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Anti-Diabetic Effects of Gynura Bicolor Aqueous Extract in Mice
Pei-Ying Pai1, Mei-Chin Mong2, Ya-Cheng Yang2
1Division of Cardiology, China Medical Univ. Hospital, China Medical Univ., Taichung City, Taiwan.
Abstract:
The effects of Gynura bicolor aqueous extract (GAE) upon glycemic control, coagulation disorder, lipid accumulation, and glycative, oxidative, and inflammatory stresses in diabetic mice were investigated. Mice were treated with streptozotocin to induce type 1 diabetes. Diabetic mice were divided into four groups, consumed GAE at 0%, 0.25%, 0.5%, or 1%. Normal group consumed standard mouse basal diet. After 8-week treatments, mice were sacrificed after overnight fasting. Results showed that GAE supplement at 0.5% and 1% decreased plasma glucose level and increased plasma insulin level. Diabetes lowered plasma level of protein C and anti-thrombin III; and raised plasminogen activator inhibitor-1 activity and fibrinogen level in plasma. GAE supplement at 0.5% and 1% reversed these alterations. Histological data, assayed by Oil Red O stain, indicated that GAE supplement decreased lipid accumulation in liver. GAE supplement at 0.5% and 1% reduced aldose reductase activity in heart and kidney; and lowered the levels of carboxymethyllysine and pentosidine in plasma and two organs. Diabetes decreased glutathione content, and increased reactive oxygen species, interleukin (IL)-1β, IL-6, and tumor necrosis factor-α production in heart and kidney. GAE supplement at three test doses reversed these changes. Diabetes upregulated the mRNA expression of p38 and nuclear factor kappa (NF-κ)B in heart and kidney. GAE supplement suppressed the mRNA expression of both p38 and NF-κB. These novel findings suggest that Gynura bicolor is a potent functional food for diabetic prevention or alleviation.
Insights
Gynura bicolor aqueous extract (GAE) effectively improved glycemic control and reduced oxidative stress in diabetic mice. This functional food shows promise for preventing or alleviating diabetes complications.
Area of Science:
- Biochemistry
- Pharmacology
- Nutrition Science
Background:
- Type 1 diabetes is characterized by hyperglycemia, coagulation disorders, and increased oxidative and inflammatory stresses.
- Diabetic complications involve lipid accumulation, glycative stress, and organ damage in the heart and kidneys.
- Gynura bicolor is a plant with potential therapeutic properties, but its effects on diabetes require detailed investigation.
Purpose of the Study:
- To investigate the effects of Gynura bicolor aqueous extract (GAE) on glycemic control in diabetic mice.
- To evaluate GAE's impact on coagulation, lipid accumulation, and oxidative and inflammatory stresses associated with diabetes.
- To explore GAE's potential role in preventing or alleviating diabetic complications.
Main Methods:
- Type 1 diabetes was induced in mice using streptozotocin.
- Diabetic mice were treated with varying doses of GAE (0.25%, 0.5%, 1%) for 8 weeks.
- Key metabolic parameters, coagulation factors, lipid accumulation, oxidative stress markers, inflammatory cytokines, and gene expression were analyzed.
Main Results:
- GAE supplementation (0.5% and 1%) significantly decreased plasma glucose and increased insulin levels.
- GAE reversed diabetes-induced alterations in coagulation factors (protein C, anti-thrombin III, PAI-1, fibrinogen).
- GAE reduced liver lipid accumulation, aldose reductase activity, and levels of advanced glycation end products (AGEs) like carboxymethyllysine and pentosidine.
- GAE normalized glutathione levels, reduced reactive oxygen species (ROS), and suppressed pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and NF-κB signaling pathways.
Conclusions:
- Gynura bicolor aqueous extract demonstrates significant anti-diabetic effects by improving glycemic control and coagulation.
- GAE mitigates lipid accumulation, glycative stress, and oxidative and inflammatory damage in diabetic mice.
- Gynura bicolor shows potential as a functional food for the prevention and management of diabetes and its associated complications.
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