Gallic acid reduces experimental colitis in rats by downregulation of cathepsin and oxidative stress

Objective: Ulcerative colitis (UC) is an idiopathic inflammatory bowel disease (IBD) with common, repetitive inflammation of the colon and rectum, which is highly defined by loss of blood on colon mucosa, ulceration and acute inflammation. The present study aimed to investigate the potential protective effects of gallic acid (GA) through a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis rat model, using biochemical and histopathological parameters. Materials and Methods: The study consisted of four groups, each including seven rats, namely control group, colitis group, colitis-GA 50 mg/kg group and colitis-GA 100 mg/kg group. Colon tissue samples were analyzed for malondialdehyde (MDA), myeloperoxidase (MPO), cathepsin B and cathepsin L values. Results: Tissue MDA, MPO, cathepsin L and cathepsin B values increased significantly in colitis group (p=0.028, p=0.038, p=0.024, p=0.019, respectively). However, MDA, MPO, cathepsin L and cathepsin B values showed a significant decrease in animals with GA (at a dose of 100 mg/kg) administration in TNBS-induced colitis in rats (p=0.021, p=0.026, p=0.019, p=0.031, respectively). Colitis group was defined by the severe detriment of surface epithelium, submucosal edema and inflammatory cell infiltration. Treatment with GA significantly decreased inflammatory cell infiltration. Conclusion: GA can be used as an effective agent in the treatment of colitis due to its inhibitory properties in multiple pathways and its potent antioxidant effect

The examination of protective effects of gallic acid against damage of oxidative stress during induced-experimental renal ischemia-reperfusion in experiment

Aim: In this study, probable effects of gallic acid were investigated in experimentally induced renal I/R injury in rats. Material and methods: For this purpose, each group consisted of 7 Sprague dawley male albino rats. Groups were defined as follows; Group I: control group; Group II: I/R group; Group III, IV and V: I/R+Gallic acid (50, 100 and 200 mg.kg(-1) respectively-i.p.). Left kidney was removed by nephrectomy except for Group I. I/R was induced in the other kidney. Gallic acid was given 15 mins before ischemia induction. SOD, CAT and Gpx activities were determined by electrophoresis. MDA, MPO levels were determined spectrophotometrically. Histopathological investigations were also performed in kidney tissues. BUN and Creatinine levels in serum were determined. Results: BUN, Creatinine and MDA levels were statistically significant but MPO level was not statistically significantly increased in Group II. For SOD, CAT, Gpx activities in Group II, an increase was determined with respect to Group I. Histopathological investigations revealed widespread hyperemia in glomerulus, expansion of the structure between tubules and cell disruptions in Group II. In Group V (200 mg.kg-1 gallic acid), in terms of biochemical parameters, in spite of the significant decrease in BUN, Creatinine and MDA levels; a decrease was determined in SOD, CAT and Gpx isoenzyme activities. Group V showed histologically that I/R injury had been prevented to a greater extent and appearances were close to the control. Conclusion: As a result, in terms of our study, evaluations regarding kidney functions and histopathology have shown that gallic acid has protective effects in renal I/R injury (Tab. 2, Fig. 5, Ref. 36). Text in PDF www.elis.sk

Fetal alcohol syndrome-induced oxidative stress and antioxidant mechanism

İstanbul Bilim Üniversitesi, Sağlık Hizmetleri Meslek Yüksekokulu.Alkol birçok organ ve dokuda (özellikle beyin ve karaciğer) doza ve kullanım süresine bağlı olarak hasar oluşturabilen bir toksindir. Doğum öncesi (prenatal) dönemde anne tarafından kullanılan alkol, fetal alkol sendromuna neden olabilmektedir. Fetal alkol sendromu ilk olarak 1970’li yılların başında, alkol kullanma alışkanlığını gebelikte de sürdüren anneden doğan bebeklerde görülen büyüme bozukluğu, yüz bölgesi anormallikleri ve mental gerilik olarak tanımlanmıştır. Gebeliğin ilk üç ayında kullanılan alkol fetus üzerinde düşüğe, organogenez döneminde organlarda hasara, gebeliğin ikinci üç aylık döneminde hücrelerdeki fetotoksik etkisiyle merkezi sinir sisteminde ağır hasara neden olabilmektedir. Bu derlemede doğum öncesi alkol kullanımı sonucu oluşan oksidatif stres ve antioksidan savunma mekanizması hakkında bilgiler sunulmuştur.Alcohol is a toxin that can generate damage on many organs and tissues (especially brain and liver) depending on the dose and duration of use. The alcohol consumed by the mother during the prenatal period may cause fetal alcohol syndrome. Fetal alcohol syndrome was first identified in the beginning of 1970s by observing developmental defects, facial abnormalities and mental retardation in the babies of mothers who continued their alcohol habit during pregnancy. Consumption of alcohol may cause miscarriage at the first trimester of pregnancy, damage the organs during organogenesis and starting with the secondary trimester, it may strike the central nervous system with the fetotoxic effect in the cells. In this review, we present information about prenatal alcohol consumption-induced oxidative stress and antioxidant defense mechanism