Protective effects of the aqueous extract of Crocus sativus against ethylene glycol induced nephrolithiasis in rats.

This study evaluated the possible protective effect of Crocus sativus L. (saffron) in the treatment of renal calculi. Aqueous extract of saffron (25, 50 and 100 mg/kg, daily) was administered intraperitoneally in two regimens of protective or curative, using male Wistar rats. Urolithiasis was induced by ethylene glycol (% 0.75) in drinking water. Urine was collected for biochemical analysis and the kidneys were prepared for total lipid peroxide and histological evaluation. Ethylene glycol feeding resulted in an increased urine output, renal excretion of oxalate and decreased excretion of citrate and magnesium. Saffron did not show diuretic effect; however, it significantly reduced the elevated urinary oxalate in prophylactic (50 and 100 mg/kg) and curative (100 mg/kg) studies. Only the high dose of prophylactic regimen restored citrate concentration of urine. Increased number of calcium oxalate crystals deposits in the kidney tissue of calculogenic rats was significantly reverted by the prophylactic and high dose of curative saffron treatment. Malondialdehyde (MDA, a lipid peroxidation product) in the kidneys was increased following the lithogenic treatment; however, prophylactic (50, 100 mg/kg) and curative (100 mg/kg) regimens with saffron reduced the elevated levels of MDA. Results in the current study indicate that saffron can protect against ethylene glycol induced calcium oxalate (CaOx) nephrolithiasis. The mechanisms underlying this effect are mediated possibly through effect on the urinary concentration of stone-forming constituents and an antioxidant effect.

Antilithiatic effects of crocin on ethylene glycol-induced lithiasis in rats.

In this study, the antilithiatic potential of crocin, a pharmacologically active constituent of Crocus sativus L. (saffron), was evaluated against ethylene glycol (EG)-induced nephrolithiasis in rats. Negative control rats were provided with EG (1 %) in drinking water for 30 days. crocin (10, 20 and 40 mg/kg, i.p.) was administered simultaneously once daily for 30 days (prophylactic regimen) or 14 days after stone induction (therapeutic study). For biochemical analysis, 24-h urine was collected from all experimental animals at the beginning (day 0) and end of the experiment (day 30). The urine output was evaluated during the first 24 h (day 1). Ethylene glycol feeding resulted in decreased hyperoxaluria (P < 0.01) and total protein loss (P < 0.001), along with decreased excretion of citrate and magnesium (P < 0.01) compared with the intact animals. Treatment with prophylactic regimen of crocin (20 and 40 mg/kg) significantly reduced the elevated oxalate, and increased the citrate and magnesium levels of urine. The attenuation of protein loss was only seen with a high dose of crocin in a prophylactic study. Urine volume was not significantly altered after EG or crocin administration. The increased number of calcium deposits in the kidney tissue of lithiatic rats was decreased after prophylactic treatment with 20 and 40 mg/kg of crocin. The urinary ionic parameters and crystal count were not significantly altered after the therapeutic study. A marked increase in malondialdehyde (MDA, a lipid peroxidation product) level was observed in the EG-given group. Treatment with crocin (20 and 40 mg/kg) reduced the elevated levels of MDA. Results indicate that crocin can be effective in preventing urine calculi formation and recurrence of the disease. The mechanism underlying this effect is mediated possibly through balancing promoter and inhibitor factors and an antioxidant effect.

Effect of aqueous extract of Crocus sativus L. (saffron) stigma against subacute effect of diazinon on specific biomarkers in rats.

In this study, the effect of aqueous extract of Crocus sativus L. (saffron) stigma was studied against subacute toxicity of diazinon (DZN) on specific biochemical markers in rats. Vitamin E (200 IU/kg) and the aqueous extract of saffron at doses 50, 100 and 200 mg/kg were injected intraperitoneally three times per week alone or with DZN (20 mg/kg/day, orally) for 4 weeks. Red blood cell (RBC) cholinesterase activity was inhibited by DZN and this effect was not affected by vitamin E or saffron plus DZN. The levels of serum tumor necrosis factor-α (inflammation marker), direct 8-iso-prostaglandin F(2α) (oxidative stress marker) and soluble protein-100 ß (S100ß, neuronal damage marker) were increased significantly by DZN. The saffron extract inhibited the effect of DZN on these biomarkers levels. However, vitamin E was able to only reduce 8-iso-prostaglandin F(2α) and S100ß levels. This study showed that the aqueous extract of saffron prevents DZN-induced rise of several specific inflammation, oxidative stress and neuronal damage biomarkers.

The effect of crocin and safranal, constituents of saffron, against subacute effect of diazinon on hematological and genotoxicity indices in rats.

In this study, the effect of crocin and safranal was studied against subacute toxicity of diazinon (DZN) on hematological and genotoxicity indices in rats. The rats were divided into 16 groups consisted of 6 rats in control, diazinon, vitamin E, vitamin E and DZN, crocin (3 doses), crocin (3 doses) and DZN, safranal (3 doses), safranal (3 doses) and DZN groups. Vitamin E (200 IU/kg), safranal at doses 0.025, 0.05 and 0.1 ml/kg and crocin at doses 50, 100 and 200 mg/kg were injected intraperitoneally to rats three times per week alone or with DZN (20 mg/kg/day, orally) for 4 weeks. Hematological parameters were evaluated at the end of 4 weeks. The evaluation of genotoxicity was done using the micronucleus assay. Vitamin E and, at lower doses, safranal (0.025 and 0.05 ml/kg) and crocin (50 mg/kg) restored the reduction of red blood cell, hemoglobin and hematocrit indices induced by DZN. These agents at some doses also prevented the reduction in platelets counts indices in diazinon treated group. A significant increase in reticulocyte was induced by diazinon. Vitamin E, safranal (0.025 or 0.05 ml/kg) and all doses of crocin decreased this effect of diazinon. In all doses vitamin E, crocin and safranal did not inhibit the effect of diazinon on RBC cholinesterase activity. A significant increase in micronucleus indices was seen with diazinon. Vitamin E, safranal and crocin could not prevent this genotoxicity. This study showed that vitamin E, safranal and crocin (without effects on cholinesterase) reduced diazinon hematological toxicity, but they did not prevent the genotoxicity induced by diazinon.