Chrysophanol at 25 μmol/L enhanced the viability-reducing effect of etoposide in HepG2 cells but weakened that of cisplatin under the tested conditions. Mitochondrial-potential measurements followed the same directions. These comparisons do not establish a formal synergy coefficient. [1]
Mitochondrial dysfunction and necrotic staining in HepG2 cells
Cell-based study · Human HepG2 liver cancer cells [1]
Chrysophanol reduced mitochondrial membrane potential, ATP and GSH/GSSG, increased mitochondrial superoxide, and produced PI-positive staining. These are cellular associations; no direct protein-binding or purified-enzyme inhibition claim is made.
Literature-Reported Treatment Conditions
- Treatment concentration
- 0, 50, 100 μmol/L
- Exposure duration
- 6, 12, 24 and 48 h for mitochondrial/redox assays; 48 h for Hoechst/PI staining
- Method
- Addition to cell culture
- Vehicle
- Not specified in retrieved methods
- Co-treatment
- None for selected panels
- Reported limits
- Solvent/final vehicle not specified. No quantitative IC50 adopted because Results 3.2 and Fig. 2E appear discordant.
Methods and source locations
Compound reported in the paper: Chrysophanol; Compound label in the paper: Chry
Compound-level research observations; no Adooq lot validation or clinical efficacy inference.
Methods 2.1,2.2,2.5,2.6,2.9; Results 3.2; Fig. 2A–D,F
Mitochondrial potential, ATP, superoxide and redox balance: TMRE, ATP kit, MitoSOX and GSH/GSSG kit — Results 3.2; Fig. 2A–D; Methods 2.5
Cell death phenotype: Hoechst/PI staining; n = 3, means ± SD in caption — Fig. 2F and caption; Methods 2.6
Different combination responses with etoposide and cisplatin
Cell-based study · Human HepG2 liver cancer cells [1]
At fixed chrysophanol concentration, combination with VP-16 lowered viability more than VP-16 alone, whereas combination with Cis-Pt increased viability relative to Cis-Pt alone. Potential changes followed the same direction. A formal interaction index was not reported in the selected experiment.
Literature-Reported Treatment Conditions
- Treatment concentration
- Chry 25 μmol/L; MTT: VP-16 10, 20, 30, 60 μmol/L or Cis-Pt 5, 10, 20, 40 μmol/L; TMRE panel: VP-16 15, 30, 60 μmol/L or Cis-Pt 10, 20, 40 μmol/L
- Exposure duration
- 48 h for MTT; 30 h for TMRE (Fig. 6 caption)
- Method
- Addition to cell culture
- Vehicle
- Not specified in retrieved methods
- Co-treatment
- Separate Chry + VP-16 and Chry + Cis-Pt comparisons with each drug alone
- Reported limits
- No formal synergy/antagonism model, confidence interval or interaction coefficient supplied. TMRE doses read from panel labels differ from MTT dose series.
Methods and source locations
Compound reported in the paper: Chrysophanol; Compound label in the paper: Chry
Compound-level research observations; no Adooq lot validation or clinical efficacy inference.
Methods 2.3,2.9; Results 3.5; Fig. 6A,B
Viability with combinations relative to chemotherapy alone: MTT; n = 3, means ± SD — Fig. 6A; Results 3.5; Methods 2.3
Mitochondrial membrane potential with combinations: TMRE flow cytometry; n = 3, means ± SD — Fig. 6B and caption; Results 3.5
Adipocyte lipid accumulation and AMPK-associated signaling
Cell-based study · Mouse 3T3-L1 adipocytes [2]
CA reduced lipid staining and adipogenic markers while increasing AMPKα phosphorylation. Compound C weakened the suppression of PPARγ and C/EBPα, supporting pathway involvement without proving direct or selective AMPK activation.
Literature-Reported Treatment Conditions
- Treatment concentration
- CA 1, 5, 10 μM; inhibitor comparison CA 10 μM with Compound C 500 nM
- Exposure duration
- 48 h exposure described for gene-expression experiment; treatment staging differs between Results and cell-differentiation Methods
- Method
- Addition to cell culture
- Vehicle
- CA stock dissolved in 100% DMSO; final concentration not specified
- Co-treatment
- Compound C mechanistic comparison; EGCG/GW positive comparators and troglitazone comparator where shown
- Reported limits
- Exact common treatment schedule across Oil Red O, qPCR and immunoblots is not unambiguously established: Methods add CA on differentiation days 2–4; Results describe fully differentiated cells exposed for 48 h. Compound C timing not specified.
Methods and source locations
Compound reported in the paper: Chrysophanic acid; Compound label in the paper: CA
Compound-level research observations; no Adooq lot validation or clinical efficacy inference.
Chemical Reagents; Cell Culture and Adipocyte Differentiation; Oil Red O; Western Blot; Results adipocyte/AMPK subsections; Fig. 4,5,7A,B
Lipid accumulation: Oil Red O, absorbance at 500 nm; three independent experiments, means ± SD; *p < 0.05 versus MDI-induced cells — Fig. 4A,B and caption; Results CA Inhibits Lipid Accumulation
AMPKα phosphorylation and PPARγ/C/EBPα response: Western blot; induced/uninduced and inhibitor-alone comparisons; GAPDH control; three independent experiments, means ± SD — Fig. 7A,B and caption; Results CA Suppresses Adipogenesis and Induces Thermogenesis via Activation of AMPK Pathway
