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Hexahydrocurcumin (HHC), a major metabolite of curcumin, has been reported to have protective effects against ischemic and reperfusion damage. The goal of the present research was to examine whether HHC could alleviate brain damage and ameliorate functional outcomes by diminishing the blood-brain barrier (BBB) damage that follows cerebral ischemia/reperfusion.
Middle cerebral artery occlusion was induced for 2 h in rats followed by reperfusion. The rats were divided into three groups: sham-operated, vehicle-treated, and HHC-treated groups. At the onset of reperfusion, the rats were immediately intraperitoneally injected with 40 mg/kg HHC. At 48 h after reperfusion, the rats were evaluated for neurological deficits and TTC staining. At 24 h and 48 h after reperfusion, animals were sacrificed, and their brains were extracted.
Treatment with HHC reduced neurological scores, infarct volume, morphological changes, Evans blue leakage and immunoglobulin G extravasation. Moreover, HHC treatment reduced BBB damage and neutrophil infiltration, downregulated myeloperoxidase, ICAM-1, and VCAM-1, upregulated tight junction proteins (TJPs), and reduced aquaporin 4 expression and brain water content.
These results revealed that HHC treatment preserved the BBB from cerebral ischemia/reperfusion injury by regulating TJPs, attenuating neutrophil infiltration, and reducing brain edema formation.
Blood-brain barrier; Cerebral edema; Cerebral ischemia/reperfusion; Neutrophil infiltration; Tight junction proteins
Hexahydrocurcumin alleviated blood-brain barrier dysfunction in cerebral ischemia/reperfusion rats.
2020 Jan 13
Curcumin, one of the most precious pharmacologically relevant natural products, has gained considerable attention among scientists for decades because of its multi-pharmacological activities in the clinical. However, critical studies on its pharmacological and toxicological activities are needed to understand how this compound can have these biological functions considering its poor oral bioavailability and the low plasma concentration. Moreover, curcumin undergoes extensive and rapid metabolism in vivo, indicating that the pharmacological activity of consuming curcumin might be mediated partly by its metabolites. And as one of the major curcumin metabolites, hexahydrocurcumin (HHC), exhibits similar or more potent bioactivity than curcumin by in vitro and in vivo studies, such as antioxidant, anti-inflammatory, antitumor and cardiovascular protective properties, which may provide important information for us to have a profound comprehension of the effectiveness of curcumin. This review mainly summarizes the current knowledge and underlying molecular mechanisms of the biological activities of HHC and its potential effects on the development of various human diseases.
Anti-inflammatory; Anticancer; Antioxidant; Cardiovascular protective; Curcumin; Hexahydrocurcumin (HHC)
Biological and pharmacological effects of hexahydrocurcumin, a metabolite of curcumin.
2018 May 15
This study was to investigate the anti-angiogenic effect of hexahydrocurcumin (HHC) to evaluate gene (p-basic fibroblast growth factor (bFGF)-SAINT-18 & p-vascular endothelial growth factor (VEGF)-SAINT-18 complex)-induced corneal neovascularization (CorNV) in rats.
CorNV was induced in 24 eyes of 24 rats. Four groups (Group A: 0 μg, B: 0.01 μg, C: 0.1 μg, and D: 1 μg) of HHC were prepared and implanted into the rat subconjunctival substantia propria 1.5 mm from the limbus at temporal side. The 1 μg of p-bFGF-SAINT-18 & p-VEGF-SAINT-18 complex were prepared and implanted into the rat corneal stroma 1.5 mm from the limbus at the same side. Inhibition of CorNV was observed and quantified from day 1 to day 60. bFGF and VEGF protein expression were analyzed by biomicroscopic examination, western blot analysis, and immunohistochemistry.
Subconjunctival injection by 1 μg HHC successfully inhibited gene-induced CorNV in rats. bFGF and VEGF protein expression were reduced after 6 days. Meanwhile, the reduction of HLA-DR expression was detected.
Our study showed that the HHC might provide an important anti-angiogenesis factor to inhibit CorNV development at the corneal experimental angiogenesis model.
Angiogenesis; Corneal neovascularization; Hexahydrocurcumin; VEGF; bFGF
Anti-angiogenic effect of hexahydrocurcumin in rat corneal neovascularization.
Kuo CN1,2,3,4, Chen CH5, Chen SN6,7, Huang JC1,2,3, Lai LJ1,2,3, Lai CH1,2,3, Hung CH2,3,8, Lee CH9, Chen CY10.