| Description: |
Licochalcone D has anti-inflammatory, and anti-allergic activities, it shows suppression ability of nitric oxide (NO) production, it also suppresses degranulation by decreasing the intracellular Ca2+ level and tyrosine phosphorylation of ERK in RBL-2H3 cells. Licochalcone D has cardioprotective potential against myocardial ischemia/reperfusion injury in langendorff-perfused rat hearts. It may be a potential drug for human melanoma treatment by inhibiting proliferation, inducing apoptosis via the mitochondrial pathway and blocking cell migration and invasion.
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| Targets: |
ROS | MMP(e.g.TIMP) | Bcl-2/Bax | Caspase | Akt | p65 | NF-kB | p38MAPK | PARP | NOS | NO | MEK | ERK | Calcium Channel | PKA |
| In vitro: |
| Oncol Rep. 2018 May;39(5):2160-2170. | | Licochalcone D induces apoptosis and inhibits migration and invasion in human melanoma A375 cells.[Pubmed: 29565458] | The aim of the present study was to determine the effects of Licochalcone D (LD) on the apoptosis and migration and invasion in human melanoma A375 cells.
METHODS AND RESULTS:
Cell proliferation was determined by sulforhodamine B assay. Apoptosis was assessed by Hoechst 33258 and Annexin V‑FITC/PI staining and JC‑1 assay. Total intracellular reactive oxygen species (ROS) was examined by DCFH‑DA. Wound healing and Transwell assays were used to detect migration and invasion of the cells. The activities of matrix metalloproteinase (MMP‑2 and MMP‑9) were assessed via gelatin zymography. Tumor growth in vivo was evaluated in C57BL/6 mice. RT‑PCR, qPCR, ELISA and western blot analysis were utilized to measure the mRNA and protein levels. Our results showed that LD inhibited the proliferation of A375 and SK‑MEL‑5 cells in a concentration‑dependent manner. After treatment with LD, A375 cells displayed obvious apoptotic characteristics, and the number of apoptotic cells was significantly increased. Pro‑apoptotic protein Bax, caspase‑9 and caspase‑3 were upregulated, while anti‑apoptotic protein Bcl‑2 was downregulated in the LD‑treated cells. Meanwhile, LD induced the loss of mitochondrial membrane potential (ΔΨm) and increased the level of ROS. ROS production was inhibited by the co‑treatment of LD and free radical scavenger N‑acetyl‑cysteine (NAC). Furthermore, LD also blocked A375 cell migration and invasion in vitro which was associated with the downregulation of MMP‑9 and MMP‑2. Finally, intragastric administration of LD suppressed tumor growth in the mouse xenograft model of murine melanoma B16F0 cells.
CONCLUSIONS:
These results suggest that LD may be a potential drug for human melanoma treatment by inhibiting proliferation, inducing apoptosis via the mitochondrial pathway and blocking cell migration and invasion. | | Bioorg Med Chem Lett. 2014 Jan 1;24(1):181-5. | | Synthesis of licochalcone analogues with increased anti-inflammatory activity.[Pubmed: 24316124 ] | Licohalcones have been reported to have various biological activities. However, most of licochalcones also showed cytotoxicity even though their versitile utilities.
METHODS AND RESULTS:
Licochalcone B and Licochalcone D, which have common substituents at aromatic ring B, are targeted to modify the structure at aromatic ring A for inflammatory studies.
CONCLUSIONS:
Licochalcone Derivatives (1-6) thus prepared are compared for their suppression ability of nitric oxide (NO) production and showed 9.94, 4.72, 10.1, 4.85, 2.37 and 4.95μM of IC50 values, respectively. |
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| In vivo: |
| PLoS One. 2015 Jun 9;10(6):e0128375. | | Cardioprotective Effect of Licochalcone D against Myocardial Ischemia/Reperfusion Injury in Langendorff-Perfused Rat Hearts.[Pubmed: 26058040] | Flavonoids are important components of 'functional foods', with beneficial effects on cardiovascular function.
METHODS AND RESULTS:
The present study was designed to investigate whether Licochalcone D (LD) could be a cardioprotective agent in ischemia/reperfusion (I/R) injury and to shed light on its possible mechanism. Compared with the I/R group, LD treatment enhanced myocardial function (increased LVDP, dp/dtmax, dp/dtmin, HR and CR) and suppressed cardiac injury (decreased LDH, CK and myocardial infarct size). Moreover, LD treatment reversed the I/R-induced cleavage of caspase-3 and PARP, resulting in a significant decrease in proinflammatory factors and an increase in antioxidant capacity in I/R myocardial tissue. The mechanisms underlying the antiapoptosis, antiinflammation and antioxidant effects were related to the activation of the AKT pathway and to the blockage of the NF-κB/p65 and p38 MAPK pathways in the I/R-injured heart. Additionally, LD treatment markedly activated endothelial nitric oxide synthase (eNOS) and reduced nitric oxide (NO) production.
CONCLUSIONS:
The findings indicated that LD had real cardioprotective potential and provided support for the use of LD in myocardial I/R injury. |
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