Pistia stratiotes has renoprotective potentials in ischemia reperfusion injury in normal and diabetic rats.

OBJECTIVE: Even though oxidative and inflammatory bursts are a big part of renal reperfusion injury (RI/R), Pistia stratiotes (PS) has been used for a long time to stop these overreactions. People have said that it can drop both blood sugar and cholesterol. Hence, the goal of this study was to show how PS changed kidney reperfusion damage in both diabetic and normal rats. MATERIALS AND METHODS: In the study, 30 min of renal ischemia (RI) was followed by 1 h of recovery for each rat. Before the test, PS (100 mg/kg p. o.) was given to the animals for 7 days. Then, using the mixture from the separated kidney tissues, the antioxidant, inflammation, and histopathological effects were determined. RESULTS: When compared to RI/R, diabetic rats given PS had lower blood sugar, aspartate aminotransferase, blood urea nitrogen, and creatinine, myeloperoxidase, C-reactive protein, and tumor necrosis factor-alpha levels in their urine. CONCLUSION: PS potentially worked in hyperglycemic rats protecting them against RI/R. It is possible that PS's ability to protect the kidneys of the test rats is due to its ability to fight free radicals, lower blood sugar, and stop inflammation.

Protective Effect of Eichhornia Crassipes Against Cerebral Ischemia Reperfusion Injury in Normal and Diabetic rats.

Eichhornia crassipes (EC) is well reported to modify inflammatory response, oxidative stress which are key pathophysiological finding of cerebral reperfusion injury, alongside it is reported to reduce cholesterol and blood glucose levels, and therefore present work was designed to investigate the effect of EC on cerebral reperfusion injury in normal and diabetic rats. Each protocol comprised cerebral ischemia (CI) for 30 min followed by reperfusion(R) for 1 h. Animals were treated with EC (100 mg/kg p.o) for seven days. At the end of the experiment, brain tissue was utilized for the measurement of oxidative stress markers, inflammatory response, infarct size and histopathological findings. EC treated rats demonstrated a significant reduction in infarct sizes when compared with CI/R and Diabetic CI/R (DCI/R) group of rats. EC treatment demonstrated a significant decreased in malondialdehyde, nitric oxide and blood glucose levels and a significant increase in the level of reduced glutathione, superoxide dismutase catalase and insulin levels, showed modification in oxidative stress. EC treatment confirmed a significant decrease in myeloperoxidase, C - reactive protein and TNF-α levels indicated a change in the inflammatory response. Histopathological findings revealed a reversal of damage in EC treated rats. EC treatmen reduced DNA fragmentation of brain tissue in treated animals. EC was found to be cerebroprotective against CI/R along with DCI/R group of rats by anti-inflammatory and antioxidant activities.

Cardio protective effect of vitamin A against isoproterenol-induced myocardial infarction.

Vitamin A is beneficial in counteracting free radical damage, therefore the present study is designed to investigate the effect of vitamin A against isoproterenol-induced myocardial infarction in rats. Male Wistar rats were divided into three groups, namely a normal control group, an isoproterenol group (150 mg/kg, s.c.), and a vitamin A treatment (4,500 IU/kg/d, orally) group. Vitamin A-treated rats demonstrated significant reduction in ST-segment (p<0.001) and infarct sizes (p<0.05) when compared with the isoproterenol group of rats, suggesting that vitamin A markedly attenuated myocardial injury. Vitamin A treatment resulted in a significant decrease in the serum level of troponin I (p<0.001), creatinine kinase-MB (p<0.01), creatine kinase (p<0.05), lactate dehydrogenase (p<0.05), aspartate aminotransferase (p<0.01) and alanine aminotransferase (p<0.01). Vitamin A treatment resulted in a significant decrease in malondialdehyde (p<0.001), and significant increases were observed in reduced glutathione (p<0.01), superoxide dismutase (p<0.05) and catalase (p<0.001). Vitamin A treatment resulted in a significantly increased level of Na(+)-K(+) ATPase (p<0.05) and Mg(2+)-ATPase (p<0.01) and a significant reduction of Ca(2+) ATPase (p<0.01). Vitamin A treatment also demonstrated a significantly decreased level of C-reactive protein (p<0.05) and myeloperoxidase activity (p<0.01). In conclusion, vitamin A attenuated the myocardial infarction and prevention was shown via membrane stabilization, reduction in oxidative stress, and prevention of neutrophil infiltration.

