| Description: |
Luteolin-7-O-glucoside has cardioprotective, anti-asthmatic, anticancer, anti-inflammatory, and antioxidative activities, it can suppress leukotriene C(4) production and degranulation by inhibiting the phosphorylation of mitogen activated protein kinases and phospholipase Cγ1 in activated mouse bone marrow-derived mast cells.Luteolin-7-O-glucoside modulated the Nrf2/MAPK/ PTEN/Akt /ERK/AP-1/PI3K-Akt signaling pathways, it suppressed the expression of β-catenin. |
| In vitro: |
| Nutr Cancer. 2011;63(1):130-8. | | Cancer chemopreventive potential of luteolin-7-O-glucoside isolated from Ophiorrhiza mungos Linn.[Pubmed: 21161823 ] | The anticarcinogenic potential of the phytocompound Luteolin-7-O-glucoside (LUT7G), isolated from the leaves of Ophiorrhiza mungos Linn, was studied against 4 different cancer cell lines (COLO 320 DM, AGS, MCF-7, and A549) and normal VERO cell line.
METHODS AND RESULTS:
The ability of LUT7G to induce apoptosis was determined by its antiradical activity, DNA fragmentation, expression of β-catenin, and chemopreventive efficacy in vivo by administering rats with DMH (20 mg/kg b.w., s.c.) for 4 consecutive wk and supplementing with 3 different doses throughout the experimental period of 16 wk. LUT7G scavenged 80% of DPPH radicals generated in vitro at 1000 μM and suppressed the expression of β-catenin to 40% at 120 μM concentrations. LUT7G induced apoptosis by scavenging ROS and suppressing the expression of β-catenin in COLO 320 DM cells and effectively inhibited ACF development in DMH-induced experimental carcinogenesis.
CONCLUSIONS:
Hence LUT7G can be a potent anticancer drug for colon carcinogenesis. | | Cardiovasc Toxicol. 2016 Apr;16(2):101-10. | | Protection of Luteolin-7-O-Glucoside Against Doxorubicin-Induced Injury Through PTEN/Akt and ERK Pathway in H9c2 Cells.[Pubmed: 25724325] | Luteolin-7-O-glucoside (LUTG) was isolated from the plants of Dracocephalum tanguticum Maxim.
Previous research has showed that LUTG pretreatment had a significant protective effect against doxorubicin (DOX)-induced cardiotoxicity by reducing intracellular calcium overload and leakage of creatine kinase and lactate dehydrogenase. But the underlying mechanisms have not been completely elucidated.
METHODS AND RESULTS:
In the present study, we investigated the effects of LUTG on H9c2 cell morphology, viability, apoptosis, reactive oxygen species generation, and the mitochondrial transmembrane potentials. The expression of p-PTEN, p-Akt, p-ERK, p-mTOR, and p-GSK-3β were detected by Western blotting. Compared with DOX alone treatment group, the morphological injury and apoptosis of the cells in groups treated by DOX plus LUTG were alleviated, cell viability was increased, ROS generation was lowered remarkably, and mitochondrial depolarization was mitigated. In DOX group, the expression of p-PTEN was lower than normal group and the expression of p-Akt and p-ERK was higher than normal group. In the groups treated with LUTG (20 μM), the expression of p-PTEN was upregulated and the expression of p-Akt, p-ERK, p-mTOR, and p-GSK-3β was downregulated.
CONCLUSIONS:
These results indicated that the protective effects of LUTG against DOX-induced cardiotoxicity may be related to anti-apoptosis through PTEN/Akt and ERK pathway. |
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