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.

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.