Dihydromyricetin promotes GLP-1 release and glucose uptake by STC-1 cells and enhances the effects of metformin upon STC-1 cells and diabetic mouse model

Yao, Yuanzhi; Li, Xiaoying; Yang, Xi-shan; Mou, Hai; Wei, Lin

doi:10.1016/j.tice.2023.102108

Cited by 1 publication

(1 citation statement)

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“…Such active ingredients have fewer toxic effects and side effects than others, and according to the World Health Organisation, 80% of people rely on herbal medicines because of their significant use in our lives [ 19 ]. Interestingly, DHM showed a wide range of biological activities including antioxidant [ 20 ], anticancer [ 21 ], antitumour [ 22 ], antidiabetic [ 23 ] and neuroprotection [ 24 ], etc. Importantly, a study found that DHM has a significant therapeutic effect on liver injury and liver cancer, and that DHM promotes cell proliferation, inhibits apoptosis, and regulates intracellular redox balance [ 25 ].…”

Section: Introductionmentioning

confidence: 99%

Study on Dihydromyricetin Improving Aflatoxin Induced Liver Injury Based on Network Pharmacology and Molecular Docking

Zhu,

Liu,

Pei

et al. 2023

Toxics

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Aflatoxin B1 (AFB1) is a toxic food/feed contaminant and the liver is its main target organ, thus it poses a great danger to organisms. Dihydromyricetin (DHM), a natural flavonoid compound, can be used as a food additive with high safety and has been shown to have strong hepatoprotective effects. In this experiment, PPI network and KEGG pathway analysis were constructed by network pharmacological analysis technique using software and platforms such as Swiss, String, and David and Cytoscape. We screened AFB1 and DHM cross-targets and pathways of action, followed by molecular docking based on the strength of binding affinity of genes to DHM. In addition, we exposed AFB1 (200 μg/kg) to mice to establish a liver injury model. Histological observation, biochemical assay, oxidative stress indicator assay, TUNEL staining and Western blot were used to evaluate the liver injury. Network pharmacological results were screened to obtain 25 cross-targets of action and 20 pathways of action. It was found that DHM may exert anti-hepatic injury effects by inhibiting the overexpression of Caspase-3 protein and increasing the expression of Bcl-2 protein. DHM (200 mg/kg) was found to reduce AFB1-induced liver indices such as alanine aminotransferase (ALT) and aspartate acyltransferase (AST), and attenuate hepatic histopathological damage through animal models. Importantly, DHM inhibited malondialdehyde (MDA) formation in liver tissue and attenuated AFB1-induced oxidative stress injury by increasing glutathione-S-transferase (GST) glutathione (GPX) catalase (CAT) and superoxide dismutase (SOD). Meanwhile, DHM also restored the expression of anti-apoptotic protein Bcl-2 and antioxidant proteins, Nrf2, Keap1 and its downstream HO-1, and down-regulated the expression of pro-apoptotic proteins Bax and Caspase-3 in AFB1-induced liver tissues. The results confirmed that liver injury caused by AFB1 exposure could be alleviated by DHM, providing valuable guidance for in-depth study of DHM in the treatment of liver-related diseases, and laying the foundation for in-depth development and utilization of DHM.

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