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1.
Article in English | WPRIM (Western Pacific) | ID: wpr-889884

ABSTRACT

Objectives@#. Diabetic auditory neuropathy is a common complication of diabetes mellitus that has a major impact on patients’ quality of life. In this study, we assessed the efficacy of rutin in treating diabetic auditory neuropathy in an experimental rat model. @*Methods@#. Forty Sprague-Dawley rats were randomly assigned to the following groups: group 1, control; group 2, diabetic rats; and groups 3–5, rats treated with rutin (at doses of 50, 100, and 150 mg/kg, respectively). We used auditory brain stem response, stereology of the spiral ganglion, and measurements of superoxide dismutase (SOD) and malondialdehyde (MDA) to evaluate the effects of treatment. @*Results@#. Significant improvements in auditory neuropathy were observed in the rutin-treated groups in comparison with the diabetic group (P<0.05). Auditory threshold, wave latency, wave morphology, the volume and number of neurons in the spiral ganglion, and SOD and MDA activity showed improvements following treatment. @*Conclusion@#. Rutin shows promise as a treatment modality for diabetic auditory neuropathy, but more trials are warranted for its clinical application.

2.
Article in English | WPRIM (Western Pacific) | ID: wpr-897588

ABSTRACT

Objectives@#. Diabetic auditory neuropathy is a common complication of diabetes mellitus that has a major impact on patients’ quality of life. In this study, we assessed the efficacy of rutin in treating diabetic auditory neuropathy in an experimental rat model. @*Methods@#. Forty Sprague-Dawley rats were randomly assigned to the following groups: group 1, control; group 2, diabetic rats; and groups 3–5, rats treated with rutin (at doses of 50, 100, and 150 mg/kg, respectively). We used auditory brain stem response, stereology of the spiral ganglion, and measurements of superoxide dismutase (SOD) and malondialdehyde (MDA) to evaluate the effects of treatment. @*Results@#. Significant improvements in auditory neuropathy were observed in the rutin-treated groups in comparison with the diabetic group (P<0.05). Auditory threshold, wave latency, wave morphology, the volume and number of neurons in the spiral ganglion, and SOD and MDA activity showed improvements following treatment. @*Conclusion@#. Rutin shows promise as a treatment modality for diabetic auditory neuropathy, but more trials are warranted for its clinical application.

3.
Article in English | WPRIM (Western Pacific) | ID: wpr-31698

ABSTRACT

The present study aimed to quantitatively compare the normal and diabetic hearts of rats using stereological methods. Diabetic and control rats received streptozotocin (60 mg/kg) and no treatments, respectively. On the 56th day, the hearts were removed and their total volume was estimated using isotropic Cavalieri method. The total volume of the connective tissues and vessels, total length and diameter of the vessels, total number of cardiomyocytes nuclei, and the mean volume of the cardiomyocytes were estimated, as well. In comparison to the control animals, 60 and 43% increase was observed in the total volume of the connective tissue and microvessels of the diabetic rats, respectively (P<0.05). The percent of the vessel profiles with the diameter of 2-4 microm was decreased, while the percent of the vessel profiles with the diameter of 4.1-8 microm was increased in the diabetic hearts (P<0.05). No significant difference was found in the vessels with more than 8 microm diameters. The total number of the cardiomyocytes' nuclei and the number-weighted mean volume were respectively decreased by 37 and 64% in the diabetic group (P<0.01). A significant difference was observed between the two groups concerning the left ventricle volume to body weight ratio as an index for ventricular hypertrophy (P<0.05), while no difference was found regarding the right ventricle to body weight ratio. It can be concluded that diabetes can induce structural changes, including loss and/or atrophy of the cardiomyocytes, accompanied with increase in the connective tissue in the rats' hearts.


Subject(s)
Animals , Humans , Male , Rats , Atrophy , Body Weight , Connective Tissue , Glycosaminoglycans , Heart , Heart Ventricles , Hypertrophy , Microvessels , Myocytes, Cardiac , Streptozocin
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