The antiferroptotic effect of indigo on ulcerative colitis

Sun, Shaopeng; Lv, Bin

doi:10.1007/s00535-023-02063-x

Cited by 2 publications

(1 citation statement)

References 5 publications

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“…Due to its excellent anti-inflammatory effects, IN is clinically used to treat UC, acute promyelocytic leukemia, and psoriasis. , The active ingredients of IN are mainly indigo, indirubin, and tryptanthrin (indolo[2,1- b ]quinoline-6,12-dione, TRYP) (Figure B). Multiple studies have shown that indigo, indirubin, and TRYP exhibited excellent anti-inflammatory activities. − Our previous study also found that TRYP exerted an anti-inflammatory effect on UC mice by modulating the secretion of inflammatory factors and decreasing the expression of NF-κB p65 in mouse colon tissues. , In addition, it has been reported that TRYP could reduce the production of inflammatory factors in BV2 cells by regulating the Nrf2/HO-1 and NF-κB signaling pathways …”

Section: Introductionmentioning

confidence: 87%

Exploring the Anti-Inflammatory Effect of Tryptanthrin by Regulating TLR4/MyD88/ROS/NF-κB, JAK/STAT3, and Keap1/Nrf2 Signaling Pathways

Zhu,

Cheng,

et al. 2024

ACS Omega

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Tryptanthrin (TRYP) is the main active ingredient in Indigo Naturalis. Studies have shown that TRYP had excellent anti-inflammatory activity, but its specific mechanism has been unclear. In this work, the differentially expressed proteins resulting from TRYP intervention in LPS-stimulated RAW264.7 cells were obtained based on tandem mass tag proteomics technology. The anti-inflammatory mechanism of TRYP was further validated by a combination of experiments using the LPS-induced RAW264.7 cell model in vitro and the DSS-induced UC mouse model (free drinking 2.5% DSS) in vivo. The results demonstrated that TRYP could inhibit levels of NO, IL-6, and TNF-α in LPS-induced RAW264.7 cells. Twelve differential proteins were screened out. And the results indicated that TRYP could inhibit upregulated levels of gp91phox, p22phox, FcεRIγ, IKKα/β, and p-IκBα and reduce ROS levels in vitro. Besides, after TRYP treatment, the health conditions of colitis mice were all improved. Furthermore, TRYP inhibited the activation of JAK/STAT3, nuclear translocation of NF-κB p65, and promoted the nuclear expression of Nrf2 in vitro and in vivo. This work preliminarily indicated that TRYP might suppress the TLR4/MyD88/ROS/NF-κB and JAK/STAT3 signaling pathways to exert anti-inflammatory effects. Additionally, TRYP could achieve antioxidant effects by regulating the Keap1/ Nrf2 signaling pathway.

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