JOURNAL ARTICLE

Protective effect of cyanidin-3-O-β-D-glucopyranoside fraction from mulberry fruit pigment against oxidative damage in streptozotocin-induced diabetic rat bladder

U-Syn Ha, Woong-Jin Bae, Su-Jin Kim, Byung-Il Yoon, Hoon Jang, Sung-Hoo Hong, Ji-Yeoul Lee, Seung-Yeon Hwang, Sae-Woong Kim
Neurourology and Urodynamics 2013, 32 (5): 493-9
23129268

AIMS: To determine whether cyanidin-3-O-β-D-glucopyranoside (C3G) fraction from mulberry fruit pigment has protective effects against bladder dysfunction on streptozotocin-induced diabetic rats

METHODS: Sprague-Dawley rats were divided into three groups (n = 12 in each): normal, diabetes (DM), and DM treated with C3G fraction (DM + C3G). The DM and DM + C3G groups received a single injection of streptozotocin (50 mg/kg) intraperitoneally. Four weeks after the induction of diabetes, the DM + C3G group was treated with daily oral C3G (10 mg/kg) dissolved in water, for 8 weeks. After 12 weeks of streptozotocin injections, rats in each group underwent cystometrography and bladders were used for evaluation of apoptosis and oxidative stress.

RESULTS: The DM group showed a markedly lower maximal intravesical pressure than that observed in the control group, whereas rats in the DM + C3G group showed improved maximum intravesical pressure associated with minimization of apoptosis, and increased levels of Akt and Bad phosphorylation, implying inhibition of pro-apoptotic stimuli. The level of 8-hydroxy-2-deoxyguanosine, a marker of oxidative stress, was significantly greater in the DM group compared to the control group and it was significantly reduced in the C3G treated group. Immunoblotting revealed a significant decrease in the levels of the superoxide dismutase protein and nerve growth factor in the DM group compared with the control group; however, these proteins were upregulated in the DM + C3G group compared with the DM group.

CONCLUSIONS: The study is the first to suggest that C3G fraction have a potency to protect the bladder under conditions of diabetes-induced oxidative stress.

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