The present study was carried out to investigate the nephroprotective effect of the ethanolic extract of Allium saralicum R.M. Fritsch (ASRMF) in mice. Thirty-five male mice were divided into five groups (n=7). Group 1 (positive control) received 1 mL/kg olive oil intraperitoneally (i.p.) and 0.5 mL distilled water orally; Group 2 (negative control) received CCl 4 (50% in olive oil, 1 mg/kg; i.p.); Groups 3, 4 and 5 received CCl 4 and 200, 800 and 1600 µg/kg of ASRMF extract, respectively. The renal volume and cortex in Groups 1 and 2 were increased by 55% and 62% (p≤0.001) following CCl 4 administration, respectively, and were improved after ASRMF administration. The volume of proximal convoluted tubules (PCTs), glomeruli, vessels and interstitial tissue increased 80%, 150%, 83% and 64% (p≤0.05), respectively, in CCl 4treated mice, and decreased significantly with 800 and 1600 µg/kg of ASRMF. The length of PCTs and vessels increased 51% and 45% and decreased (p≤0.05) with 200, 800 and 1600 µg/kg of ASRMF, respectively. CCl 4-treated mice lost 22.5% of glomeruli; the loss was inhibited significantly (p≤0.05) by ASRMF. Urea and creatinine concentrations were increased (p≤0.05) in CCl 4-induced nephrotoxicity as compared to the controls, whereas different doses of ASRMF restored the levels of these biomarkers compared to the negative controls. In conclusion, ASRMF has a potent nephroprotective property and can improve renal structural and serum biomarkers in CCl 4-induced nephrotoxicity in mice.
Objective:Polycystic ovary syndrome (PCOS) is a common endocrine disorder associated with obesity. Human and animal studies showed a direct relationship between leptin level and obesity, however, results from different studies were mixed. This study investigated the status of leptin level in PCOS and its relationship with body mass index (BMI) in a group of Iranian women with PCOS.Methods:In this cross-sectional study, 40 women with PCOS and 36 healthy women were assigned to experimental and control groups, respectively. Those in the PCOS group were not prescribed any medications for 3 months prior to the study. Fasting blood samples were then collected during the 2nd or 3rd day of menstruation for laboratory measurement of serum total leptin, blood glucose (fasting blood sugar), serum insulin, follicle-stimulating hormone, and luteinizing hormone (LH).Results:Mean BMI of the PCOS and control groups were 26.62 ± 4.03 kg/m2 and 23.52 ± 2.52 kg/m2, respectively (P = 0.006). The mean total leptin in the PCO group was also 10.69 ± 5.37 ng/mL and 5.73 ± 2.36 ng/mL in the control group (P = 0.0001). A significant relationship was found between leptin level and BMI as well as LH level among women with PCOS (P < 0.05). However, there was no significant correlation between leptin and insulin (P > 0.05).Conclusion:The results of this study indicated an increased leptin level among women with PCOS that positively associated with BMI and LH.
Our findings indicate that oxidative stress, impairment of the antioxidant system and abnormal lipid metabolism may play a role in the pathogenesis and progression of ESRD and its related complications. These data suggest that patients with ESRD are more susceptible to vascular diseases.
Severe envenoming was induced in two groups of experimental dogs after subcutaneous (SQ) injection of venom of the scorpion (Mesobuthus tamulus concanesis, Pocock) (3.0 and 3.5 mg/kg body weight). The circulating levels of blood sugar, insulin, glucagon, and cortisol were assayed at 0, and 30, 60, 90 and 120 min after venom injection. There was an increase in the circulating levels of blood sugar, insulin, glucagon, and cortisol following envenoming. Scorpion envenoming causes an autonomic storm resulting in a massive release of catecholamines, angiotensin II, glucagon, and cortisol accompanied by changes in insulin secretion. The rise in the counter-regulatory hormones (glucagon, cortisol, and catecholamines) oppose the anabolic actions of insulin resulting in a variety of clinical manifestations. These changes may lead to a syndrome of fuel-energy deficits and to an inability of the vital organs to utilise the existing metabolic substrates, ultimately resulting in multisystem organ failure (MSOF) and death
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