Indigo Naturalis Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice by Modulating the Intestinal Microbiota Community

Liang, Yanni; Yu, Jin-Gao; Zhang, Dongbo; Zhang, Zhen; Ren, Langlang; Li, Luhan; Zheng, Wei; Tang, Zhishu

doi:10.3390/molecules24224086

Cited by 54 publications

(35 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a 3% DSS Kunming mouse model, IN significantly downregulated the expression of the pro-inflammatory cytokines IL-6, IL-8, and TNF-α, and upregulated the expression of the anti-inflammatory factor IL10. Combination 16 s rDNA sequence analysis showed that IN decreases the relative number of Turicibacter bacilli and increases the relative number of Peptococcus 64 . In RAW264.7 cells induced by LPS, IN inhibits the degradation of IκB-α, the production of TNF-α and IL-6, and the expression of COX-2 and iNOS 65 .…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of indigo naturalis on treating ulcerative colitis explored by GEO gene chips combined with network pharmacology and molecular docking

Xue

Gao

et al. 2020

Sci Rep

View full text Add to dashboard Cite

Oral administration of indigo naturalis (IN) can induce remission in ulcerative colitis (UC); however, the underlying mechanism remains unknown. The main active components and targets of IN were obtained by searching three traditional Chinese medicine network databases such as TCMSP and five Targets fishing databases such as PharmMapper. UC disease targets were obtained from three disease databases such as DrugBank,combined with four GEO gene chips. IN-UC targets were identified by matching the two. A protein–protein interaction network was constructed, and the core targets were screened according to the topological structure. GO and KEGG enrichment analysis and bioGPS localization were performed,and an Herbs-Components-Targets network, a Compound Targets-Organs location network, and a Core Targets-Signal Pathways network were established. Molecular docking technology was used to verify the main compounds-targets. Ten core active components and 184 compound targets of IN-UC, of which 43 were core targets, were enriched and analyzed by bioGPS, GO, and KEGG. The therapeutic effect of IN on UC may involve activation of systemic immunity, which is involved in the regulation of nuclear transcription, protein phosphorylation, cytokine activity, reactive oxygen metabolism, epithelial cell proliferation, and cell apoptosis through Th17 cell differentiation, the Jak-STAT and IL-17 signaling pathways, toll-like and NOD-like receptors, and other cellular and innate immune signaling pathways. The molecular mechanism underlying the effect of IN on inducing UC remission was predicted using a network pharmacology method, thereby providing a theoretical basis for further study of the effective components and mechanism of IN in the treatment of UC.

show abstract

Section: Discussionmentioning

confidence: 99%

Mechanisms of indigo naturalis on treating ulcerative colitis explored by GEO gene chips combined with network pharmacology and molecular docking

Xue

Gao

et al. 2020

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Indirubin, a component of indigo naturalis, which is derived from the leaves and stems of indigo plants, is used in traditional Chinese medicine to treat inflammatory bowel disease [ 52 ]. A study of the molecular structure of indirubin indicates that it has a more three-dimensional structure compared to the more planar structure of the indigo molecule which is another component of indigo naturalis [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

Functions of Small Organic Compounds that Mimic the HNK-1 Glycan

Wang

Theis

Kabat

et al. 2020

IJMS

View full text Add to dashboard Cite

Because of the importance of the HNK-1 carbohydrate for preferential motor reinnervation after injury of the femoral nerve in mammals, we screened NIH Clinical Collection 1 and 2 Libraries and a Natural Product library comprising small organic compounds for identification of pharmacologically useful reagents. The reason for this attempt was to obviate the difficult chemical synthesis of the HNK-1 carbohydrate and its isolation from natural sources, with the hope to render such compounds clinically useful. We identified six compounds that enhanced neurite outgrowth from cultured spinal motor neurons at nM concentrations and increased their neurite diameter, but not their neurite branch points. Axons of dorsal root ganglion neurons did not respond to these compounds, a feature that is in agreement with their biological role after injury. We refer to the positive functions of some of these compounds in animal models of injury and delineate the intracellular signaling responses elicited by application of compounds to cultured murine central nervous system neurons. Altogether, these results point to the potential of the HNK-1 carbohydrate mimetics in clinically-oriented settings.

show abstract

“…Clinical treatment UC is usually treated with anti-in ammatory or immunosuppressive drugs that have the disadvantages of relapse after discontinuation, long-term adverse drug reactions, and unsatisfactory results in some refractory cases [18]. Other studies have proved that INN, IND and INB can improve UC, but their therapeutic mechanism is not clear [19][20][21].…”

Section: Discussionmentioning

confidence: 99%

Study on the mechanism of Indigo naturalis and its two main compounds (indigo and indirubin) in the treatment of ulcerative colitis based on TLR4/MyD88/NF-κB pathway and intestinal microorganisms

Yang¹,

He²,

Ma³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Indigo naturalis is a natural dye extracted from plants and has a good anti-inflammatory effect. Clinical studies have shown that it can improve ulcerative colitis (UC), but the active constituents and the mechanism are unclear. Methods: The anti-UC activity of Indigo naturalis and its two main compounds (indigo and indirubin) were investigated in dextran sulfate sodium (DSS)-induced UC mice. Indigo naturalis, indigo and indirubin were administrated to DSS-induced UC rats by oral gavage for 1 weeks. The anti-UC effect was evaluated by pathological section, inflammatory cytokine production, western blotting, and gut microbiota analysis via 16S rRNA sequencing. Results: Indigo naturalis, indigo and indirubin can improve the UC induced by DSS. Their effect intensity is Indigo naturalis > indirubin > indigo based on disease activity index, body weight, colon length and pathological section. Indigo naturalis, indigo and indirubin also decrease the expression of NF-κB，TLR4 and MYD88 proteins, thus reducing the level of related inflammation cytokines (IL-1β, IL-6 and TNF-α) both in serum and tissue. In addition, Indigo naturalis and indigo improved symptoms of gut microbial disturbance, and decreased Firmicutes/Bacteroidetes ratio and the significantly increased probiotics such as Lactobacillus. Indirubin has little effect on the regulation of gut microbial. Conclusions: Indigo naturalis could attenuate the DSS-induced UC in mice, by means of ameliorating intestinal inflammation, improving intestinal mucosa, and regulating the disturbed gut microbiota. Indigo and indirubin could also attenuate the DSS-induced UC in mice, but their comprehensive effect is not as good as Indigo naturalis.

show abstract

Indigo Naturalis Ameliorates Dextran Sulfate Sodium-Induced Colitis in Mice by Modulating the Intestinal Microbiota Community

Cited by 54 publications

References 64 publications

Mechanisms of indigo naturalis on treating ulcerative colitis explored by GEO gene chips combined with network pharmacology and molecular docking

Mechanisms of indigo naturalis on treating ulcerative colitis explored by GEO gene chips combined with network pharmacology and molecular docking

Functions of Small Organic Compounds that Mimic the HNK-1 Glycan

Study on the mechanism of Indigo naturalis and its two main compounds (indigo and indirubin) in the treatment of ulcerative colitis based on TLR4/MyD88/NF-κB pathway and intestinal microorganisms

Contact Info

Product

Resources

About