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ABSTRACT Objective: To investigate the protective effect of wolfberry (WB) against acetic acid-induced colitis in rats. Methods: The rats were divided into four groups with eight rats in each group: the control group, WB group, colitis group and WB + colitis group. Distal colitis was induced in rats by intracolonic instillation of 4% acetic acid. Wolfberry + colitis group received 100 mg/kg of WB extract dissolved in saline through the intraperitoneal route for 7 days. Acute colitis was created on the 8th day, and the rats were sacrificed 48 hours later. Colonic damage was assessed by macroscopic and histological criteria as well as biochemical markers. Results: Mean total antioxidant capacity (TAC), total oxidant status (TOS), tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 levels were significantly higher in the colitis group compared with the control and WB groups (p < 0.05). The WB + colitis group had significantly lower TAC, TOS, TNF-α, IL-1β and IL-6 levels compared with the colitis group (p < 0.05). The analyses of the histopathological findings indicated that the colitis group had a significantly higher histopathological damage score than the control group (3.12 ± 0.45, 0 ± 0.00, respectively; p < 0.05). Histopathological damage score was significantly higher in the WB + colitis group than in the control group and statistically significantly lower than the colitis group (1.62 ± 0.44, 0 ± 0.00, respectively; 3.12 ± 0.45, respectively; p < 0.05 for both comparisons). Conclusion: Wolfberry extract is an agent that is effective for preventing acetic acid-induced colitis in rats.
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ABSTRACT Objective: Ethyl alcohol (EA) is a substance that is used commonly worldwide and known to have toxic effects on the liver. The aim of this study was to investigate the effect of montelukast sodium (MK) on acute hepatopathy induced by a single dose of EA in rats. Methods: The study consisted of four groups each containing eight Wistar albino male rats. The groups were classified as follows: the control group received distilled water; the EA group received 6 g/kg EA diluted with distilled water orally by gavage; the MK group received 30 mg/kg MK orally by gavage; the EA + MK group received, 2 hours after the EA administration, ie 30 mg/kg MK orally by gavage. After 24 hours, all the rats were sacrificed, and their blood and liver tissue samples were taken for biochemical and histopathological examinations. Results: The administration of EA caused a statistically significant increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels compared with the control group (220.50 ± 66.90 and 92.38 ± 5.90 versus 84.88 ± 15.66 and 43.75 ± 10.22). The administration of EA + MK caused a statistically significant decrease in the AST and ALT levels compared with the EA alone group. Ethyl alcohol administered to the rats caused lesion in the liver including congestions, hydropic degeneration and irregular shaped area caused coagulation necrosis. The histopathological changes seen in the EA group were not detected in the EA + MK group. Conclusion: Consequently, these data suggested that MK had beneficial effects in alleviating EA-induced hepatotoxicity in rats.
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OBJECTIVE: This study aimed to determine a possible correlation between oral mucosal disease and salivary concentrations of the antimicrobial peptides human beta-defensin-1 (hβD-1) and human betadefensin- 2 (hβD-2). METHOD: The present work focussed on the establishment of a reversed phase-high performance liquid chromatography (RP-HPLC) procedure to quantify human beta-defensins (hβD-1 and hβD-2) in saliva samples of patients with oral diseases such as lichen planus (n = 10), Behçet (n = 10) and recurrent apthous stomatitis (n = 10). RESULTS: Linear calibration range for hβD-1 and hβD-2 defensins was 1.67−200 µg mL-1 and 3.13− 100 µg mL-1 with R2 values of 0.9998 and 0.996, correspondingly. The concentration of beta-defensins in saliva was determined by comparing the peak areas of eluted hβD-1 and hβD-2 with that of their standards. The variation of the amount of beta-defensins was evaluated by comparisons of the results obtained from the patients with oral mucosal diseases before and after treatments and the control subjects. The limit of detection (LOD) and limit of quantification (LOQ) were found to be 1.62 µg mL- 1 and 5.39 µg mL-1 for hβD-1 and 0.94 µg mL-1 and 3.13 µg mL-1 for hβD-2, respectively. CONCLUSION: The salivary beta-defensin concentration was significantly higher in patients with oral mucosal diseases than in healthy volunteers; furthermore, in patients with oral mucosal diseases, the concentration was significantly higher before treatment than after treatment.
OBJETIVO: Este estudio tuvo por objeto determinar una posible correlación entre la enfermedad de la mucosa oral y las concentraciones salivales de la beta-defensina humana 1 (hβD-1) y la beta-defensina humana 2 (hβD-2) de los péptidos antimicrobianos. MÉTODO: El presente trabajo estuvo encaminado al establecimiento de un procedimiento de cromatografía líquida de alta eficacia de fase reversa (RP-HPLC) para cuantificar las beta-defensinas humanas (hβD-1 y hβD-2) en muestras de saliva de pacientes con enfermedades orales como el liquen plano (n = 10), Behçet (n = 10), y la estomatitis aftosa recurrente (n = 10). RESULTADOS: El rango de calibración lineal de las defensinas hβD-1 y hβD-2 fue 1.67-200 µg mL-1 y 3.13-100 µg mL-1 con valores R2 de 0.9998 y 996, respectivamente. La concentración de beta-defensinas en la saliva se determinó utilizando el área de sus estándares. La variación de la cantidad de beta defensinas fue evaluada por comparaciones de los resultados obtenidos de los pacientes con enfermedades de la mucosa oral, antes y después de los tratamientos y los sujetos de control. Se halló que el límite de detección (LDD) y el límite de cuantificación (LDC) fueron 1.62 µg mL-1 y 5.39 µg mL- 1 para hβD-1 y 0.94 µg mL-1 y 3.13 µg mL-1 hβD-2, respectivamente. CONCLUSIÓN: La concentración de beta-defensina salival fue significativamente mayor en los pacientes con enfermedades de la mucosa oral que en los voluntarios sanos. Además, en pacientes con enfermedades de la mucosa oral, la concentración fue significativamente mayor antes del tratamiento que después del tratamiento.