Effects of curcumin and melatonin on bone formation in orthopedically expanded suture in rats: A biochemical, histological and immunohistochemical study.

OBJECTS: To investigate the effects of curcumin (CUR) and melatonin (MEL) on new bone formation following rapid maxillary expansion (RME) in rats. SETTING AND SAMPLE POPULATION: For this study, 24 12-week-old adult male Wistar albino rats from the Animal Laboratory at Adnan Menderes University, Faculty of Medicine, were used. MATERIALS AND METHODS: The rats were randomly divided into the following 3 groups (n = 8 each): only expansion (OE), expansion plus MEL (MEL) and expansion plus CUR (CUR). CUR and MEL were given to the rats during the study period. After the sacrifice of the animals, biochemical, histological and immunohistochemical examinations were performed. RESULTS: Serum bone alkaline phosphatase levels in the MEL group were statistically (P = .007) higher than in the OE group. Serum glutathione peroxidase and catalase activities in the CUR and MEL groups were significantly higher than in the OE group (P = .007 and P = .021, respectively). Inflammatory cell infiltration, new bone formation and capillary intensity parameters did not demonstrate statistically significant differences between the groups (P = .865, P = .067 and P = .055, respectively). The immunohistochemical findings revealed that IL-1, IL-6 and TNF-α H scores showed considerable differences between the groups (all P < .001). The highest IL-1, IL-6 and TNF-α H scores were found in the OE groups rather than in the other groups (P < .001). CONCLUSION: CUR and MEL treatments may be effective in accelerating new bone formation and beneficial in preventing relapse following the RME procedures.

The effects of dexpanthenol in streptozotocin-induced diabetic rats: histological, histochemical and immunological evidences.

This study was designed to investigate the effects of Dexpanthenol (Dxp) on liver and pancreas histology and cytokine levels in streptozotocine (STZ)-induced diabetic rats. Twenty-four Wistar albino male rats were divided into four groups: control, Dxp, STZ-induced diabetic (STZ) and diabetic treatment with Dexpanthenol (STZ-Dxp) groups. Experimental diabetes was induced by single dose STZ (50 mg/kg) intraperitoneally (i.p.). After administration of STZ, the STZ-Dxp group began to receive a 300 mg/kg/day i.p. dose of Dxp for 6 weeks. Liver and pancreas tissues of the control group were in normal morphology. Liver tissue of STZ group showed vacuolisation of hepatocytes in the liver parenchyma with enlargement of sinusoidal spaces and increasing amounts of connective tissue in the portal area. Pancreatic section of STZ group displayed ß-cells with of cytoplasmic mass, reduction of islet size, and atrophy. The STZ-Dxp group that received Dxp treatment exhibit partially normal hepatic parenchyma. Histochemical examinations revealed that the diabetes-induced glycogen depletion markedly improved with the Dxp treatment (p⟨0.001). The severity of degenerative alteration was lessened by Dxp supplementation in the STZ-Dxp group. Induction of STZ presented a significant increase both in interleukin-1α (IL-1α) (p=0.033) and monocyte chemotactic protein-1 (MCP-1) (p=0.011) levels, when compared with the control rats. DXP-treated diabetic rats' IL-1α and MCP-1 levels were similar to control value. This evidence suggests that Dxp is effective in reducing STZ-induced, diabetic-related complications and may be beneficial for the treatment of diabetic patients.

Multi-organ injuries caused by lipopolysaccharide-induced periodontal inflammation in rats: role of melatonin.

BACKGROUND AND OBJECTIVE: Periodontitis, a chronic inflammatory disease caused by oral bacterial infection, is considered to be a risk factor for systemic diseases including diabetes mellitus, bacterial pneumonia, hyperlipidemia and atherosclerosis. The aim of this study was to evaluate the effectiveness of melatonin against periodontal inflammation-induced multiple organ injury in rats. MATERIAL AND METHODS: Eighteen female Wistar albino rats were randomly divided into three groups of six rats each: control; lipopolysaccharide (LPS); and LPS + melatonin. During the experimental period (10 d) all rats in the LPS and LPS + melatonin groups were given 10 µL of LPS (from a 10 mg/mL standard solution of LPS dissolved in saline) on days 1, 3 and 5. The rats in the LPS + melatonin group were given 50 mg/kg of melatonin, daily for 10 d, starting on day 1 after the administration of LPS. All rats were killed at the end of the experimental period. Liver, kidney and lung tissues were removed for investigation by light microscopy. RESULTS: The levels of serum aspartate aminotransferase (AST), alanine transaminase (ALT) and blood urea nitrogen (BUN) were significantly increased in the LPS group compared with the LPS + melatonin group (p < 0.05). There was no significant change in the serum creatinine levels in the groups. However, the changes in serum AST, ALT and BUN levels in the experimental groups did not correlate with changes in histological data. Both LPS and LPS + melatonin groups displayed structural features similar to those of the control group. CONCLUSION: The results revealed that increased serum AST, ALT and BUN levels following periodontitis are ameliorated with melatonin treatment.

Involvement of NMDA receptors and nitric oxide in the thermoregulatory effect of morphine in mice.

Morphine has long been known to have potent effects on body temperature. It has been suggested that both N-methyl-D-aspartate (NMDA) receptors and nitric oxide (NO) pathway are involved in thermoregulation and also known to play important roles in some of morphine effects. The aim of this study was therefore to investigate the contribution of NMDA receptors and NO to the thermoregulatory effect of morphine. Morphine produced a hypothermic effect, especially at the dose of 10mg/kg. Ketamine (5-40mg/kg, i.p.) and N(G)-nitro-L-arginine-methyl ester (L-NAME, 1-100mg/kg, i.p.) also produced hypothermic effects with their higher doses. At doses which themselves produced no effect on colonic temperature in mice, both ketamine (10mg/kg, i.p.) and L-NAME (10mg/kg, i.p.) enhanced the hypothermic effect of morphine (10mg/kg, i.p.). These results further support the relationship between NO and NMDA receptors and suggest a possible role of NMDA-NO pathway in the thermoregulatory effect of morphine.