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| Author | Possible hepatic toxicity components | Conclusion |
|
| Furukawa et al. [16] | Anthraquinones and contaminants (mycotoxins, heavy metals, and pesticides) | The incorrect use of HSW might be the leading cause |
| Yu et al. [49] | Anthraquinones | The toxicity of water extractions of RHSW and PHSW < any other solvent (50% ethanol and 95% ethanol) |
| Wu et al. [41] | The content of tetrahydroxystilbene glucosides | The toxicity of water decocta > acetone extract. Meanwhile, the toxicity of acetone extract of RHSW > acetone extract of PHSW. |
| Lin et al. [47] | Anthraquinone, emodin-O-(malonyl)-hex, emodin-O-glc, emodin, emodin-8-O-glc, emodin-O-(acetyl)-hex, and emodin-O-hex-sulfate | RHSW ethanol extract > RHSW water extract > PHSW ethanol extract > PHSW water extract |
| Lv et al. [50] | Modin, physcion, EG, and physcion-8-O-β-D-glucoside (PG) | Ethanol extract has much stronger hepatotoxicity, the contents of emodin-8-O-β-d-glucopyranoside, physcion-8-O-β-d-glucopyranoside, emodin and physcion are significantly higher in ethanol extract than in water extract |
| Ma et al. [51] | Anthraquinones | Administration of high-dose HSW extract (20 g/kg) for 3 weeks can cause hepatic lesions, while the low-dose treatment (1 g/kg) is safe |
| Zhang et al. [52] | Vitamin A | The toxicity of alcohol extraction > water extraction. |
| Yang et al. [53] | Rhein, emodin, physcion-8-O-β-D-glucopyranoside, and physcion-8-O-(6′-O-acetyl)-β-D-glucopyranoside | Which anthraquinones are the prime constituents of the hepatotoxicity of HSW are still not be proved |
| Ma et al. [32] | Aloe emodin, emodin, rhein, and gallic acid | The anthraquinones of HSW have potential hepatotoxicity, and the liver injury caused by HSW is related to mitochondrial abnormalities. |
| Li et al. [54] | Emodin | HSW ethyl acetate extracts have close association with the idiosyncratic hepatotoxicity of HSW |
| Jiang et al. [55] | Anthraquinones | Conjugation with glutathione is a major detoxification route |
| Hong et al. [56] | Rhein | Caspase 3 (CASP3), peroxisome proliferator-activated receptor gamma (PPARG), and myeloid cell leukemia-1 (MCL1) are main potential targets for HSW-induced liver injury |
| Li et al. [34] | 2,3,5,4′-tetrahydroxy cis -stilbene-2-O-β-glucoside (cis-THSG) | cis-THSG is closely associated with the idiosyncratic hepatotoxicity of HSW |
| Lin et al. [48] | tetrahydroxystilbene-O-(galloyl)-hex and emodin-O-hex-sulfate | The toxicity of the total fraction > the 30% ethanol fraction > the 70% ethanol fraction > the dichloromethane fraction and the water fraction |
| Wang et al. [30] | Some quinones and stilbenes, especially emodin and rhein | HILI may result from a combination of active compounds rather than a single chemical entity |
| Meng et al. [57] | cis-THSG combined with LPS | cis-THSG is the major factor responsible for HSW-induced liver injury, but it is not the only component |
| Quan, et al. [58] | Emodin, rhein, aloe emodin, emodin-1-O-glucoside, physcion-8-O-glucoside, and aloe emodin-8-O-glucoside | The hepatotoxicity of HSW may be mediated by anthraquinone compounds, and its material basis is related to the 6 anthraquinone compounds mentioned above, which are mainly on the combined anthraquinones |
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