INDUSTRIAL CROPS AND PRODUCTS
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2019
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IF 4.191
Wenjing Wang,Yuan Wu,Huihui Xu,Yuan Shang,Yichen Chen,Miaoer Yan,Zhaohui Li,David R. Walt
The harvest time of a plant usually affects the yield of its metabolites. Polygonum tinctorium ( Polygonum tinctorium Ait., P. tinctorium ) is an important cultivated plant that produces the natural blue dye indigo and the medicinal metabolite indirubin. To explore the mechanism of indigo and indirubin accumulation, the leaves of P. tinctorium at different harvest times, namely July, August, and October, were investigated by metabolite and de novo transcriptome analyses. The results revealed that the indigo and indirubin content varied at different harvest times. Moreover, their contents were significantly higher (p < 0.05) in August than in either July or October. Transcriptome analysis showed different gene expression patterns of P. tinctorium leaves in August. Almost all the identified differentially expressed genes (DEGs) that were responsible for the biosynthesis of indigo and indirubin, including four anthranilate synthase (AS) genes, two indole-3-glycerolphosphate synthase (IGPS) genes, three tryptophan synthase (TS) genes and seven cytochrome P450 (CYP450) genes were expressed at significantly higher levels in August ( p < 0.05), which correlated with the increase of the two compounds. Overall, the results of this study provide useful information for understanding the accumulation mechanism of indigo and indirubin in P. tinctorium , which may promote the development of agricultural breeding and industrial production of P. tinctorium. Moreover, sequence data obtained by de novo transcriptome sequencing of P. tinctorium provides a platform for future molecular biological studies.
研究领域:
植物学
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分子生物学
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产品关联
DOI
高影响因子
Frontiers in Pharmacology
·
2025
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IF 4.8
Yancen Li,Chengyu Wan,Fan Li,Guang Xin,Tao Wang,Qilong Zhou,Tingyu Wen,Shiyi Li,Xiaoting Chen,Wen Huang
Background: Isatidis Folium, a botanical drug widely used in traditional medicine, is known for its anti-inflammatory properties, including heat-clearing, detoxifying, and blood-cooling effects. Although its potential in sepsis treatment has been suggested, the bioactive metabolites and underlying mechanisms remain poorly understood.Methods: Network pharmacology and molecular docking were employed to identify the therapeutic effects and mechanisms of Indirubin, the major bioactive metabolite of Isatidis Folium, in sepsis treatment. In vivo, a cecal ligation and puncture (CLP)-induced mouse sepsis model was used to evaluate the protective effects of Indirubin through histopathological analysis, ELISA, and biochemical assays. In vitro, RAW264.7 cells were stimulated with LPS and treated with varying concentrations of Indirubin. The anti-inflammatory effects of Indirubin were assessed using ELISA, apoptosis assays, and Western blotting.Results: Network pharmacology analysis identified Indirubin as the major bioactive metabolite of Isatidis Folium and EGFR and SRC as its key molecular targets. Experimental validation demonstrated that Indirubin significantly improved survival rates, alleviated tissue injury, and suppressed inflammatory responses in sepsis models. Mechanistically, Indirubin inhibited LPS-induced activation of the EGFR/SRC/PI3K and NF-κB/MAPK pathways in macrophages, significantly reducing cell death and inflammation in RAW264.7 cells.Conclusion: Indirubin, the primary bioactive metabolite of Isatidis Folium, exerts protective effects against sepsis by targeting the EGFR/SRC/PI3K and NF-κB/MAPK signaling pathways in macrophages. These findings provide a mechanistic basis for the development of Indirubin as a multi-target therapeutic agent for sepsis treatment.
研究领域:
药理学
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免疫学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
BMC Complementary Medicine and Therapies
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2020
·Vol. 20
·期 1
·1-10
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IF 0
Liu Shou Gang,Luo Guang Pu,Qu Yong Bin,Chen Yong Feng
Background Psoriasis is a common inflammatory skin disease. Abnormal proliferation of keratinocytes is one of the psoriatic histopathological features. Indirubin has an essential effect on the proliferation and activation of keratinocytes; however, in psoriasis, the specific mechanism of action of indirubin on keratinocytes is unclear. In the present study, we revealed the effects of indirubin on DNA methyltransferase 1 (DNMT1), wnt inhibitory factor 1 (wif-1), and wnt/β-catenin signal pathway, in the meantime, we explored the effects of indirubin on proliferation, cell cycle and the apoptosis of HaCaT cells.Methods The expression of DNMT1, wif-1, Frizzled2, Frizzled5, and β-catenin in HaCaT cells treated with different concentrations of indirubin were detected by Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR). The expression levels of DNMT1 and wif-1 were observed after treated with different concentrations of indirubin by enzyme-linked immunosorbent assay (ELISA). The wif-1 promoter methylation status was detected by DNA methylation-specific PCR (MSP). The transcriptional activities of wif-1 and β-catenin were discovered by a luciferase reporter gene system. Cell viability was determined by Cell Counting Kit-8 (CCK8) method. The cell cycle was detected by flow cytometry. The apoptotic cells were surveyed by the apoptosis kit. The expression of Inolucrin, Loricrin, Filaggrin, Keratin 17, and transcriptional activation of transglutaminase 1(TGase1) were detected by Western blotting.Results Indirubin inhibited the expression of DNMT1 and the methylation of the wif-1 promoter. In the wnt signal pathway, indirubin restored the protein expression of wif-1 and inhibited expression of Frizzled2, Frizzled5, and β-catenin. Besides, indirubin inhibited the proliferation of HaCaT cells, induced apoptosis, and arrest cell cycle. We also reported that indirubin could down-regulate the expression of Involucrin, TGase 1, and keratin 17, but the expression of Filaggrin and Loricrin had no significant effect.Conclusion Our research showed that indirubin promoted the demethylation of wif-1 and suppressed the wnt/β-catenin signal pathway, thereby exerted an anti-proliferative effect. This study reveals the anti-proliferation mechanism of indirubin, which may provide an effective option for the treatment of proliferative diseases.
研究领域:
皮肤科
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分子生物学
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药理学
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产品关联
DOI
PubMed
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