Angelicin promoted osteogenic differentiation in primary rat calvarial osteoblasts. Mineralization after 12 days increased at 1 and 10 µM, while 0.1 µM did not differ from control. ALP activity increased after 7 days. [1]
In a 48-hour CCK8 assay, the reported angelicin IC50 values were 90±6.565 µM in HepG2 hepatoblastoma cells and 60±4.256 µM in Huh-7 hepatocellular carcinoma cells. These are cell-viability measurements rather than biochemical target-inhibition constants. [2]
Osteogenic differentiation in primary rat calvarial osteoblasts
Cell-based study · Primary calvarial osteoblasts from 1-day-old female Wistar rats, cultured in osteoblast differentiation medium [1]
Angelicin increased ALP activity and mineralization relative to the 0 µM control. Mineralization increased at 1 and 10 µM, whereas 0.1 µM did not differ from control. These are cell-culture differentiation endpoints.
Literature-Reported Treatment Conditions
- Treatment concentration
- 0, 0.1, 1, 10 µM
- Exposure duration
- ALP activity: 7 days; ALP staining: 9 days; mineralization: 12 days
- Method
- ALP activity normalized to total protein; ALP staining and Alizarin red S with cetylpyridinium chloride quantification
- Reported limits
- Supplier, purity and solvent/vehicle not specified in the inspected original; 0 µM control is identified but vehicle matching cannot be independently assessed.
Methods and source locations
Compound reported in the paper: Angelicin
Findings apply to the reported angelicin research material and model; no Adooq lot equivalence or clinical efficacy is established.
Figure 3A–C; Results: Angelicin promotes the osteogenic differentiation of osteoblasts; Methods: ALP activity and ALP/Alizarin red S staining
ALP activity at day 7: p-Nitrophenyl phosphate substrate; absorbance 405 nm normalized to total protein — Figure 3B and caption; ALP activity methods
Mineralized nodule formation at day 12: Alizarin red S staining and 10% cetylpyridinium chloride quantification at 560 nm — Figure 3C and caption; Results osteogenic differentiation paragraph; ALP/Alizarin red S methods
Dkk-1 attenuation of angelicin-associated osteogenesis
Cell-based study · Primary rat calvarial osteoblasts; four conditions: control, Dkk-1 alone, angelicin alone, and angelicin plus Dkk-1 [1]
Dkk-1 attenuated the angelicin-associated increases in β-catenin protein, mineralization and ALP activity. This supports involvement of Wnt/β-catenin signaling in this model; it does not identify a direct molecular binding target.
Literature-Reported Treatment Conditions
- Treatment concentration
- Angelicin 10 µM; Dkk-1 0.1 µg/ml
- Method
- Dkk-1 co-treatment with western blot densitometry (β-catenin/GAPDH), mineralization and ALP readouts
- Co-treatment
- Angelicin plus Dkk-1; single-agent and untreated controls included
- Reported limits
- The Figure 5 caption does not specify endpoint-specific co-treatment durations. Do not substitute the 24-hour immunofluorescence protocol of Figure 6. Supplier, purity and vehicle are not specified in the inspected original.
Methods and source locations
Compound reported in the paper: Angelicin
Findings apply to the reported angelicin research material and model; no Adooq lot equivalence or clinical efficacy is established.
Figure 5A–C and caption; Results: Effect of angelicin on the Wnt signaling pathway in osteoblasts; shared ALP/mineralization and western blot methods
β-Catenin protein, mineralization and ALP in the Dkk-1 co-treatment comparison: Western blot normalized to GAPDH, Alizarin red S mineralization and ALP activity — Figure 5A–C and caption; Results Wnt signaling subsection
48-hour viability in HepG2 and Huh-7 cells
Cell-based study · HepG2 hepatoblastoma and Huh-7 hepatocellular carcinoma cells [2]
Angelicin reduced CCK8 viability in both cell lines. The authors reported 48-hour IC50 values of 90±6.565 µM for HepG2 and 60±4.256 µM for Huh-7. These viability endpoints do not establish target potency or selective killing of cancer over normal cells.
Literature-Reported Treatment Conditions
- Treatment concentration
- 0, 2.5, 5, 10, 20, 40, 60, 80, 100, 120, 160, 200 µM
- Exposure duration
- 48 h
- Method
- CCK8 viability, absorbance 450 nm; control viability set to 100%
- Vehicle
- 0.5% DMSO control
- Reported limits
- IC50 fitting procedure and an explicit definition of the ± term for fitted IC50 estimates are not specified. Vehicle concentration across individual angelicin doses is not separately stated.
Methods and source locations
Compound reported in the paper: Angelicin
Findings apply to the reported angelicin research material and model; no Adooq lot equivalence or clinical efficacy is established.
Figure 1B and caption; Results: Angelicin inhibits hepatic cancer cell growth in vitro; Methods: Reagents, Cell lines and cell culture, Cellular viability assay
HepG2 cell viability at 48 h: CCK8 viability assay; ± reproduced as reported, not relabeled as fitted SD/SEM — Results first subsection, first paragraph; Figure 1B; Cellular viability assay
Huh-7 cell viability at 48 h: CCK8 viability assay; ± reproduced as reported, not relabeled as fitted SD/SEM — Results first subsection, first paragraph; Figure 1B; Cellular viability assay
