Effects of Apocynin on Liver Ischemia-Reperfusion Injury in Rats.

OBJECTIVE: Ischemia-reperfusion (IR) injury is associated with various clinical conditions, such as myocardial infarction, shock, and surgery under vascular occlusion. We aimed to investigate the protective and therapeutic effects of apocynin (AP) on liver injury induced by IR in an in vivo rat model. METHODS: Thirty-two rats were randomly divided into 4 experimental groups with n = 8 in each group: sham, IR, AP, and IR + AP. AP (20 mg/kg) was intraperitoneally administered to rats in the AP and IR + AP groups for 30 minutes before 60 minutes of ischemia and followed by 60 minutes of reperfusion. All rats were killed on the same day to evaluate tissue levels of oxidants and antioxidants (catalase, malondialdehyde, myeloperoxidase, superoxidedismutase (SOD), and total glutathione). RESULTS: IR decreased SOD levels in IR group when compared with the sham group. AP supplementation to IR group significantly ameliorated SOD levels (P < .05). Also, IR caused elevation of myeloperoxidase production when compared with the sham group, whereas AP treatment prevented these hazardous effects (P < .05). However, plasma total glutathione, catalase, and malondialdehyde levels did not differ between the AP + IR and the IR rats. CONCLUSION: The main finding of the present study was that AP may be protective against liver IR injury. Our results suggested that AP pretreatment suppressed oxidative stress and increased antioxidant levels in an rat model of liver IR.

Effects of melatonin on acetylsalicylic acid induced gastroduodenal and jejunal mucosal injury.

We evaluated the effects of melatonin on acetylsalicylic acid (ASA) induced gastroduodenal and jejunal mucosal injury. We used 40 postpubertal rats divided randomly into five groups of eight animals. The control group consisted of untreated animals. The Mel group was injected intraperitoneally (i.p.) with 5 mg/kg melatonin. The ASA group was injected i.p. with 200 mg/kg ASA. The ASA + Mel group was injected i.p. with 5 mg/kg melatonin 45 min after administering 200 mg/kg ASA i.p. The Mel + ASA group was injected i.p. with 5 mg/kg melatonin 45 min before administering 200 mg/kg ASA i.p. We found no statistically significant differences in mean histopathological scores in the ASA + Mel group compared to the ASA group. ASA caused shortened villi and loss of the apical villus in the duodenum. The histopathological score was increased and villus height was decreased in the ASA group compared to untreated controls. Treatment with melatonin attenuated the histological damage. In the ASA group, occasional areas showed erosion of villi in the jejunum; however, differences in mean histopathological score in ASA group compared to the other groups were not statistically significant. Malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) activities were measured in stomach, duodenal and jejunum tissue. We found increased MDA activity in both stomach and duodenal tissues in the ASA group compared to the control group (p < 0.05). We found no statistically significant changes in MDA levels in jejunal tissue in the ASA group compared to the control group. We found no change in SOD activity in either stomach or duodenal tissues in the ASA group compared to the control group. We observed decreased SOD activity in jejunal tissue in the ASA group compared to the control group (p < 0.05). We detected no change in GSH activity in stomach, duodenal or jejunal tissues in the ASA group compared to the control group. The stomach damage was less in melatonin treated groups, but the lesions were not completely eliminated. The jejunum in the ASA group retained a nearly normal appearance. We found that melatonin exhibited some healing effects on ASA induced duodenal mucosal injury.

The protective effect of melatonin in lungs of newborn rats exposed to maternal nicotine.

We investigated possible healing effects of melatonin (MEL) on biochemical and histological changes in the lungs of rat offspring caused by exposure to nicotine (NT) in utero. Pregnant rats were divided randomly into five groups. The SP group was treated with physiological saline. The EA group was treated with ethyl alcohol. The MEL group was treated with MEL. The NT group was treated with NT. The NT + MEL group was treated with NT and MEL. At the end of the study, the biochemistry and histopathology of lung tissue of the offspring were examined. Reduced alveolar development and increased numbers of alveolar macrophages and mast cells were observed in the NT group compared to the SP, EA and MEL groups. We also found increased malondialdehyde (MDA) levels and decreased total glutathione (GSH) levels in the NT group. Application of MEL ameliorated the histological and biochemical damage caused by NT. The number of alveoli was greater in the NT + MEL group than in the NT group. Also, the increased numbers of alveolar macrophages and mast cells resulting from exposure to NT were decreased following MEL treatment. We found that MEL caused a significant decrease in the level of MDA. Maternal exposure to NT caused significant structural and biochemical changes in the lungs of the offspring and administration of MEL ameliorated the changes.