Retraction on “Dihydromyricetin attenuates inflammation through TLR4/NF-kappa B pathway”

Jing, Nianshui; Li, Xinnan

doi:10.1515/med-2021-0331

Cited by 1 publication

(1 citation statement)

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“…Several preclinical studies have revealed that DHM can inhibit the growth of a variety of cancer cells by modulating various cellular signalling pathways; for example, DHM can protect the cardiovascular system through the PI3K/Akt, Nrf2/HO-1 and SIRT3 signalling pathways ( 18-20 ) and can prevent or inhibit the growth of a variety of cancer cells through the ERK/Akt, AMPK/MAPK/XAF1, Akt-mTOR, ROS/NF-κB and mitochondrial apoptosis signalling pathways to prevent or inhibit hepatocellular carcinoma, lung cancer, colorectal cancer, breast cancer, leukaemia and melanoma ( 21-23 ). DHM can also prevent or inhibit neurodegenerative diseases through the TRL4/NF-κB and p53/p21 signalling pathways ( 24 , 25 ). In addition, DHM has anti-inflammatory, antibacterial, antiviral and skin-protective effects, thus it has great potential for the treatment of tumours ( 10 ).…”

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confidence: 99%

Multiple molecular and cellular mechanisms of the antitumour effect of dihydromyricetin (Review)

Xia,

Zhu

2024

Biomed Rep

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Dihydromyricetin (DHM) is a natural flavonoid compound with multiple antitumour effects, including inhibition of proliferation, promotion of apoptosis, inhibition of invasion and migration, clearance of reactive oxygen species (ROS) and induction of autophagy. For example, DHM can effectively block the progression of the tumour cell cycle and inhibit cell proliferation. In different types of cancer cells, DHM can regulate the PI3K/Akt pathway, mTOR, and NF-κB pathway components, such as p53, and endoplasmic reticulum stress can alter the accumulation of ROS or induce autophagy to promote the apoptosis of tumour cells. In addition, when DHM is used in combination with various known chemotherapy drugs, such as paclitaxel, nedaplatin, doxorubicin, oxaliplatin and vinblastine, it can increase the sensitivity of tumour cells to DHM and increase the therapeutic effect of chemotherapy drugs. In the present review, the multiple molecular and cellular mechanisms underlying the antitumour effect of DHM, as well as its ability to increase the effects of various traditional antitumour drugs were summarized. Through the present review, it is expected by the authors to draw attention to the potential of DHM as an antitumour drug and provide valuable references for the clinical translation of DHM research and the development of related treatment strategies.

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