Kuijieling regulates the differentiation of Treg and Th17 cells to ameliorate experimental colitis in rats

Yu, Liang; Li, Sixin; Qin, Jingchun; Xie, Liwei; Gan, Liping; Jie, Fengming; Wu, Yanli; Li, Yanwu; Du, Qun

doi:10.1016/j.biopha.2018.06.011

Cited by 23 publications

(17 citation statements)

References 36 publications

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“…Traditional Chinese medicine has a long history and has been widely used in Asia. An increasing number of animal experiments have confirmed that Chinese medicine monomers or compounds have good anti-inflammatory effects [14, 22, 45–47]. However, the aim of this research is to treat patients, and drugs are ultimately used on people.…”

Section: Discussionmentioning

confidence: 99%

“…Abelmoschus manihot (L.) Medik (huang shu kui hua), Euphorbia humifusa Willd (di jin cao), Pteris multifida Poir (feng wei cao), Lithospermum erythrorhizon Siebold & Zucc (zi cao), Rubia cordifolia L. (qian cao), and Rhus chinensis Mill (wu bei zi) were mixed in a ratio of 6:6:6:3:3:1, and they were purchased from Suzhou Tianling Chinese Medicine Pieces Co., Ltd. All herbs were used in accordance with the Chinese Pharmacopoeia standards identified by the Pharmacy Department of Suzhou Traditional Chinese Medicine Hospital. After the herbs were washed with water, they were soaked in distilled water equivalent to 5 times the amount of the medicine for 60 minutes, boiled for 30 minutes, and filtered; the dregs were added to 3 times the amount of distilled water, boiled for another 20 minutes, and filtered [22]. The two decoctions were mixed and diluted to 1.92 g of crude drug/mL of drug solution in a water bath for use.…”

Section: Methodsmentioning

confidence: 99%

“…Real-time fluorescence quantitative polymerase chain reaction (qPCR) was chosen to measure mRNA expression in the colonic mucosa [22]. Total RNA was extracted from the colonic mucosa by the Trizol method; 1 μ g RNA was reverse transcribed in a 20 μ L reaction mixture in Prime Script RT Master Mix (TaKaRa, Japan).…”

Section: Methodsmentioning

confidence: 99%

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Huangkui Lianchang Decoction Ameliorates DSS-Induced Ulcerative Colitis in Mice by Inhibiting the NF-kappaB Signaling Pathway

Zhou

Wen

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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Background. The nuclear factor kappa beta (NF-κB) signaling pathway plays an important role in ulcerative colitis (UC). Huangkui Lianchang decoction (HLD) is an effective traditional Chinese medicinal compound used in the treatment of UC. HLD has good effects in the clinic, but the mechanism by which HLD acts is unclear. This study aims to reveal the exact molecular mechanism of HLD in the treatment of UC. Methods. Mouse ulcerative colitis was induced by dextran sulfate sodium (DSS) and treated with HLD. Intestinal damage was assessed by disease activity index (DAI), colon macroscopic lesion scores, and histological scores. Interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β were detected in colon tissue using ELISA. Myeloperoxidase (MPO) and superoxide dismutase (SOD) activities in the colonic mucosa were measured. The levels of IL-6, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) in the colon were determined by real-time quantitative polymerase chain reaction (qPCR). The expression of NF-κB, IκBα, and p-IκBα in the colon was measured by Western blot. Results. After treatment with HLD, the DAI scores, macroscopic lesion scores, and histological scores decreased, and the levels of inflammatory cytokines related to the NF-κB signaling pathway, such as IL-6, TNF-α, and IL-1β, as well as those of iNOS and COX-2, were reduced; at the same time, colonic pathological damage was alleviated, and the MPO and SOD activities decreased. Western blot confirmed that HLD can inhibit the NF-κB signaling pathway in DSS-induced ulcerative colitis. Conclusion. HLD can alleviate the inflammation caused by ulcerative colitis. In particular, high doses of HLD can significantly alleviate intestinal inflammation and have comparable efficacy to Mesalazine. We propose that the anti-inflammatory activity of HLD on DSS-induced colitis in mice may involve the inhibition of the NF-κB pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Huangkui Lianchang Decoction Ameliorates DSS-Induced Ulcerative Colitis in Mice by Inhibiting the NF-kappaB Signaling Pathway

Zhou

Wen

et al. 2019

Evidence-Based Complementary and Alternative Medicine

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“…Furthermore, several anti-inflammatory molecules ameliorating disease activity in experimental colitis are associated with modulation of JAK/STAT-signaling in lymphocytes. In detail, decreased expression or activation of JAK1 and JAK2[ 77 ], STAT1[ 77 ], STAT3[ 77 - 79 ] and STAT4[ 77 , 79 ] as well as enhancement of STAT5[ 78 ] phosphorylation in T-cells, have been linked to effective pharmacological treatment of DSS-induced murine colitis and TNBS-induced rat colitis. Additionally, inflammatory activity was reduced by general STAT1 knockout in DSS-treated STAT1-null mice[ 80 ] and by specific inhibition of STAT1 in T-cells in TNBS-induced colitis[ 81 ].…”

