Effect of corticosteroid (triamcinolone acetonide) and chlorhexidin on chemotherapy- induced oxidative stress in buccal mucosa of rats.

Oral mucositis (OM) refers to erythematous and ulcerative lesions of the oral mucosa. This pathology can occur by various causes. Cancer therapy is one of the well-known causes of OM such as chemotherapy and/or with radiation therapy. It has been widely mentioned that oxidative stress parameters such as lipid peroxidation (LP) levels increase during cancer process. Glutathione (GSH) is one of the major intracellular enzymes to detoxify oxidant molecules. The aim of this study was to investigate and compare the effects of Triamcinolone Acetonide (TA), a synthetic steroid chlorhexidine (CHX), a chemical antiseptic, on 5- fluorouracil (5-FU), a chemotherapeutic agent and soft abrasion induced OM in buccal mucosa of rats.OM was induced in rats through a combination of 5-FU treatment and mild abrasion of the cheek pouch with a wire brush. Buccal mucosa lipid peroxidation (LP) levels were higher (p< 0.05) in 5-FU group than in control although LP levels were lower (p<0.05) in TA group than in control group. The reduced glutathione levels were lower (p<0.05) in 5-FU group than in the control group although its level was higher (p<0.05) in TA and CHX groups than in the 5-FU group. Glutathione peroxidase activity was also higher (p<0.05) in TA group than the 5- FU group. In histopathological analyses, treatment with TA reduced 5-FU induced inflammatory cell infiltration and ulceration (p<0.001) but not with CHX.In conclusion, we observed that TA and CHX treatment modulated chemotherapy induced oxidative injury in the rat OM. However, only TA histopathologically ameliorated the 5-FU induced OM of rats. These findings suggest that TA is a useful agent for management of experimental oxidative injury and OM caused by the chemotherapy.

Effect of a corticosteroid (triamcinolone) and chlorhexidine on chemotherapy-induced oxidative stress in the buccal mucosa of rats.

Oral mucositis manifests as erythematous and ulcerative lesions of the oral mucosa. Among its various causes, cancer treatment (e.g., chemotherapy with or without radiation therapy) is one of the more well known. It has been widely mentioned that oxidative stress parameters such as lipid peroxidation levels increase during the cancer process. Glutathione is one of the major intracellular enzymes used to detoxify oxidant molecules; it exists in both a reduced and oxidized state. Reduced glutathione is used as a substrate to synthesize glutathione peroxidase. We conducted a study to investigate and compare the effects of triamcinolone (a synthetic steroid) and chlorhexidine (a chemical antiseptic) on 5-fluorouracil (5-FU; a chemotherapeutic agent)-induced oral mucositis in the buccal mucosa of 36 rats. Oral mucositis was induced through a combination of 5-FU treatment and mild abrasion of the cheek pouch with a wire brush. The rats were treated with one of four regimens: saline placebo (group I), 5-FU only (group II), 5-FU plus triamcinolone (group III), and 5-FU plus chlorhexidine (group IV). Three rats in the triamcinolone group died of unknown causes on days 7 and 8, and 3 rats in the chlorhexidine group died on days 7 and 9. On day 9, the remaining 30 rats were sacrificed and examined. Buccal mucosa lipid peroxidation levels were significantly higher in the 5-FU-only group than in the control group and significantly higher in the control group than in the triamcinolone group (p < 0.05 for both). Levels of reduced glutathione were significantly lower in the 5-FU-only group than in both the triamcinolone group and the chlorhexidine group (p < 0.05). Glutathione peroxidase activity was significantly higher in the triamcinolone group than in the 5-FU-only group (p < 0.01). Histopathologic analysis revealed that treatment with triamcinolone significantly reduced 5-FU-induced inflammatory cell infiltration and ulceration (p < 0.001); no such reduction was seen with chlorhexidine. In conclusion, we observed that triamcinolone and chlorhexidine treatment modulated chemotherapy-induced oxidative injury in rat oral mucositis. However, only triamcinolone histopathologically ameliorated 5-FU-induced oral mucositis. These findings suggest that triamcinolone is a useful agent for the management of experimental oxidative injury and oral mucositis caused by 5-FU chemotherapy.

The effects of methylprednisolone, montelukast and indomethacine in experimental otitis media with effusion.

OBJECTIVES: The present study aimed to investigate the effects of indomethacine, montelukast and methylprednisolone in management of experimental otitis media with effusion. METHODS: Forty Wistar albino rats of which the weights ranged between 310 and 370 g were included in this study. Middle ear effusion was created by transtympanic histamine injection. The presence of effusion was confirmed by otomicroscopic examination. Thirty-seven rats with effusion were divided into 4 groups (methylprednisolone, montelukast, indomethacine and saline-control groups). All agents were administered for a period of consecutive 10 days. At the 11th days of administration, the recovery of effusion was confirmed by otomicroscopic examination. Tympanic bullae of the rats were removed and histopathological examinations were carried out. In the histopathological examination, the neutrophil leukocytes accumulated in the middle ear submucosa were counted. RESULTS: The mean numbers of submucosal neutrophils in the methylprednisolone, montelukast, indomethacine, and saline groups were 24.6±8.1, 54.1±6.2, 52.3±7.3, 55.7±8.3, respectively. The otomicroscopic recovery rates of effusion in the methylprednisolone, montelukast, indomethacine, and saline groups were 18/18 (100%), 8/18 (44%), 2/14 (14%), 2/18 (11%) respectively. CONCLUSIONS: Methylprednisolone and montelukast ameliorate the middle ear effusion. However, only methylprednisolone reduces the submucosal infiltration of the neutrophil leukocytes which are the most evident cell of inflammatory process. Montelukast is effective in the resolution of experimental otitis media with effusion.