Qing Hua Chang Yin exerts therapeutic effects against ulcerative colitis through the inhibition of the TLR4/NF-κB pathway

Ke, Xiao; Zhou, Fan; Gao, Youliang; Xie, Bin; Hu, Guanghong; Fang, Wenyi; Peng, Jun; Chen, Youqin; Sferra, Thomas J.

doi:10.3892/ijmm.2013.1458

Cited by 31 publications

(26 citation statements)

References 19 publications

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“…Moreover, its application significantly inhibits the DSS-induced expression of TLR4 and MyD88, the phosphorylation of IκB and the nuclear translocation of NF-κB. Taken together, it suggests that the suppression of the TLR4/NF-κB signaling pathway may be one of the mechanisms involved in the therapeutic effects of QHCY against UC [143]. Furthermore, QHCY (1.4 mg/mL) treatment attenuates the LPS-induced phosphorylation of JAK1 and JAK2 in differentiated Caco-2 cells, which is in accordance with the reduced phosphorylation state of STAT3.…”

Section: Heat-clearing and Drying Dampness Categorymentioning

confidence: 78%

“…Suppress NF-κB activation [135] Qingchang Huashi recipe HT-29 cells Reduce the activation of NF-κB [137] Gegenqinlian Decoction TNBS-induced colon tissue Inhibit the activation and translocation of NF-κBp65 [138] DSS-induced colonic tissues Decrease the P-NF-κBp65 [139] RAW 264.7 cells Down-regulate the expression of P-NF-κBp65 [139] Jianpi Qingchang decoction DSS-induced colon tissue Inhibit the activation of the NF-κB [140] Modified pulsatilla decoction OXZ-induced colon tissues Suppress the activation of the NF-κB [142] Qing Hua Chang Yin DSS-induced colon tissue Inhibit the expression of the nuclear translocation of NF-κB [143] QingBai decoction DSS-induced colon tissue Decrease the protein level of P-NF-κBp65 [145] Chang-An-Shuan TNBS-induced colonic tissues Down-regulate the expression levels of NF-κBp65 [146] Baishaoqiwu TNBS-induced colon tissues Inhibit expression of the NF-ĸBp65 genes [147] Xie-xin decoction TNBS-induced colon tissues Decrease expression of NF-ĸBp65 [148] Compound sophorae decoction…”

Section: Shaoyao Decoction Aom/dss-induced Colonic Tissuesmentioning

confidence: 99%

“…Attenuate the levels of inflammatory markers via suppression of the PI3K/AKT/mTOR signaling pathway, in part through up-regulation of miRNA-126 [125] Astringent medicine Qing Hua Chang Yin DSS-induced colon tissue Inhibit the expression of the phosphorylation of IκB [143] Caco-2 cells Suppress the phosphorylation of JAK1, JAK2 and STAT3 [144] QingBai decoction DSS-induced colon tissue Strengthen mucus barrier through inhibiting p-ERK and Notch signaling [145] Chang-An-Shuan…”

Section: Dss-induced Intestinal Mucosamentioning

confidence: 99%

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Targeting NF-κB pathway for treating ulcerative colitis: comprehensive regulatory characteristics of Chinese medicines

Zhao

2020

Chin Med

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Nuclear factor-kappa B (NF-κB) is a kind of multi-functional nuclear transcription factor involved in regulating gene transcription to influence pathological evolution of inflammatory and immune diseases. Numerous literature evidence that NF-κB pathway plays an essential role in pathogenic development of ulcerative colitis (UC). UC is a chronic non-specific inflammatory bowel disease, and until now, therapeutic agents for UC including aminosalicylates, corticosteroids and immune inhibitors still cannot exert satisfied effects on patients. In recent years, Chinese medicines suggest the advantages of alleviating symptoms and signs, decreasing side-effects and recurrence, whose one of mechanisms is related to regulation of NF-κB pathway. In this review, we categorize Chinese medicines according to their traditional therapeutic functions, and summarize the characteristics of Chinese medicines targeting NF-κB pathway in UC treatment. It indicates that 85 kinds of Chinese medicines' compounds and formulae can directly act on NF-κBp65; while 58 Chinese medicines' ingredients and formulae indirectly suppress NF-κBp65 by regulation of its upstream or other related pathways. Moreover, by the analysis of Chinese medicines' category based on their traditional functions, we conclude the category of dampness-drying and detoxificating medicine targeting NF-κB pathway accounts for primary status for amelioration of UC. Simultaneously, this review also contributes to the choices of Chinese medicine category and provides curative potential of Chinese medicines for clinical UC treatment.