Section: Jak/stat-signaling In Ibd: T-cellsmentioning

confidence: 99%

Differential regulation of JAK/STAT-signaling in patients with ulcerative colitis and Crohn’s disease

Cordes

Foell

Ding

et al. 2020

WJG

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In 2018, the pan-Janus kinase (JAK) inhibitor tofacitinib was launched for the treatment of ulcerative colitis (UC). Although tofacitinib has proven efficacious in patients with active UC, it failed in patients with Crohn’s disease (CD). This finding strongly hints at a different contribution of JAK signaling in both entities. Here, we review the current knowledge on the interplay between the JAK/signal transducer and activator of transcription (STAT) pathway and inflammatory bowel diseases (IBD). In particular, we provide a detailed overview of the differences and similarities of JAK/STAT-signaling in UC and CD, highlight the impact of the JAK/STAT pathway in experimental colitis models and summarize the published evidence on JAK/STAT-signaling in immune cells of IBD as well as the genetic association between the JAK/STAT pathway and IBD. Finally, we describe novel treatment strategies targeting JAK/STAT inhibition in UC and CD and comment on the limitations and challenges of the new drug class.

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“…Candidate bioactive components in CSCC. e 119 candidate bioactive components (SFR � 30; IN � 7; BS � 6; RS � 4; LR � 72) of CSCC were determined with DL index ≥0.18, OB ≥ 30%, and Caco-2 ≥ 0.4.Evidence-Based Complementary and Alternative Medicine their hallmark cytokine, IL-17A[33][34][35]. Further experimental validation revealed that CSCC attenuated DSS-induced colitis by the suppression of the mRNA levels of IL-17A and of the cytokines it induces, such as IL-6, IL-1β, and TNF-α.…”

mentioning

confidence: 99%

Integrating Pharmacology and Microbial Network Analysis with Experimental Validation to Reveal the Mechanism of Composite Sophora Colon‐Soluble Capsule against Ulcerative Colitis

Ding

Chen

Wang

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Ulcerative colitis (UC) has multifactorial pathogenesis that acts synergistically, such as immune system dysregulation and expansion of infectious gut microbiota. Therefore, a multicomponent treatment derived from Chinese herbal medicine that interacts with multiple targets synergistically is needed. Composite sophora colon-soluble capsule (CSCC) is a Chinese herbal formula that has shown therapeutic efficacy against UC in randomized clinical trials. However, its bioactive components and potential target genes against UC remain unclear. Here, we used a network pharmacology approach to detect component-target-pathway interactions of CSCC against UC. A total of 29 gene targets, 91 bioactive components, and 20 enriched pathways of CSCC were identified. The IL-17 signaling pathway activated by infectious gastrointestinal microbes and predicted by the network analysis to be a major pathway modulated by CSCC against UC was studied in a dextran sulfate sodium-induced colitis model. CSCC showed remarkable efficacy against UC with respect to the attenuation of colon length, body weight loss, and disease activity index through gut microbiota recovery and intestinal immune homeostasis. The rectal administration of CSCC reduced the numbers of Th17 cells isolated from both mesenteric lymph nodes and lamina propria mononuclear cells and the levels of IL-17A, IL-6, IL-1β, and TNF-α. Additionally, the percentage of Treg cells and the levels of their hallmark cytokines were upregulated. Rectal administration of CSCC led to microbiota regulation with a significant correlation between suppression of Verrucomicrobiaceae and Ruminococcaceae, as well as the elevation of Lactobacillaceae, and CSCC administration via microbiome correlation heatmaps and cooccurrence network analysis at multiple time points. Thus, our study presents an effective herbal formula, CSCC, for UC treatment and explores its components and mechanisms of efficacy through the examination of gut microbiota and hallmark cytokines in the IL-17 pathway.

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Kuijieling regulates the differentiation of Treg and Th17 cells to ameliorate experimental colitis in rats

Cited by 23 publications

References 36 publications

Huangkui Lianchang Decoction Ameliorates DSS-Induced Ulcerative Colitis in Mice by Inhibiting the NF-kappaB Signaling Pathway

Huangkui Lianchang Decoction Ameliorates DSS-Induced Ulcerative Colitis in Mice by Inhibiting the NF-kappaB Signaling Pathway

Differential regulation of JAK/STAT-signaling in patients with ulcerative colitis and Crohn’s disease

Integrating Pharmacology and Microbial Network Analysis with Experimental Validation to Reveal the Mechanism of Composite Sophora Colon‐Soluble Capsule against Ulcerative Colitis

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