Similar hepatotoxicity response induced by Rhizoma Paridis in zebrafish larvae, cell and rat

Zhao, Chongjun; Wang, Mingshuang; Jing, Zhe; Li, Erwen; Zhao, Xia; Li, Farong; Lin, Rui‐Chao

doi:10.1016/j.jep.2019.112440

Cited by 16 publications

(6 citation statements)

References 35 publications

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“…Previous studies have shown that the aqueous extracts of Rhizoma Paridis exhibited hepatotoxicity to zebrafish and SD rats and cytotoxicity to L02 cells ( Zhao et al, 2020 ). However, there have been no studies on the differences in toxicity of extracts from different solvents on Rhizoma Paridis .…”

Section: Resultsmentioning

confidence: 99%

Lipidomics Indicates the Hepatotoxicity Effects of EtOAc Extract of Rhizoma Paridis

Wang

et al. 2022

Front. Pharmacol.

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Rhizoma Paridis is a traditional Chinese medicine commonly used in the clinical treatment of gynecological diseases. Previous studies have shown that aqueous extracts of Rhizoma Paridis exhibit some hepatotoxicity to hepatocytes. Here, using lipidomics analysis, we investigated the potential hepatotoxicity of Rhizoma Paridis and its possible mechanism. The hepatic damaging of different solvent extracts of Rhizoma Paridis on zebrafish larvae were determined by a combination of mortality dose, biochemical, morphological, and functional tests. We found that ethyl acetate extracts (AcOEtE) were the most toxic fraction. Notably, lipidomic responsible for the pharmacological effects of AcOEtE were investigated by Q-Exactive HF-X mass spectrometer (Thermo Scientific high-resolution) coupled in tandem with a UHPLC system. Approximately 1958 unique spectral features were detected, of which 325 were identified as unique lipid species. Among these lipid species, phosphatidylethanolamine cardiolipin Ceramide (Cer), lysophosphatidylinositol sphingosine (Sph), etc., were significantly upregulated in the treated group. Pathway analysis indicates that Rhizoma Paridis may cause liver damage via interfering with the glycerophospholipid metabolism. Collectively, this study has revealed previously uncharacterized lipid metabolic disorder involving lipid synthesis, metabolism, and transport that functionally determines hepatic fibrosis procession.

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Section: Resultsmentioning

confidence: 99%

Lipidomics Indicates the Hepatotoxicity Effects of EtOAc Extract of Rhizoma Paridis

Wang

et al. 2022

Front. Pharmacol.

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“…In the early development stage of larvae, the nutrients in yolk sac play an important role in growing and are mainly metabolized in the liver, so yolk‐sac retention can reflect the liver function of zebrafish larvae (Huang et al, 2018; Zhong et al, 2019). AO staining is an effective method to investigate the cell apoptosis of zebrafish larvae (Zhao et al, 2020). For biochemicals, ALT is the most sensitive index for liver function damage recommended by the World Health Organization.…”

Section: Discussionmentioning

confidence: 99%

Simultaneously screening multiple UGT1A1 inhibitors from Polygonum multiflorum root using ultrafiltration LC–MS

Jiang

Cai

Zheng

et al. 2022

Biomedical Chromatography

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Liver injury induced by Polygonum multiflorum root (PMR) is an immediate issue requiring global attention. UDP-glucuronosyltransferase 1A1 (UGT1A1) inhibitors are suspected to additively contribute to the hepatotoxicity of PMR. This study was deliberately designed to simultaneously screen UGT1A1 inhibitors from PMR, and their co-contribution to hepatotoxicity was determined. Using ultrafiltration coupled to LC-MS method, four compounds, namely cis-2,3,5,4 0 -tetrahydroxystilbene-2-Oβ-glucoside, trans-2,3,5,4 0 -tetrahydroxystilbene-2-O-β-D-glucoside, emodin-8-O-β-Dglucoside, and emodin, were screened, exhibiting the in vitro inhibitory activities against UGT1A1 with IC 50 values of 76.23, 18.70, 62.18, and 34.02 μM, respectively.The varying activities of the screened UGT1A1 inhibitors were demonstrated by performing a molecular docking simulation. Finally, zebrafish larvae and mice assays demonstrated that the UGT1A1 inhibitors co-contributed to the hepatotoxicity of PMR. These findings are conducive to understand the role of UGT1A1 inhibitors in PMR-induced hepatotoxicity.

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“…Quantitative proteomic analysis was performed according to the methodology published in our previous study [ 17 ]. Briefly, proteins of L-02 cells from different groups were extracted by triethyl ammonium bicarbonate (TEAB)/acetone, reduced and alkylated with DL-dithiothreitol and iodoacetamide, and digested with trypsin in TEAB.…”

Section: Methodsmentioning

confidence: 99%

The interaction between polyphyllin I and SQLE protein induces hepatotoxicity through SREBP-2/HMGCR/SQLE/LSS pathway

Fan²,

Chen³

et al. 2023

Journal of Pharmaceutical Analysis

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Similar hepatotoxicity response induced by Rhizoma Paridis in zebrafish larvae, cell and rat

Cited by 16 publications

References 35 publications

Lipidomics Indicates the Hepatotoxicity Effects of EtOAc Extract of Rhizoma Paridis

Lipidomics Indicates the Hepatotoxicity Effects of EtOAc Extract of Rhizoma Paridis

Simultaneously screening multiple UGT1A1 inhibitors from Polygonum multiflorum root using ultrafiltration LC–MS

The interaction between polyphyllin I and SQLE protein induces hepatotoxicity through SREBP-2/HMGCR/SQLE/LSS pathway

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