Research progress of dihydromyricetin in the treatment of diabetes mellitus

Wang, Ziyuan; Cao, Zhuoran; Yue, Zhiying; Yang, Zhengfeng

doi:10.3389/fendo.2023.1216907

Cited by 3 publications

References 73 publications

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Dihydromyricetin alleviates inflammatory bowel disease associated intestinal fibrosis by inducing autophagy through the PI3K/AKT/mTOR signaling pathway

Wang,

Li,

et al. 2023

Naunyn-Schmiedeberg's Arch Pharmacol

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Objective: Intestinal brosis is a common complication of in ammatory bowel disease and is characterized by tissue stiffening and luminal narrowing. Dihydromyricetin (DHM) can alleviate liver brosis and renal interstitial brosis by inducing autophagy. However, whether DHM can alleviate intestinal brosis remains unclear. This study aimed to evaluate the role and mechanism of action of DHM in in ammatory bowel disease-associated intestinal brosis .Methods: Mice were administered Dextran sulphate Sodium (DSS) in drinking water to induce in ammatory bowel disease-associated intestinal brosis. HE staining, qPCR and Western blotting were used to analyze colon in ammation. Masson' s trichrome staining, qPCR, Western blotting and immuno uorescence staining were used to evaluate the severity of brosis. Transmission electron microscopy and Western blotting were used to assess the activation of autophagosomes. The human colonic broblast line CCD-18Co, was cultured in the presence of TGF-β1 to develop a brotic phenotype.Immuno uorescence staining, Western blotting and qPCR were used to assess the alteration of brosis markers and used to investigate whether DHM-induced autophagy was involved in the inactivation of CCD-18Co cells. Additionally, the role of the PI3K/AKT/mTOR pathway was investigated.Results: DHM alleviated intestinal in ammation and inhibited the progression of intestinal brosis. Additionally, DHM induced the activation of autophagy, thereby alleviating intestinal brosis, and downregulated the PI3K/AKT/mTOR signaling pathway in vitro.Conclusions: Overall, this study demonstrated that DHM can inhibit the progression of intestinal brosis and activation of colonic broblasts by inducing autophagy through the PI3K/AKT/mTOR signaling pathway, thereby playing a preventive and therapeutic role in intestinal brosis.

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Dihydromyricetin alleviates inflammatory bowel disease associated intestinal fibrosis by inducing autophagy through the PI3K/AKT/mTOR signaling pathway

Wang,

Li,

et al. 2023

Naunyn-Schmiedeberg's Arch Pharmacol

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Effects of Nanoparticle-Mediated Dihydromyricetin to Diabetic Wounds: An In Vivo Study

Wang,

Ma,

et al. 2024

Journal of Burn Care &Amp; Research

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Diabetic wound is one of the serious complications of diabetes, and the wound is persistent and easily recurring, which seriously endangers the health and life of patients. How to effectively promote the healing of diabetic wounds has been a hot spot and difficult area of clinical research. Some previous studies have shown that dihydromyricetin has the effects of regulating blood glucose, controlling the severity and inhibiting scarring. In the present study, we used PLGA nanoparticles as a carrier to load dihydromyricetin to make drug-loaded nanoparticles and applied them dropwise (200 µL) to diabetic mice wounds by topical application to observe the healing and scar formation of diabetic wounds. We found that the healing rate of the diabetic mice was faster and the scar formation was less obvious. In addition, the elevated blood glucose level and weight loss of the mice in the treatment group were also reduced. Therefore, nanoparticle-mediated dihydromyricetin may be an effective treatment for diabetic wounds.

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Dihydromyricetin promotes GLP-1 secretion to improve insulin resistance via “gut microbiota-CDCA”

Li,

Zhang,

Lang

et al. 2024

Preprint

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Dihydromyricetin (DHM) is a polyphenolic phytochemical found mainly in plants such asAmpelopsis grossedentata,which has beneficial effects on insulin resistance. However, the specific mechanism has not been clarified. In this study, C57BL/6 mice were exposed to a high-fat diet (HFD) for eight weeks. DHM could improve insulin resistance via enhancing the incretin effect. DHM increased serum GLP-1 by improving intestinal GLP-1 secretion and inhibiting GLP-1 decomposition, associated with the alteration of intestinal intraepithelial lymphocytes (IELs) proportions and decreased expression of CD26 in IELs and TCRαβ+CD8αβ+IELs in HFD-induced mice. Meanwhile, DHM could ameliorate GLP-1 level and insulin resistance by modulation of gut microbiota and the metabolites, particularly the regulation of intestinal bile acid CDCA content, followed by the inhibition of FXR expression in intestinal L cells as well as increased Gcg mRNA expression and the secretion of GLP-1. These findings clarify the role of the “gut microbiota-CDCA” pathway in the improvement of intestinal GLP-1 levels in HFD-induced mice by DHM administration, providing a new pharmacological target for the prevention of insulin resistance.

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Research progress of dihydromyricetin in the treatment of diabetes mellitus

Cited by 3 publications

References 73 publications

Dihydromyricetin alleviates inflammatory bowel disease associated intestinal fibrosis by inducing autophagy through the PI3K/AKT/mTOR signaling pathway

Dihydromyricetin alleviates inflammatory bowel disease associated intestinal fibrosis by inducing autophagy through the PI3K/AKT/mTOR signaling pathway

Effects of Nanoparticle-Mediated Dihydromyricetin to Diabetic Wounds: An In Vivo Study

Dihydromyricetin promotes GLP-1 secretion to improve insulin resistance via “gut microbiota-CDCA”

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