Protective effect of luteolin on acute lung injury in a rat model of sepsis.

We investigated the effects of luteolin (LUT) treatment on acute lung injury caused by cecal ligation and puncture (CLP) induced septic rats. We also investigated the relation between LUT and the cytokines, interleukin-10 (IL-10) and tumor necrosis factor-α (TNF-α). LUT was administered 1 h after CLP surgery. Administration of LUT reduced the glutathione level and superoxide dismutase activity in rat lung tissues. We also found significant reduction of malondialdehyde following LUT treatment. LUT administration also reduced TNF-α and IL-10 mRNA expression in lung tissue. Histopathologic investigation of lung tissue supported our biochemical and molecular findings. Administration of LUT ameliorated lung injury in CLP induced septic rats owing to its antioxidant and anti-inflammatory properties.

Epigallocatechin-3-gallate (EGCG) exert therapeutic effect on acute inflammatory otitis media in rats.

INTRODUCTION: That EGCG has strong antioxidant and anti-inflammatory activities as well as antibacterial activity against many streptococcus species suggests that it may be beneficial in the treatment of AOM. OBJECTIVE: Aim of the study is to reveal the molecular and biochemical effects of EGCG on LPS induced otitis media in rats. METHODS: Forty-two male albino Wistar rats were randomly divided into 7 groups. Inflammation was induced by administrating 50 µL of 1 mg/ml lipopolysaccharide (LPS). EGCG used 50 and 100 mg/kg/day and combined penicillin G (PENG) 48 h after LPS injection. RESULTS: The combined EGCG 50 and PENG group and the group with EGCG 50 alone showed the best anti-inflammatory effect on LPS-induced AOM. TNF-α and IL-1ß gene expression significantly down regulated EGCG 50 and combined with PENG compared to the otitis media group. The combination of PenG and EGCG 50 led to the best histopathological improvement. Both the inflammation and the membrane thickness of this group were at almost the same level as the healthy group and tympanum was seen normal. CONCLUSION: The results of this study make it clear that EGCG plays an important role in antioxidant and anti-inflammatory activity during AOM.

Role of polymorphonuclear leukocyte infiltration in the mechanism of anti-inflammatory effect of amiodarone.

In many physiological bodily functions, and in the pathogenesis of inflammation, ions are exchanged between intracellular and extracellular areas. Amiodarone is a multiple ion channel (Ca++, Na+, K+) blocking drug, effective anti-arrhythmic drug, and phospholipase inhibitor. The aim of this study is to examine a role of polymorphonuclear leukocyte infiltration in amiodarone's anti-inflammatory effect on experimental paw inflammation. After rats had been assigned to groups, their normal right hind paw volumes were measured using a plethysmometer. Amiodarone (25, 50 and 100 mg/kg) and distilled water were administrated to the experimental and control groups, respectively, by ip route. Thirty minutes later, paw edema was induced in rats by subplantar injection of 0.1 ml of histamine (0.1%) to those paws. Subsequent volume readings for those paws were carried out at 30-min intervals. Results were expressed as percentages of change from the initial volumes. After the final measurements, the animals were killed by decapitation and their paw tissues were cut for pathological investigation. Amiodarone dose-dependently decreased the paw edema (25.05, 48.71 and 74.97%), and reduced polymorphonuclear leukocyte infiltration in the paw tissue (55.65, 69.76 and 84.58%). Our findings support the view that amiodarone dose-dependently exerts a powerful anti-inflammatory activity. This effect of amiodarone may be due to the activation of nitric oxide resulting from its calcium channel antagonistic effects, to the inhibition of phospholipase A2 and/or to a reduction in neutrophil movement and activation, which may reduce free radical production and proteolytic enzyme release.

Antioxidant effect of T-type calcium channel blockers in gastric injury.

It is known that calcium ion has an important role in the cellular function. For this reason, calcium channel blockers may have a protective action against gastric injury which is induced by various stimuli. In this study, the influence of mibefradil on ethanol-induced gastric injury was investigated in rats. Mibefradil was given at a dose 50 mg/kg intraperitoneally 30 min before administration of 1 ml absolute ethanol given by gavage. We compared this effect of mibefradil with that of omeprazol. Ethanol-induced mucosal damage was evaluated using three different approaches: analysis of biochemical parameters and pathologic and macroscopic investigation. It was found that pretreatment with mibefradil significantly reduced ethanol-induced macroscopic, pathologic, and biochemical changes in the gastric mucosa. In conclusion, it is speculated that this findings may prove important in the development of new and improved therapies for the treatment and prevention of gastric ulcers in humans.

Melatonin prevents ethanol-induced gastric mucosal damage possibly due to its antioxidant effect.

Oxygen radical release has been proposed as a pathogenic factor of the ethanol-induced acute gastric injury. Melatonin, a pineal hormone, is known to scavenge oxygen free radicals. We investigated whether parenteral administration of melatonin prevented ethanol-induced macroscopic damage, polymorphonuclear (PMN) leukocyte infiltration, depletion of total glutathione (tGSH) concentration, and glutathione reductase (GSSG-Rd) activity in the rat gastric mucosa. We compared the effects of melatonin with those of omeprazole. Ethanol-induced mucosal damage was evaluated using three different parameters: gastric total glutathione (tGSH) concentration and glutathione reductase (GSSG-Rd) activity, the number of PMN leukocytes, and macroscopic investigation. Gatric tGSH concentration and GSSG-Rd activity decreased and the number of PMNs increased after ethanol administration. It was found that pretreatment with melatonin increased both tGSH concentration and GSSG-Rd activity. Melatonin also reduced ethanol-induced PMN infiltration in the stomach. Ethanol administration damaged the entire gastric mucosa. Melatonin significantly decreased the extent of ethanol-induced macroscopic injury. In conclusion, these findings support the conclusion that the protection conferred by melatonin in gastric ulcer is presumably due to its antioxidant activity.