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 Spraque 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).
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 Spraque 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).