Propolis, a Constituent of Honey, Inhibits the Development of Sugar Cataracts and High-Glucose-Induced Reactive Oxygen Species in Rat Lenses.

Teppei Shibata,Dhirendra P Singh,Shinsuke Shibata,Naoko Shibata,Hiroshi Sasaki,Etsuko Kiyokawa,Eri Kubo

doi:10.1155/2016/1917093

Teppei Shibata, Dhirendra P Singh + Show 5 more

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https://doi.org/10.1155/2016/1917093

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Abstract

Purpose. This study investigated the effects of oral propolis on the progression of galactose-induced sugar cataracts in rats and the in vitro effects of propolis on high-glucose-induced reactive oxygen species (ROS) and cell death in cultured rat lens cells (RLECs). Methods. Galactose-fed rats and RLECs cultured in high glucose (55 mM) medium were treated with propolis or vehicle control. Relative lens opacity was assessed by densitometry and changes in lens morphology by histochemical analysis. Intracellular ROS levels and cell viability were measured. Results. Oral administration of propolis significantly inhibited the onset and progression of cataract in 15% and 25% of galactose-fed rats, respectively. RLECs cultured with high glucose showed a significant increase in ROS expression with reduced cell viability. Treatment of these RLECs with 5 and 50 μg/mL propolis cultured significantly reduced ROS levels and increased cell viability, indicating that the antioxidant activity of propolis protected cells against ROS-induced damage. Conclusion. Propolis significantly inhibited the onset and progression of sugar cataract in rats and mitigated high-glucose-induced ROS production and cell death. These effects may be associated with the ability of propolis to inhibit hyperglycemia-evoked oxidative or osmotic stress-induced cellular insults.

Highlights

Hyperglycemia is the major factor in the development of diabetic cataracts
These findings suggested that oxidative stress induced by osmotic stress and hyperglycemia is a major factor in the etiology of cell death signaling that leads to cataractogenesis
Cell viability assays showed that culture with 50 mM glucose significantly reduced cell survival but that the addition to these cells of 5 or 50 μg/mL propolis significantly enhanced their viability, more so than that of rat lens cells (RLECs) cultured with 50 mM glucose and treated with

Summary

Introduction

Hyperglycemia is the major factor in the development of diabetic cataracts. Hyperglycemia activates the aldose reductase (AR)/sorbitol (polyol) pathway and induces osmotic and/ or oxidative stress [1,2,3,4,5,6]. Hyperglycemia associated ROS are generated by the autoxidation of glucose, the nonenzymatic glycation of proteins, the glucoseinduced activation of protein kinase C, increased polyol pathway activity, and impairment of antioxidant enzymes and alterations in mitochondria [13,14,15,16,17]. Taken together, these findings suggested that oxidative stress induced by osmotic stress and hyperglycemia is a major factor in the etiology of cell death signaling that leads to cataractogenesis. The results of this study may contribute to the development of strategies to prevent or delay hyperglycemia-induced complications

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Discussion