Protective effect and potential mechanisms of propolis on streptozotocin-induced diabetic rats

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• 作者：Mohamed T. Al-Hariri ; PhD^a ; ^{mohd_alhariri@yahoo.com" class="auth_mail" title="E-mail the corresponding author} ; Tharwat A. Gamal Eldin ; PhD^a ; Mohammed M. Al-Harb ; MSc^b
• 关键词：Diabetes mellitus ; Diabetic rats ; Histopathology ; Lipid peroxidation ; Propolis ; Streptozotocin
• 刊名：Journal of Taibah University Medical Sciences
• 出版年：2016
• 出版时间：February 2016
• 年：2016
• 卷：11
• 期：1
• 页码：7-12
• 全文大小：2307 K

文摘

The objective of this study was to determine the protective effects of propolis supplementation against the toxic effect of streptozotocin (STZ) on pancreatic beta-cells and to identify the possible mechanism of actions underlying this effect.

Methods

Forty-five rats were randomly divided into three groups, with each group containing 15 rats. Group I consisted of normal rats fed a normal chow diet. Group II included diabetic rats induced with STZ. Group III consisted of rats treated with 0.3 g/Kg/day propolis for 2 weeks before the induction of diabetes by STZ. At the end of experimental period, blood samples were collected for the measurement of fasting blood glucose (FBG) and lipid peroxidation activity. Pancreatic tissues from the dissected rats were processed for morphological and immunohistochemical studies.

Results

The findings of this work showed that the treatment of rats with propolis before the induction of diabetes mellitus is associated with significantly decreased FBG levels compared to the diabetic rats. The lipid peroxidation products were significantly increased in group II compared to group I. However, these products were significantly decreased in group III compared to group II. The histopathological and immunohistochemical analysis of the pancreatic tissue showed an increase in the size of the islets of Langerhans and the enhanced staining of beta-cells of the pancreas with beta-cell antibodies in group III compared to group II.

Conclusion

Propolis showed protective and preservative effects on pancreatic beta-cell integrity in STZ-induced diabetic rats. This study suggests the need for further research to elucidate the exact mechanism of this effect.