Homocysteine-dependent endothelial dysfunction induced by renal ischemia/reperfusion injury.

BACKGROUND: Elevation of serum homocysteine is considered to contribute to endothelial dysfunction, which is considered to be the initial event in vascular disease following renal transplantation. We sought to investigate whether an association existed between serum homocysteine levels and endothelial dysfunction after renal ischemia/reperfusion (I/R) injury. MATERIALS AND METHODS: Acetylcholine (Ach)-induced endothelium-dependent and sodium nitroprusside (SNP)-induced endothelial-independent relaxation responses were determined in thoracic aortas from different I/R groups. A correlation analysis was performed between Ach responses and homocysteine levels. RESULTS: Long-term I/R injury decreased the responses to acetylcholine and the pD2 values of the concentration response curves compared with controls. While vascular responses to SNP were unchanged among all groups. Homocysteine levels correlated with the pD2 values of acetylcholine among control and I/R groups, indicating that the increase in homocysteine was associated with decreased sensitivity to acetylcholine. In short-term I/R rats, no association was observed between these parameters. CONCLUSION: These data suggest a possible link between serum homocysteine and decreased vascular reactivity to endothelium-dependent relaxation in I/R aorta.

Sitagliptin protects renal ischemia reperfusion induced renal damage in diabetes.

This study was designed to investigate the possible effect of sitagliptin on renal damage induced by renal ischemia reperfusion (I/R) in diabetic rats. T2DM in rats was induced by the administration of nicotinamide (230 mg/kg, i.p.), 15 min prior to a single dose of streptozotocin (65 mg/kg, i.v.). In vivo renal I/R was performed in both T2DM and normal rats. Each protocol comprised ischemia for 30 min followed by reperfusion for 24h and a treatment period of 14 days before induction of ischemia. Sitagliptin treated diabetic rats that underwent renal I/R demonstrated significant decrease in the serum concentrations of aspartate aminotransferase (p < 0.01), urea nitrogen (p < 0.01) and creatinine (p < 0.001) compared to renal I/R in diabetic rats. Lipid peroxidation, xanthine oxidase activity, myeloperoxidase activity and nitric oxide level in renal tissue were significantly (p < 0.05, p < 0.001, p < 0.01, p < 0.05 respectively) decreased after renal I/R in sitagliptin treated rats compared to diabetic rats. Antioxidant enzymes like glutathione (p < 0.05), glutathione peroxidase (p < 0.001), superoxide dismutase (p < 0.05) and catalase (p < 0.001) were significantly increased after renal I/R in sitagliptin treated diabetic rats compared to non treated diabetic rats. The typical DNA laddering was observed when renal I/R performed in diabetic rats, which indicates cell apoptosis. Sitagliptin treated rats demonstrated a decrease in DNA fragmentation and apoptosis. Furthermore, renal histopathology preserved in sitagliptin treated rats verified protection against renal I/R in diabetes. The results of present investigation established sitagliptin treatment attenuated renal damage induced by renal I/R in diabetic rats.

Role of fenofibrate alone and in combination with telmisartan on renal ischemia/reperfusion injury.

