Melatonin protects liver from intestine ischemia reperfusion injury in rats

Abstract

AIM:To investigate the protective effect of melatonin on liver after intestinal ischemia-reperfusion injury in rats. METHODS: One hundred and fifty male Wistar rats, weighing 190-210 g, aged 7 wk, were randomly divided into melatonin exposure group, alcohol solvent control group and normal saline control group. Rats in the melatonin exposure group received intraperitoneal (IP) melatonin (20 mg/kg) 30 min before intestinal ischemia-reperfusion (IR), rats in the alcohol solvent control group received the same concentration and volume of alcohol, and rats in the normal saline control group received the same volume of normal saline. Serum samples were collected from each group 0.5, 1, 6, 12, and 24 h after intestinal IR. Levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured with an auto-biochemical analyzer. Serum TNF-α was tested by enzyme-linked immunosorbent assay (ELISA). Malondialdehyde (MDA) in liver was detected by colorimetric assay. Pathological changes in liver and immunohistochemical straining of ICAM-1 were observed under an optical microscope. RESULTS: The levels of ALT measured at various time points after intestinal IR in the melatonin exposure group were significantly lower than those in the other two control groups (P < 0.05). The serum AST levels 12 and 24 h after intestinal IR and the ICAM-1 levels (%) 6, 12 and 24 h after intestinal IR in the melatonin exposure group were also significantly lower than those in the other two control groups (P < 0.05). CONCLUSION: Exotic melatonin can inhibit the activity of ALT, AST and TNF-α, decrease the accumulation of MDA, and depress the expression of ICAM-1 in liver after intestinal IR injury, thus improving the liver function.

Melatonin is a potent modulator of antioxidative defense and cellular proliferation against aluminum toxicity in rats

“…Another study states that Wistar albino rats administered with drinking water and aluminum chloride had edema and tissue disintegration in their brain, and showed that vitamin E and C given as antioxidants reduced the damage that occurred (Hussein et al, 2010). Mel is one of the most powerful antioxidants, terminating lipid peroxidation, by capturing peroxyl radicals (Karbownik and Reiter, 2000;Li et al, 2008;Millan-Plano et al, 2010). Mel shows an antioxidant effect in the presence of metals causing oxidative stress, thereby reducing the damage occurring or eliminating it altogether Sharma et al, 2011).…”

“…Owing to its negative effects on human health, Al has become a highly researched metal (ElMaraghy et al, 2001;Mahmoud and Elsoadaa, 2013). Mel is a small molecule, well documented as an antioxidant in numerous toxicological models of induced oxidative damage (Li et al, 2008). The small intestine plays an important role in the detoxification of various substances toxic to the body, as well as in the absorption of foods (Kierszenbaum, 2006).…”

Physiological Effects Of Melatonin on Leptin, Testosterone and Biochemical Parameters in Albino Rats

“…Also, Li et al, (2008) concluded that exogenous MEL protects liver by inhibiting the production of free radicals, reducing the concentration of tumor necrosis factor-α in systemic circulation and suppressing the expression of inter-cellular adhesion molecule 1 in liver. Also, it has been shown that liver is the final metabolic place of MEL and MEL protects liver from intestinal ischemia reperfusion injury (Xu et al, 2007) and studies have shown that MEL has no side effect when a high dose is used in rats (Pignone et al, 2006).…”

Melatonin protection against burn-induced liver injury. A review

“…Protective effect of melatonin is related not only to the inhibition of inflammatory cytokines but also to the reduction of the expression of adhesion molecules after burns [8]. Exogenous melatonin protects the liver by ischemia/reperfusion injury inhibiting the production of free radicals, reducing TNF-α concentration in systemic circulation and suppressing intercellular adhesion molecule-1 (ICAM-1) liver expression [41]. These data suggest a bidirectional and synergistic linkage of inflammation and oxidative stress contributing to burn-induced hepatic injury.…”