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Monascin from red mold dioscorea as a novel antidiabetic and antioxidative stress agent in rats and Caenorhabditis
Yeu-Ching Shi1, Vivian Hsiu-Chuan Liao, Tzu-Ming Pan
1Department of Biochemical Science and Technology, National Taiwan University, Taipei, Taiwan.
Abstract:
Monascin is a major yellow compound from red mold dioscorea. We investigated monascin to test whether this compound acts as an antidiabetic and antioxidative stress agent in diabetic rats and Caenorhabditis elegans. The mechanisms by which monascin exerts its action in vivo were also examined. Streptozotocin (STZ)-induced diabetic rats were given monascin at 30 mg/kg/day and sacrificed after 8 weeks. Blood glucose and serum insulin, triglyceride, total cholesterol, and high-density lipoprotein and antioxidative enzymes in the pancreas of rats were measured. In addition, monascin was evaluated for stress resistance and potential associated mechanisms in C. elegans. Throughout the 8-week experimental period, significantly lowered blood glucose, serum triglyceride, and total cholesterol and higher high-density lipoprotein levels were observed in monascin-treated rats. Monascin-treated rats showed higher serum insulin level, lower reactive oxygen species production, and higher activities of glutathione peroxidase, superoxide dismutase, and catalase in the pancreas compared to diabetic control rats. In addition, monascin significantly induced the hepatic mRNA levels of FOXO3a, FOXO1, MnSOD, and catalase in STZ-induced diabetic rats. Monascin-treated C. elegans showed an increased survival rate during oxidative stress and heat stress treatments compared to untreated controls. Moreover, monascin extended the life span under high-glucose conditions and enhanced expression of small heat shock protein (sHSP-16.2), superoxide dismutase (SOD-3), and glutathione S-transferase (GST-4) in C. elegans. Finally, we showed that monascin affected the subcellular distribution of the FOXO transcription factor DAF-16, whereas it was unable to enhance oxidative stress resistance in the daf-16 deletion mutant in C. elegans. Mechanistic studies in rats and C. elegans suggest that the protective effects of monascin are mediated via regulation of the FOXO/DAF-16-dependent insulin signaling pathway by inducing the expression of stress response/antioxidant genes, thereby enhancing oxidative stress resistance.
Insights
Monascin, a compound from red mold, demonstrates significant antidiabetic and antioxidative effects in diabetic rats and C. elegans by regulating the FOXO/DAF-16 insulin signaling pathway and enhancing stress resistance genes.
Area of Science:
- Biochemistry
- Pharmacology
- Gerontology
Background:
- Monascin is a yellow pigment derived from red mold.
- Diabetes mellitus is a metabolic disorder characterized by hyperglycemia and oxidative stress.
- Identifying natural compounds with antidiabetic and antioxidant properties is crucial for therapeutic development.
Purpose of the Study:
- To investigate the antidiabetic and antioxidative stress effects of monascin in streptozotocin (STZ)-induced diabetic rats and Caenorhabditis elegans.
- To elucidate the underlying mechanisms of monascin's action in vivo, focusing on insulin signaling and stress response pathways.
Main Methods:
- Diabetic rats were treated with monascin (30 mg/kg/day) for 8 weeks, with biochemical and enzymatic analyses performed.
- Monascin's effects on stress resistance, lifespan, and gene expression were evaluated in C. elegans.
- Mechanistic studies involved assessing the role of the FOXO transcription factor DAF-16 in monascin's protective effects.
Main Results:
- Monascin treatment significantly reduced blood glucose, triglyceride, and total cholesterol levels while increasing high-density lipoprotein and insulin levels in diabetic rats.
- Monascin enhanced antioxidant enzyme activities (glutathione peroxidase, superoxide dismutase, catalase) and induced hepatic mRNA levels of FOXO3a, FOXO1, MnSOD, and catalase in rats.
- In C. elegans, monascin improved survival under oxidative and heat stress, extended lifespan in high-glucose conditions, and upregulated stress response genes (sHSP-16.2, SOD-3, GST-4) in a DAF-16 dependent manner.
Conclusions:
- Monascin exhibits potent antidiabetic and antioxidative properties.
- Its protective effects are mediated through the FOXO/DAF-16 insulin signaling pathway, leading to enhanced expression of stress response and antioxidant genes.
- Monascin represents a promising natural compound for managing diabetes and mitigating oxidative stress.
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