alkanet Alkanna tinctoria and Lithospermum arvense.
Alkannin (VAN)/5,8-dihydroxy-2-[(1S)-1-hydroxy-4-methylpent-3-en-1-yl]naphthalene-1,4-dione/5,8-Dihydroxy-2-[(1S)-1-hydroxy-4-methylpent-3-en-1-yl]-1,4-naphthoquinone/Anchusa acid (VAN)/Anchusin (VAN)/C.I. Natural Red 20/(S)-5,8-Dihydroxy-2-(1-hydroxy-4-methyl-3-pentenyl)-1,4-naphthalenedione/1,4-Naphthalenedione, 5,8-dihydroxy-2-[(1S)-1-hydroxy-4-methyl-3-penten-1-yl]-/Alkanna red (VAN)/Alkannin/Anchusa acid/Anchusin/(-)-5,8-Dihydroxy-2-(1-hydroxy-4-methyl-3-pentenyl)-1,4-naphthoquinone/Alkanna Red/5,8-Dihydroxy-2-[(1S)-1-hydroxy-4-methyl-3-penten-1-yl]-1,4-naphthoquinone/C.I. Natural Red 20 (VAN)/EINECS 208-245-7/(1-Hydroxy-3-isohexenyl)naphthazarine
Alkannin, found in Alkanna tinctoria, is used as a food coloring. Alkannin shows anticancer activity, arrests cell cycle, and induces apoptosis. Alkannin improves hepatic inflammation in a Rho-kinase pathway.
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Shikonin, alkannin and their derivatives, the main ingredient of Lithospermum erythrorhizon and Arnebia euchroma (Royle) Johnst native to Inner Mongolian and Northwest of China respectively, hold promising potentials for antitumor effects via multiple-target mechanisms. This review will emphasize the importance of their antitumor activity in apoptosis, necroptosis and immunogenic cell death, and expound the relationship of their antitumor activity and naphthoquinone scaffold that could generate ROS and alkylating agent. Meanwhile, the antitumor mechanisms of naturally-occurring shikonin, alkannin and their derivatives, which were divided into the direct interaction involved in alkylating agent, covalently binding the DNA and protein, as well as the indirect interaction mediated by ROS, nonspecifically influencing the mitochondria or multiple signal pathways, will be systematically summarized and discussed.
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Alkannin; DNA; ROS; anti-tumor mechanisms; bioalkylation; shikonin
Advance in Anti-tumor Mechanisms of Shikonin, Alkannin and their Derivatives.
Zhang X1, Cui JH2, Meng QQ2, Li SS2, Zhou W3, Xiao S1.
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. In our study, we aimed to investigate the effects of alkannin on HCC cells growth, migration and invasion.
Huh7 and Hep3B2.1-7 cells were treated with alkannin. Expression of miR-92a in cell was altered by transfection with miR-92a-mimic (miR-92a-M) or miR-92a-inhibitor (miR-92a-I). Cell viability, proliferation, apoptosis, migration and invasion were detected by Cell Counting Kit-8, BrdU assay, flow cytometry, and transwell assay, respectively. The expression of miR-92a was determined by quantitative real-time PCR. The expression of proteins associated with proliferation, apoptosis and metastasis was measured by Western blot.
Alkannin decreased cell viability and proliferation, executed cell apoptosis, and inhibited the migration and invasion of Huh7 and Hep3B2.1-7 cells. Alkannin negatively regulated the expression of miR-92a, and transfection with miR-92a-M impeded alkannin’s anti-tumor functions. PTEN and TP53INP1 were found to be target genes of miR-92a. Alkannin inhibited PTEN-dependent PI3K/AKT pathway. Furthermore, the biological effects of miR-92a-I in alkannin treated cells were eliminated by PTEN silencing.
Alkannin exerted anti-tumor activities by downregulation of miR-92a. This process might be executed by inactivating PTEN/PI3K/AKT signal pathways through the binding effects of miR-92a on PTEN.
Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.
lkannin; Hepatocellular carcinoma; PTEN/PI3K/AKT; miR-92a
Alkannin inhibits proliferation, migration and invasion of hepatocellular carcinoma cells via regulation of miR-92a.
Sun B1, Zhang J2, Liu M3, Guan L4.
Lupus nephritis (LN) is a fatal complication induced by systemic lupus erythematosus (SLE). As the current therapeutic approaches for LN are not a permanent cure, we studied the potential therapeutic effects of alkannin (ALK) on LPS-treated human proximal tubular cells (HK-2 cells), aiming to find novel therapeutic drugs for LN treatment.
Cell viability, apoptotic cells, expression of p53 and proteins associated with apoptosis, and release of IL-6 and TNF-α in LPS-treated HK-2 cells were measured by using CCK-8 assay, flow cytometry assay, Western blot analysis and RT-qPCR/ELISA, respectively. Effects of ALK on LPS-treated HK-2 cells were evaluated, and miR-210 expression was determined by RT-qPCR. Afterwards, whether ALK affected LPS-treated cells via regulating miR-210 was verified, and the involvements of the NF-κB and p38MAPK pathways were finally studied using Western blot analysis.
LPS-induced decrease of cell viability, increase of apoptosis, and release of IL-6 and TNF-α were attenuated by ALK treatment. We found miR-210 level in LPS-treated cells was elevated by ALK, and miR-210 inhibition could effectively reverse the effects of ALK on LPS-treated cells. Moreover, we found the phosphorylation levels of key kinases in the NF-κB and p38MAPK pathways were reduced by ALK via up-regulating miR-210 in LPS-treated cells.
ALK attenuated LPS-induced inflammatory injury in HK-2 cells possibly through up-regulating miR-210. The LPS-induced activation of the NF-κB and p38MAPK pathways was attenuated by ALK via regulation of miR-210.
Copyright © 2018. Published by Elsevier Masson SAS.
Alkannin; Inflammatory injury; Lupus nephritis; NF-κB/p38MAPK; microRNA-210
Alkannin protects human renal proximal tubular epithelial cells from LPS-induced inflammatory injury by regulation of microRNA-210.
Chen Y1, Li H2.