Inhibitors | Comment | Organism | Structure |
---|---|---|---|
D-saccharic acid 1,4-lactone | SAL, a beta-glucuronidase inhibitor | Mus musculus |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
baicalin + H2O | Mus musculus | - |
baicalein + D-glucuronate | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Mus musculus | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
liver | - |
Mus musculus | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
baicalin + H2O | - |
Mus musculus | baicalein + D-glucuronate | - |
? |
Synonyms | Comment | Organism |
---|---|---|
beta-glucuronidase | - |
Mus musculus |
General Information | Comment | Organism |
---|---|---|
physiological function | the protective effect of baicalin (the main active compound in Scutellariae radix (Huangqin)) against aminoacetophen (APAP or paracetamol)-induced hepatotoxicity is not altered through enzyme inhibition by D-saccharic acid 1.4-lactone. SAL, a beta-glucuronidase inhibitor, strongly decreased the intestinal beta-glucuronidase activity in mice, but the baicalin-provided protection against APAP-induced cytotoxicity in L-02 cells is not altered after the application of SAL, thus protection of baicalin against APAP-induced hepatotoxicity does not require the conversion into its aglycone baicalein | Mus musculus |