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Section: Heat-clearing and Drying Dampness Categorymentioning

confidence: 78%

Section: Shaoyao Decoction Aom/dss-induced Colonic Tissuesmentioning

confidence: 99%

Section: Dss-induced Intestinal Mucosamentioning

confidence: 99%

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Targeting NF-κB pathway for treating ulcerative colitis: comprehensive regulatory characteristics of Chinese medicines

Zhao

2020

Chin Med

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“…TLR4/NF-κB, regulating inflammatory factors secretion, is closely associated with colitis initiation and development. 33 TLR4 was upregulated in patients with IBD 34 and colitis model. 35 NF-κB was also upregulated in TNBSinduced colitis.…”

Section: Discussionmentioning

confidence: 91%

Inhibition of proprotein convertase subtilisin/kexin type 9 attenuates 2,4,6‐trinitrobenzenesulfonic acid‐induced colitis via repressing toll‐like receptor 4/nuclear factor‐kappa B

Lei

Yuan

et al. 2020

The Kaohsiung J of Med Scie

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Inflammatory bowel disease (IBD) is characterized by recurring inflammatory disorders in digestive system, and devoid of effective treatment. Proprotein convertase subtilisin/kexin type 9 (PCSK9), stimulated via inflammation whose inhibition could decrease secretion of inflammatory factors. We then determined whether inhibition of PCSK9 could improve the inflammation. First, rats model of colitis was first established via administration of 2,4,6‐trinitrobenzenesulfonic acid (TNBS), and then verified via determination of body weight loss, myeloperoxidase (MPO) activity, and histopathological analysis of colonic damage. Results showed that treatment with TNBS induced a great body weight loss, MPO activity increase, and serious colonic damage, showing an obviously character of IBD. PCSK9 was elevated in TNBS‐induced rats, and PCSK9 inhibition delivered by adenovirus vector increased the body weight, decreased MPO activity, and ameliorated histological change of colon. Second, the protective effect of PCSK9 inhibition against TNBS‐induced colitis was accompanied by decrease of proinflammatory factors secretion, including tumor necrosis factor‐α, interleukin‐1β, interleukin‐6, intercellular adhesion molecule 1, and monocyte chemoattractant protein‐1. TNBS could activate toll‐like receptor 4 (TLR4)/nuclear factor‐kappa B (NF‐κB) signaling pathway, while PCSK9 inhibition suppressed activation of TLR4/NF‐κB in TNBS‐induced rats. In conclusion, PCSK9 inhibition attenuated TNBS‐induced rat colitis through anti‐inflammatory effect under inactivation of TLR4/NF‐κB, suggesting potential therapeutic strategy in IBD.

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“…In vivo mouse colitis study. Mouse colitis model was established as we described previously (51). Briefly, acute colitis was induced by administration with 3% DSS in the drinking water for 8 days.…”

Section: Methodsmentioning

confidence: 99%

Pien Tze Huang ameliorates DSS‑induced colonic inflammation in a mouse colitis model through inhibition of the IL‑6/STAT3 pathway

Shen

Chu

et al. 2018

Mol Med Report

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Interleukin‑6 (IL‑6)/signal transducer and activator of transcription 3 (STAT3) pathway plays essential roles in the development of inflammatory diseases including ulcerative colitis (UC). Therefore, suppression of IL‑6/STAT3 signaling provides a promising therapeutic strategy in UC. Pien Tze Huang (PZH), a well‑known traditional Chinese formula, has been used in China and Southeast Asia for centuries as a folk remedy for various inflammatory diseases. However, the molecular mechanisms of its anti‑inflammatory effects remain to be elucidated. In the present study, we generated a mouse colitis model by using dextran sulfate sodium (DSS) and evaluated the therapeutic efficacy of PZH against UC by observing the clinical manifestations. We found that PZH obviously alleviated DSS‑induced colitis symptoms, including body weight loss, rectal bleeding and stool consistency. In addition, administration of PZH profoundly prevented DSS‑induced colon shortening, and ameliorated colonic histopathological changes such as mucosal ulceration, infiltration of inflammatory cells, crypt distortion and hyperplastic epithelium. Moreover, PZH markedly inhibited the serum level of the inflammatory biomarker serum amylase A (SAA) in UC mice. Furthermore, PZH treatment significantly inhibited DSS‑induced expression of IL‑6 in colon tissues. Finally, the increased phosphorylation level of STAT3, induced either by DSS in experimental mice or by IL‑6 in the differentiated human colorectal carcinoma cells, was significantly suppressed by PZH. These results suggest that the inhibition of IL‑6/STAT3 signaling is a potential mechanism by which PZH is used in the treatment of UC.

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Qing Hua Chang Yin exerts therapeutic effects against ulcerative colitis through the inhibition of the TLR4/NF-κB pathway

Cited by 31 publications

References 19 publications

Targeting NF-κB pathway for treating ulcerative colitis: comprehensive regulatory characteristics of Chinese medicines

Targeting NF-κB pathway for treating ulcerative colitis: comprehensive regulatory characteristics of Chinese medicines

Inhibition of proprotein convertase subtilisin/kexin type 9 attenuates 2,4,6‐trinitrobenzenesulfonic acid‐induced colitis via repressing toll‐like receptor 4/nuclear factor‐kappa B

Pien Tze Huang ameliorates DSS‑induced colonic inflammation in a mouse colitis model through inhibition of the IL‑6/STAT3 pathway

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