The results obtained in this study suggest that RES is a promising supplement against catecholamine exposure as it improves antioxidant defense mechanisms in the heart. In the light of above-mentioned data, RES can be assumed as a promising agent in ameliorating the oxidative injury of the myocardium.
ABSTRACT
AIM: Spinal cord injury (SCI) leads to an inflammatory response that generates substantial secondary damage within the tissue besides the primary damage. Ghrelin, 28 amino-acid peptide, has been shown to modulate the release of proinflammatory cytokines and exert antiinflammatory effects. The aim of the current study was to investigate the anti-inflammatory effects of ghrelin, in a rat model of SCI. MATERIAL AND METHODS: Wistar albino rats were divided as control, SCI, and ghrelin-treated (10 µg/kg/day, ip) SCI groups. In order to induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10, was used. Injured animals were given either ghrelin or saline 15 min post-injury. RESULTS: In plasma samples, neuron-specific enolase (NSE) and S-100ß protein levels were evaluated. Spinal cord samples were taken for histological examination or determination of myeloperoxidase (MPO) activity and DNA fragmentation. SCI caused significant increases in plasma NSE and S-100ß levels and tissue MPO activity and DNA damage. On the other hand, ghrelin treatment improved histological findings as well as biochemical parameters while it failed to improve the impairment of the neurological functions due to SCI. CONCLUSION: The present study suggests that ghrelin could reduce SCI-induced oxidative stress and exert anti-inflammatory effects in the spinal cord following trauma.
