Although the gastroprotective potential of folic acid has been reported, little is known about the role of inflammation and apoptosis in the said activity. This study, therefore, assessed lipid peroxidation (LPO), Neu...Although the gastroprotective potential of folic acid has been reported, little is known about the role of inflammation and apoptosis in the said activity. This study, therefore, assessed lipid peroxidation (LPO), Neutrophil-lymphocyte ratio (NLR), C-reactive protein (CRP) as markers of inflammation and, p53 and BCl-2 as markers of apoptosis in ethanol-induced gastric ulcer pretreated with Folic acid (FA) for twenty-one (21) days. Adult male Wistar rats were arranged into experimental groups (n = 5) viz: 1) Control;2) Ulcer control;3) 2FA (2 mg/kg folic acid + Ulcer);4) 3FA (3 mg/kg folic acid + Ulcer);5) OMEP (20 mg/kg omeprazole + Ulcer);6) 2FA + OMEP + Ulcer;and 7) 3FA + OMEP + Ulcer. Ulcer score, LPO, NLR, serum CRP were all determined one hour post ulcer induction. Paraffin gastric sections were stained first with H & E, then immunostained for p53 and BCl-2. Ethanol caused gastric lesion with an index of 3.0 ± 0.2. Ulcer severity and LPO was significantly decreased in the 2FA, 3FA, OMEP, 2FA + OMEP and 3FA + OMEP groups. NLR reduced significantly in the 2FA, 3FA, OMEP and OMEP + 3FA group. Qualitatively, there was absence of C-reactive protein in the 2FA group while quantitatively, presence of CRP appeared sustained in the 3FA and OMEP treated groups. Unlike p53, the expression and labeling index of BCl-2 were significantly enhanced more in the FA and OMEP combination than OMEP alone. Folic acid ameliorates the development of gastric ulcer in rats via its anti-inflammatory and anti-apoptotic activities.展开更多
文摘Although the gastroprotective potential of folic acid has been reported, little is known about the role of inflammation and apoptosis in the said activity. This study, therefore, assessed lipid peroxidation (LPO), Neutrophil-lymphocyte ratio (NLR), C-reactive protein (CRP) as markers of inflammation and, p53 and BCl-2 as markers of apoptosis in ethanol-induced gastric ulcer pretreated with Folic acid (FA) for twenty-one (21) days. Adult male Wistar rats were arranged into experimental groups (n = 5) viz: 1) Control;2) Ulcer control;3) 2FA (2 mg/kg folic acid + Ulcer);4) 3FA (3 mg/kg folic acid + Ulcer);5) OMEP (20 mg/kg omeprazole + Ulcer);6) 2FA + OMEP + Ulcer;and 7) 3FA + OMEP + Ulcer. Ulcer score, LPO, NLR, serum CRP were all determined one hour post ulcer induction. Paraffin gastric sections were stained first with H & E, then immunostained for p53 and BCl-2. Ethanol caused gastric lesion with an index of 3.0 ± 0.2. Ulcer severity and LPO was significantly decreased in the 2FA, 3FA, OMEP, 2FA + OMEP and 3FA + OMEP groups. NLR reduced significantly in the 2FA, 3FA, OMEP and OMEP + 3FA group. Qualitatively, there was absence of C-reactive protein in the 2FA group while quantitatively, presence of CRP appeared sustained in the 3FA and OMEP treated groups. Unlike p53, the expression and labeling index of BCl-2 were significantly enhanced more in the FA and OMEP combination than OMEP alone. Folic acid ameliorates the development of gastric ulcer in rats via its anti-inflammatory and anti-apoptotic activities.