It was demonstrated that fenofibrate and telmisartan exerted renoprotective effects in ischemia/reperfusion (I/R) injury. Because the combination of fenofibrate and telmisartan synergistically enhanced peroxisome proliferator-activated receptor (PPAR) activation, we hypothesized that the combination of both drugs may exert prolonged beneficial effects in renal I/R injury than fenofibrate alone. Forty-eight male Wistar albino rats were divided into eight groups. Hyperlipidemia was induced by cholesterol feeding for 4 weeks. At the end of the fourth week, renal I/R injury was performed by occlusion of both renal vascular pedicles for 60 minutes, followed by 24 hours of reperfusion. In the treatment group, fenofibrate alone and in combination with telmisartan was administered 2 weeks prior to renal ischemia. At the end of the experiment, blood and kidneys were isolated for biochemical and histological analysis. I/R in hyperlipidemic rat shows significantly increased lipid peroxidation, nitric oxide, and myeloperoxidase activity, and depletion of antioxidant enzyme compared with control rats, and that was significantly restored after fenofibrate and telmisartan treatment. Also, significant increases in serum homocysteine level were detected following I/R. Fenofibrate treatment further elevated homocysteine level, which was reduced by telmisartan in combination with fenofibrate. The most significant histological damage was found in the hyperlipidemic rat subjected to renal I/R, which was reduced significantly with combination therapy. The results of this study concluded that fenofibrate alone and in combination with telmisartan significantly ameliorated renal I/R injury. The additive beneficial effect of telmisartan is predicted to reduce homocysteine-induced oxidative stress through reduced nitric oxide production during I/R.

Exaggerated liver injury induced by renal ischemia reperfusion in diabetes: effect of exenatide.

BACKGROUND/AIM: This study was designed to investigate the possible effect of exenatide (Glucagon like Peptide-1 receptor agonist) on liver injury (distant organ) induced by renal ischemia reperfusion (IR) in diabetic rats. MATERIALS AND METHODS: In vivo renal IR was performed in both type 2 diabetic and normal rats. Each protocol comprised ischemia for 30 minutes followed by reperfusion for 24 hours and a treatment period of 14 days before induction of ischemia. RESULTS: Lipid peroxidation, xanthine oxidase activity, myeloperoxidase activity and nitric oxide level in liver tissue were significantly increased (P < 0.01, P < 0.001, P < 0.001, P < 0.05, respectively), after IR in diabetic rats compared to normal rats. Antioxidant enzymes like glutathione, superoxide dismutase, catalase and glutathione peroxidase were significantly reduced (P < 0.05, P < 0.05, P < 0.01, P < 0.05, respectively), after IR in diabetic rats compared to normal rats. Exenatide treatment significantly normalized (P < 0.01), these biochemical parameters in treated rats compared to diabetic IR rats. Serum creatinine phosphokinase activity and liver function enzymes were also significantly normalized (P < 0.001, P < 0.001, respectively), after administration of exenatide. CONCLUSION: Exenatide exerted protective effect on exaggerated remote organ (liver) injury induced by renal IR in diabetes.

Renoprotective activity of benincasa cerifera fruit extract on ischemia/reperfusion-induced renal damage in rat.

INTRODUCTION: Evidence suggests that reactive oxygen species play a role in the pathophysiology of renal ischemia/reperfusion (I/R) injury. This study was designed to investigate the renoprotective activity of methanolic fruit extract of Benincasa cerifera in I/R-induced kidney failure in rats. MATERIALS AND METHODS: Renal pedicles of 12 rats were occluded for 60 minutes followed by 24 hours of reperfusion. Six days prior to induction of I/R, 6 of the rats received Benincasa cerifera, 500 mg/kg, orally. Serum creatinine, urea, and uric acid levels were measured after the operation. At the end of reperfusion period, the rats were sacrificed. Superoxide dismutage, catalase, reduced glutathione, and renal malondialdehyde content were determined in the renal tissues. Results were compared with a group of rats with sham operation. RESULTS: Renal I/R caused significant impairment of kidney function. Six-day administration of Benincasa cerifera, however, minimized this effect. Rats with renal I/R only showed significantly decreased activity of superoxide dismutage, catalase, and reduced glutathione compared with the sham-operated rats. These declining trends were significantly less in the group treated with Benincasa cerifera compared with those in the I/R-only group (P = .008, P = .07, and P < .001, respectively). Renal I/R produced a significant increase in malondialdehyde level, while pretreatment with Benincasa cerifera was associated with a significantly lower malondialdehyde level (P < .001). CONCLUSIONS: These findings imply that reactive oxygen species play a crucial role in I/R-induced kidney injury and Benincasa cerifera exerts renoprotective activity probably by the radical scavenging activity.