Anti-inflammatory and anti-diabetic role of Ashwagandha (Withania somnifera) in a type 2 diabetes mellitus mouse model.
Anti-inflammatory and anti-diabetic role of Ashwagandha (Withania somnifera) in a type 2 diabetes mellitus mouse model: a study using histological, molecular, and pathological parameters.
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Abstract
Type 2 diabetes mellitus (T2DM) is an extensive metabolic disorder that imposes significant health and economic problems worldwide. It is characterized by chronic hyperglycemia, insulin resistance, and systemic inflammation. T2DM is linked with an increased risk of terrible difficulties, including cardiovascular disease, neuropathy, and nephropathy. The developing proofs suggest that natural compounds such as Ashwagandha (Withania somnifera) may have therapeutic potential due to their anti-inflammatory, antioxidant, and glucose-regulating properties. Ashwagandha is a traditional medicinal herb that is rich in withanolides and has demonstrated efficacy in previous studies; however, its comprehensive role in mitigating T2DM-related complications is underexplored. The current study seeks to assess the anti-inflammatory and antidiabetic effects of Ashwagandha in a high-fat diet (HFD) and low-dose streptozotocin (STZ)-induced T2DM mouse model. We have selected male C57BL/6 mice, which were allocated into four experimental groups, i.e. controls, STZ-induced diabetic controls, diabetic mice treated with Ashwagandha (200 mg/kg), and diabetic mice treated with metformin. The mice were treated for 8 weeks and then we assisted histological changes in pancreatic and hepatic tissues, with analysis of molecular markers of inflammation and glucose metabolism, and biochemical parameters such as blood glucose, insulin levels, lipid profiles, and oxidative stress markers. We have found a significant reduction in systemic inflammation, enhanced glucose tolerance, improved insulin sensitivity, and restored function of pancreaticβ-cell. Furthermore, Ashwagandha treatment is predicted to relieve hepatic steatosis and adipose tissue inflammation by altering key oxidative stress and inflammatory pathways.
Affiliation
Reem Hasaballah Alhasani
External References
- PubMed ID:
- 40717151
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