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Specification
Zhang S, et al. The Journal of Nutritional Biochemistry, 2025, 146, 110034.
Tetrahydrocurcumin was experimentally evaluated for its capacity to modulate metabolic dysfunction associated with obesity through integrated in vitro and in vivo models. Hepatic lipid accumulation was first assessed in Hepa1-6 hepatocytes, where tetrahydrocurcumin treatment significantly suppressed intracellular lipid deposition under lipogenic conditions. In vivo validation employed glucose-induced obese Caenorhabditis elegans and high-fat diet (HFD) C57BL/6J mice. Lipid accumulation and oxidative stress markers were quantified alongside hepatic injury indicators (AST/ALT). Molecular mechanisms were investigated using Western blotting and RT-qPCR, which demonstrated downregulation of key lipogenic enzymes SCD1 and DGAT1. Furthermore, fecal 16S rRNA sequencing was performed to characterize gut microbiota alterations, revealing a reduced Firmicutes/Bacteroidetes ratio and decreased Desulfobacterota. Short-chain fatty acid production was also quantified. These experimental findings demonstrate that tetrahydrocurcumin mitigates obesity-associated metabolic disturbances through coordinated regulation of lipid metabolism, oxidative stress, and intestinal microbial homeostasis.
Wu J, et al. Biomedicine & Pharmacotherapy, 2024, 178, 117297.
The therapeutic potential of tetrahydrocurcumin in nonalcoholic steatohepatitis (NASH) was investigated using complementary in vivo and cellular steatosis models. A high-fat diet-induced NASH rat model was established to evaluate hepatic steatosis, inflammation, and oxidative stress following tetrahydrocurcumin administration. Parallel in vitro experiments were conducted using palmitic acid-induced steatotic L02 and HepG2 hepatocytes, where intracellular lipid accumulation was quantified after treatment. Lipophagy activation was examined by Western blot and immunofluorescence, revealing increased LC3B-II and reduced P62, indicating enhanced autophagic flux. The mechanistic pathway was analyzed via qRT-PCR, protein expression analysis, and molecular docking, demonstrating that tetrahydrocurcumin inhibited mTORC1 and promoted TFEB nuclear translocation, thereby stimulating lysosomal biogenesis. Pharmacological validation using chloroquine and the mTORC1 activator MHY1485 confirmed pathway involvement. These results establish tetrahydrocurcumin as an effective experimental modulator of hepatocyte lipophagy and lipid metabolism in NASH.
The molecular formula of Tetrahydrocurcumin is C21H24O6.
The molecular weight of Tetrahydrocurcumin is 372.4 g/mol.
Some synonyms for Tetrahydrocurcumin are 1,7-bis(4-hydroxy-3-methoxyphenyl)heptane-3,5-dione, Sabiwhite, and Tetrahydro Curcumin.
The IUPAC name of Tetrahydrocurcumin is 1,7-bis(4-hydroxy-3-methoxyphenyl)heptane-3,5-dione.
Tetrahydrocurcumin is found in Curcuma longa.
The InChIKey for Tetrahydrocurcumin is LBTVHXHERHESKG-UHFFFAOYSA-N.
Tetrahydrocurcumin has 2 hydrogen bond donor counts.
The exact mass of Tetrahydrocurcumin is 372.15728848 g/mol.
Tetrahydrocurcumin has 10 rotatable bond counts.
The topological polar surface area of Tetrahydrocurcumin is 93.1 Å^2.
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