Antihypertriglyceridemia and anti-inflammatory activities of monascus-fermented dioscorea in streptozotocin-induced diabetic rats

Yeu-Ching Shi, Jiunn-Wang Liao, Tzu-Ming Pan, Yeu-Ching Shi, Jiunn-Wang Liao, Tzu-Ming Pan

Abstract

The rice fermented by Monascus, called red mold rice (RMR), and has a long tradition in East Asia as a dietary staple. Monascus-fermented dioscorea called red mold dioscorea (RMD) contains various metabolites to perform the ability of reducing oxidative stress and anti-inflammatory response. We used Wistar rats and induced diabetes by injecting streptozotocin (STZ, 65 mg/kg i.p.). RMD was administered daily starting six weeks after disease onset. Throughout the experimental period, significantly (P < .05) lowered plasma glucose, triglyceride, cholesterol, free fatty acid and low density lipoprotein levels were observed in the RMD-treated groups. The RMD-treated diabetic rats showed higher activities of glutathione disulfide reductase, glutathione reductase, catalase and superoxide dismutase (P < .05) in the pancreas compared with the diabetic control rats. RMD also inhibited diabetes-induced elevation in the levels of interleukin (IL)-1β, IL-6, interferon-γ and tumor necrosis factor-α. Pancreatic β-cells damaged by STZ in the RMD supplemented groups were ameliorated. The results of this study clearly demonstrated that RMD possesses several treatment-oriented properties, including the control of hyperglycemia, antioxidant effects, pancreatic β-cell protection and anti-inflammatory effects. Considering these observations, it appears that RMD may be a useful supplement to delay the development of diabetes and its complications.

Figures

Figure 1
Figure 1
Chromatograms for phenolic acid. Phenolic acid standards (a). Phenolic acids composition of red mold dioscorea (b).
Figure 2
Figure 2
Effect of red mold dioscorea on antioxidant enzyme activity in the pancreas. Superoxide dismutase (SOD) (a). Glutathione reductase (GR) (b). Glutathione peroxidase (GPx) (c). Catalase (CAT) (d). NC: normal control; DC: diabetic control; DM: diabetes mellitus; D: dioscorea; RMD: red mold dioscorea. Data are presented as the means ± SD (n = 6). *P < .05 versus the diabetic control.
Figure 3
Figure 3
Relative proliferation of splenocyte from rats with red mold dioscorea treatment. Splenocytes were stimulated with PHA (a) and LPS (b). NC: normal control; DC: diabetic control; DM: diabetes mellitus; D: dioscorea; RMD: red mold dioscorea. *P < .05 versus the diabetic control.
Figure 4
Figure 4
Immunohistochemical evaluation on pancreas (400x). Normal control (a). Diabetic control (b). Diabetic + 1X D (dioscorea) (c). Diabetic + 0.5X RMD (red mold dioscorea) (d). Diabetic + 1X RMD (red mold dioscorea) (e). Diabetic + 5X RMD (red mold dioscorea) (f).
Figure 5
Figure 5
Comparative evaluation of the expression of insulin immunoreactivity in pancreas. NC: normal control; DC: diabetic control; DM: diabetes mellitus; D: dioscorea; RMD: red mold dioscorea. Data are presented as the means ± SD (n = 6). *P < .05 versus the diabetic control.
Figure 6
Figure 6
The hypothetical diagram of prevention approach of red mold dioscorea with diabetic oxidative stress and inflammatory response.

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