ABSTRACT
Background: Acute kidney injury [AKI] often occurs as a result of ischemia-reperfusion. AKI is a major renal disease associated with high mortality rate. We investigated the renal protective effects of gallic acid and L-carnitine on the blood factors in rat model of renal ischemia-reperfusion
Materials and methods: In this experimental study, forty male Wistar rats were randomly divided into 4 groups: controls, ischemia/reperfusion group [I/R], ischemia-reperfusion+L-carnitine [I/R+Lc, 500mg/kg], and ischemia/reperfusion + gallic acid [I/R+GA, 100mg/kg]. Animals of the experimental groups were subjected to unilateral nephrectomy and received Gallic acid and L-carnitine for 14 days. Then, ischemia was induced by clamping the renal pedicle for 45 minutes. 72 h later, they were sacrificed, and the blood level of BUN, uric acid and creatinine were analyzed
Results: The results showed a significant increase in BUN and creatinine of I/R group compared to the controls. Also, BUN and creatinine were significantly decreased in I/R+Lc and I/R+GA groups in comparison with I/R group. On other hand, blood level of uric acid was decreased in I/R+GA group compared to I/R group
Conclusion: The results indicated that ischemia/reperfusion induced acute renal injury in rat model, and pretreatment with L-carnitine and gallic acid can prevent the kidney tissue damage from renal ischemia
ABSTRACT
Objective: The present study investigated the effects of gallic acid [GA] administration on trimethyltin chloride [TMT] induced anxiety, depression, and hippocampal neurodegeneration in rats
Materials and Methods: In this experimental study, the rats received intraperitoneal [i.p.] injections of TMT [8 mg/kg]. The animals received either GA [50, 100 and 150 mg/kg] or saline as the vehicle for 14 consecutive days. We measured depression and anxiety levels of the rats by conducting the behavioral tail suspension [TST], elevatedplusmaze [EPM], and novelty suppressed feeding [NSF] tests. Histological analyses were then used to determine the cell densities of different hippocampal subdivisions. The data were analyzed with ANOVA and Tukey's post hoc test
Results: GA administration ameliorated anxiety and depression in the behavioral tests. The cell densities in the CA1, CA2, CA3 and DG hippocampal subdivisionsfrom GA-treated rats were higher than saline treated rats
Conclusion: GA treatment against TMT-induced hippocampal degeneration altered cellular loss in the hippocampus and ameliorated the depression-anxiety state in rats
ABSTRACT
Regarding the therapeutic properties of Nigella sativa [NS], the effects of the plant hydroalcoholic extract on learning, memory and brain tissues oxidative damage were investigated in penthylenetetrazole [PTZ]-induced repeated seizures. There were 4 experimental groups including: 1- control group; received saline, 2- PTZ group; received saline and PTZ [50 mg/Kg, i.p], 3- PTZ-NS 200 and 4- PTZ-NS 400 ; received 200 and 400 mg/Kg of NS extract respectively, before PTZ injection in 5 consecutive days. Seizure scores were lower in PTZNS 200 and 400, furthermore the seizure onset latencies were higher in these groups than PTZ group [P<0.05 and P<0.01]. In Morris water maze, the time spent in target quadrant by PTZ group was lower than control group [P<0.05]; while, 400 mg/Kg of the extract increased it [P<0.01]. In the passive avoidance test, delay time to enter the dark by PTZ group was lower than control at 1 and 24 hours after training [P<0.01 - P<0.001]; while, 400 mg/Kg of the extract increased it [P<0.05]. The total thiol concentration in hippocampal and cortical tissues of PTZ group was reduced while, MDA concentration was higher than control [p<0.05 - p<0.001]. Administration of the extract increased the total thiol and decreased the MDA concentrations [p<0.01 - p<0.001]. It is concluded that the hydro-alcoholic extract of NS possess beneficial effects on learning and memory impairments in repeated seizures model which is accompanied by antioxidant effects in the brain
Subject(s)
Animals, Laboratory , Plant Extracts , Memory/drug effects , Brain/drug effects , Oxidative Stress , Seizures , Rats, Wistar , PentylenetetrazoleABSTRACT
The cerebellum is a key structure involved in coordinated motor planning, cognition, learning and memory functions. This study presents a permanent model of a toxin produced cerebellar lesion characterized according to contemporary motor and cognitive abnormalities. In this experimental study, slow administration of quinolinic acid [QA, 5 microl of 200 micromol, 1 microl/minute] in the right cerebellar hemisphere [lobule VI] caused noticeable motor and cognitive disturbances along with cellular degeneration in all treated animals. We assessed behavioral and histopathological studies over ten weeks after QA treatment. The data were analyzed with ANOVA and the student's t test. The QA treated group showed marked motor learning deficits on the rotating rod test [p = 0.0001], locomotor asymmetry on the cylinder test [p = 0.0001], dysmetria on the beam balance test [p = 0.0001], abnormalities in neuromuscular strength on the hang wire test [p = 0.0001], spatial memory deficits in the Morris water maze [MWM, p = 0.001] and fear conditioned memory on the passive avoidance test [p = 0.01] over a ten-week period compared with the control animals. Histopathological analysis showed loss of Purkinje cells [p = 0.001] and granular cell density [p = 0.0001] in the lesioned hemisphere of the cerebellum. Results of the present study show that QA can remove numerous cells which respond to this toxin in hemispheric lobule VI and thus provide a potential model for functional and cell-based studies