| Identification | Back Directory | [Name]
b-D-Glucopyranosiduronic acid,(3b)-17-carboxy-28-norolean-12-en-3-yl | [CAS]
26020-14-4 | [Synonyms]
C08964
Silphioside F
Calenduloside E
Calunduloside E
CALENDULOSIDE E (CE)
Oleanolic acid 3-glucuronide
Oleanoic acid 3-o-glucuronide
Oleanolic acid 3-O-glucuronide
Oleanolic acid 3-β-D-glucuronoside
17β-Carboxy-28-norolean-12-en-3β-yl β-D-glucopyranosiduronic acid
β-D-Glucopyranosiduronic acid, (3β)-17-carboxy-28-norolean-12-en-3-yl
b-D-Glucopyranosiduronic acid,(3b)-17-carboxy-28-norolean-12-en-3-yl | [Molecular Formula]
C36H56O9 | [MDL Number]
MFCD11113461 | [MOL File]
26020-14-4.mol | [Molecular Weight]
632.82 |
| Chemical Properties | Back Directory | [Melting point ]
243-245 °C (decomp) | [Boiling point ]
750.8±60.0 °C(Predicted) | [density ]
1.27±0.1 g/cm3(Predicted) | [form ]
Solid | [pka]
2.82±0.70(Predicted) | [color ]
White to off-white |
| Hazard Information | Back Directory | [Description]
Calenduloside E (CE), a natural pentacyclic triterpenoid saponin, is a significant component of saponin isolated from the bark and root of Aralia elata (Miq.) ?AS are usually used as an antihypertensive, anti-arrhythmic and anti-diabetic agent in traditional Chinese medicine (Wang et al. 2014). In human umbilical vein endothelial cells (HUVECs), CE and CE analog can repress ox-LDL induced apoptosis (Tian et al. 2019). | [Uses]
Oleanolic Acid 3-O-Glucuronide exhibits hypoglycemic activities by suppressing the transfer of glucose from the stomach to the small intestine and by inhibiting glucose transport at the brush border of the small intestine in oral glucose-loaded rats. | [Definition]
ChEBI: Oleanolic acid 3-O-beta-D-glucosiduronic acid is a beta-D-glucosiduronic acid. It is functionally related to an oleanolic acid. | [in vivo]
Calenduloside E (11 mg/kg; i.g.; once daily for 16 weeks) reduces atherosclerotic plaque size, enhanced plaque stability, and reduced inflammatory responses in ApoE-/- mice[2].
Calenduloside E (15 and 30 mg/kg; i.g.; once daily for 7 days) inhibits hepatocyte apoptosis and reduced oxidative stress and immune inflammation in mice with acute liver injury induced by LPS (HY-D1056) and D-GalN[3].
Calenduloside E (7.5-30 mg/kg; i.g.; once daily for 3 days) restores sarcomere contraction and calcium transients in adult rat ventricular myocytes (ARVMs)[4].
Calenduloside E (5 and 10 mg/kg; i.g.; once daily for 4 weeks) improves liver injury, lipid accumulation, and profibrotic phenotypes in nonalcoholic fatty liver disease model mice and inhibits inflammasome activation and pyroptosis in the liver of mice[5]. | Animal Model: | HFD-fed ApoE-/- mice[2] | | Dosage: | 11 mg/kg | | Administration: | i.g.；Once a day for 16 weeks | | Result: | Reduced the levels of IL-1β, IL-6, TNF-α, and monocyte chemoattractant protein-1 (MCP-1) in the serum of ApoE-/- mice. |
| Animal Model: | LPS (HY-D1056)/dGalN-induced acute liver injury in mice[3] | | Dosage: | 15 and 30 mg/kg | | Administration: | i.g.; 1 time per day for 7 consecutive days | | Result: | Improved hepatocyte infiltration and reduced hepatocyte necrosis and shrinkage.
Reduced hepatocyte ROS levels and serum MDA levels, and increased GSH-Px and SOD levels.
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| Animal Model: | Rat Model of MI/R Injury[4] | | Dosage: | 7.5, 15 and 30 mg/kg | | Administration: | i.g.; 1 time per day for 3 consecutive days | | Result: | Myocardial infarction area/risk area decreased to 53%, 38% and 43% respectively.
Restored the expression of calcium-regulating proteins, including calcium transporters (SERCA, a1C, RyR2, and NCX) to normal levels.
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| Animal Model: | Establishment of NAFLD model in apoE-/- mice by western diet[5] | | Dosage: | 5 and 10 mg/kg | | Administration: | i.g.; 1 time per day for 4 weeks | | Result: | Reduced the expression of TNF-α, MCP-1, CCL2, Ly6c and cd68 in the liver.
Reversed the upregulation of lipogenic genes FASN, Srebpf, ACC and PPARγ and lipid uptake gene cd36.
Reduced the expression of NLRP3, pNLRC4, NLRC4, cleaved GSDMD, cleaved Caspase1 and IL-1β.
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| [References]
[1] JIANXIONG LI. Calenduloside E alleviates cerebral ischemia/reperfusion injury by preserving mitochondrial function[J]. Journal of Molecular Histology, 2022, 53 4: 713-727. DOI:10.1007/s10735-022-10087-5.
[2] YIFEI LE . Calenduloside E ameliorates non-alcoholic fatty liver disease via modulating a pyroptosis-dependent pathway.[J]. Journal of ethnopharmacology, 2023, 319: Article 117239. DOI:10.1016/j.jep.2023.117239.
[3] LANFANG LI . Calenduloside e modulates macrophage polarization via KLF2-regulated glycolysis, contributing to attenuates atherosclerosis[J]. International immunopharmacology, 2023, 117: Article 109730. DOI:10.1016/j.intimp.2023.109730.
[4] RUIYING WANG . Calenduloside E suppresses calcium overload by promoting the interaction between L-type calcium channels and Bcl2-associated athanogene 3 to alleviate myocardial ischemia/reperfusion injury[J]. Journal of Advanced Research, 2021, 34: Pages 173-186. DOI:10.1016/j.jare.2020.10.005.
[5] MIN WANG. Calenduloside E Ameliorates Myocardial Ischemia-Reperfusion Injury through Regulation of AMPK and Mitochondrial OPA1.[J]. Oxidative Medicine and Cellular Longevity, 2020: 2415269. DOI:10.1155/2020/2415269. |
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