Low dose of carvacrol prevents rat pancreas tissue damage after L-arginine application, while higher doses cause pancreatic tissue impairment.

Carvacrol (5-isopropyl-2-methylphenol) is a biologically active monoterpene phenol abundantly present in the essential oils of many Lamiaceae aromatic/ethnomedicinal plants. Herein, we aimed to evaluate the damaging effect of carvacrol to rat pancreatic tissue, but also to assess its possible ameliorative impact on pancreatic damage induced by L-arginine. The toxic and beneficial (in a dose of 10 mg/kg) properties of carvacrol were assessed by measuring serum α-amylase and lipase activities, tissue malondialdehyde (MDA) content, and pathohistological changes in pancreatic tissue. Application of 100/500 mg/kg of carvacrol produced a significant increase in α-amylase activity, followed by inflammatory-cell infiltration and patchy interlobular edema in the pancreas. In the L-arginine-induced pancreatitis model, a dose of 10 mg/kg of carvacrol prevented an increase in α-amylase and lipase activities, and MDA formation, when compared to the animals that received L-arginine only. Animals treated with carvacrol prior to L-arginine administration displayed mild edema and inflammatory infiltration with few necrotic areas. Contrary to that, animals that received only L-arginine showed a massive leukocyte infiltrate with edema and substantial necrotic areas. In our study carvacrol showed significant protective effects and a potential to modulate leukocyte recruitment in pancreatic tissue after L-arginine injection.

Pre- vs. post-treatment with melatonin in CCl4-induced liver damage: Oxidative stress inferred from biochemical and pathohistological studies.

AIMS: The present study was designed to compare the ameliorating potential of pre- and post-treatments with melatonin, a potent natural antioxidant, in the carbon tetrachloride-induced rat liver damage model by tracking changes in enzymatic and non-enzymatic liver tissue defense parameters, as well as in the occurring pathohistological changes. MAIN METHODS: Rats from two experimental groups were treated with melatonin before and after CCl4 administration, while the controls, negative and positive, received vehicle/melatonin and CCl4, respectively. Serum levels of transaminases, alkaline phosphates, γ-GT, bilirubin, and albumin, as well as a wide panel of oxidative stress-related parameters in liver tissue, were determined in all experimental animals. Liver tissue specimens were stained with hematoxylin and eosin and further evaluated for morphological changes. KEY FINDINGS: Both pre- and post-treatment with melatonin prevented a CCl4-induced increase in serum (ALT, AST, and γ-GT) and tissue (MDA and XO) liver damage markers and a decrease in the tissue total antioxidant capacity, in both enzymatic and non-enzymatic systems. The intensity of pathological changes, hepatocyte vacuolar degeneration, necrosis and inflammatory cell infiltration, was suppressed by the treatment with melatonin. SIGNIFICANCE: In conclusion, melatonin, especially as a post-intoxication treatment, attenuated CCl4-induced liver oxidative damage, increased liver antioxidant capacities and improved liver microscopic appearance. The results are of interest due to the great protective potential of melatonin that was even demonstrated to be stronger if applied after the tissue damage.