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Showing 2 results for Royal Jelly

Mojtaba Asgari, Masoumeh Asle-Rousta, Mohammad Sofiabadi,
Volume 20, Issue 5 (8-2017)
Abstract

Abstract

Background: Diabetes is the most common endocrine disorder that leads to hyperglycemia and hyperlipidemia. Royal jelly is as a bee-collected natural product has diverse biological properties and that is rich in natural antioxidants. The aim of this study was to investigate the effects of royal jelly on serum glucose and lipids profile in streptozotocin induced type 1 diabetic rats.

Materials and Methods: In this experimental study, 40male Wistar rats were divided into 5 groups(8 in each): control, diabetic rats, Glibenclamide, and two groups of royal jelly- treated diabetic. Diabetes was induced in the rats by injection of streptozotocin (60 mg/kg b.w) intraperitoneally. The royal jelly was gavaged at doses of 100 and 200 mg/kg after streptozotocin injection for30 days. At the end of this period, levels of glucose, cholesterol, triglyceride, LDL and HDL in serum were measured.

Results: Royal jelly and Glibenclamide significantly decreased the levels of glucose, cholesterol, triglyceride and LDL in diabetic rats (p<0.01). In addition, significant increase (p<0.01) in HDL level was observed in royal jelly-treating rats in comparison to the diabetic rats.

Conclusion: The results indicated that royal jelly may be used effectively in controlling and attenuating the complications of diabetes. The hypoglycemic and hypolipidemic effects of royal jelly may be due to the presence of antioxidants.


Hojat Anbara, Hassan Morovvati, Masoud Adib Moradi, Rasoul Shahrooz,
Volume 20, Issue 7 (10-2017)
Abstract


Abstract
Background: Phenylhydrazine (PHZ) as a strong oxidant agent causes variety of toxic effects including alterations in the biochemical and cardiac tissue. The aim of the present study was to investigate the effects of royal jelly (RJ) and vitamin C (vit C) against PHZ-induced cardiotoxicity in mice.
Materials and Methods: Adult male mice were randomly assigned to eight groups of eight mice each. PHZ was administered to four groups of mice at a dose of 60 mg/kg per 48 hours intraperitoneally for 35 days. Three of these groups received vit C (250 mg/kg per day) intraperitoneally, RJ (100 mg/kg per day) orally and vit C+RJ with same doses four hours before PHZ administration, respectively. A vehicle-treated control group and vit C, RJ and vit C+RJ control groups were also included.
Results: RJ and vit C significantly decreased (p< 0.05) the serum level of malondialdehyde and creatine kinase (CK-BM) that had been increased by PHZ. Also, RJ and vit C increased the total antioxidant capacity and supraxoid dismutase serum that had been decreased by induced PHZ. Moreover, RJ and vit C could improve the tissue damages induced by PHZ such as diffused edema, hemorrhage, congestion, hyaline exudates, necrosis and also fibrosis tissue in heart tissue.
Conclusion: It seems that Vit C and RJ can minimize PHZ-induced cardiotoxicity in mouse through oxidative reactions inhibition.

 


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