Therapeutic effects of triptolide on interleukin-10 gene-deficient mice with colitis

Wei, Xiaowei; Gong, Jianfeng; Zhu, Jing; Niu, Lingying; Zhu, Weiming; Li, Jieshou

doi:10.1016/j.intimp.2008.08.019

Cited by 24 publications

(13 citation statements)

References 26 publications

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“…Triptolide, a diterpene triepoxide, has been identified to be one of the major active components in the TwHF extract. Previous studies have shown that triptolide exerts potent immunosuppressive, anti-inflammatory, anti-proliferative and anti-oxidative effects (11–13). Our previous study and an investigation from another laboratory have indicated that triptolide may inhibit inflammatory responses, thereby reducing albuminuria and improving renal functions in type II diabetic rats and patients with type II diabetes (14,15).…”

Section: Introductionmentioning

confidence: 99%

Triptolide markedly attenuates albuminuria and podocyte injury in an animal model of diabetic nephropathy

Liu

et al. 2013

Experimental and Therapeutic Medicine

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Triptolide is a major active component of Tripterygium wilfordii Hook F, which exerts marked immunosuppressive, anti-inflammatory and podocyte-protective effects. In this study, the ability of triptolide to inhibit inflammation and attenuate podocyte injury was examined in a rat model of diabetic nephropathy (DN). Type II diabetic rats with DN were treated with triptolide at a dose of 100 μg.kg−1.day−1. Following 8 weeks of triptolide treatment, the urine albumin level, kidney weight/body weight and the number of cells positive for ED-1 (a marker for rat mononuclear macrophages) in the kidney were assessed. The effects of triptolide on podocyte injury and chronic inflammation were analyzed using quantitative polymerase chain reaction (qPCR), western blotting and immunohistochemistry. Following triptolide treatment, the albuminuria in the type II diabetic rats was significantly reduced. Furthermore, the glomerular hypertrophy and foot process effacement were improved, and there was a recovery of the slit diaphragm associated with nephrin and podocin expression. The inflammation in the kidneys was also attenuated. Furthermore, triptolide significantly reduced the expression of transforming growth factor-β1 and osteopontin, and the infiltration of ED-1-positive cells into the kidney. The results demonstrated that triptolide markedly attenuated albuminuria and podocyte injury in the rat model of DN, which may have been correlated with the inhibition of inflammation and macrophage infiltration in the kidneys.

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Section: Introductionmentioning

confidence: 99%

Triptolide markedly attenuates albuminuria and podocyte injury in an animal model of diabetic nephropathy

Liu

et al. 2013

Experimental and Therapeutic Medicine

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“…These results suggested that TL may have a therapeutic effect in experimental colitis and indicated TL as a potential therapeutic agent for the treatment of Crohn's disease. Wei et al (35) have previously demonstrated that TL administration for 8 weeks results in a significant decrease in the severity of colitis, which was accompanied by reduced expression of TNF-α, IFN-γ and IL-4 in the colon. Serum amyloid A levels were decreased in TL-treated mice and IL-12 and IL-23 gene expression levels in the colon were also downregulated following treatment.…”

Section: Discussionmentioning

confidence: 98%

Therapeutic effects of triptolide via the inhibition of IL-1β expression in a mouse model of ulcerative colitis

Zhang

Chen

et al. 2016

Experimental and Therapeutic Medicine

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The present study aimed to investigate the effect of triptolide (TL) on ulcerative colitis (UC) and explore the potential association between the therapeutic effects of TL and IL-1β expression using a 4,4-dimethyl-4-silapentane-1-sulfonic acid (DSS)-induced mouse model to simulate human UC. A total of 70 BALB/c female mice were randomly allocated into seven equal groups: Group A, blank control; group B, normal saline injection; group C, propylene glycol injection; group D (TL1), 0.2 mg/kg TL; group E (TL2), 0.4 mg/kg TL; group F (TL3), 0.6 mg/kg TL; and group G, dexamethasone injection. Mice activity, diet and stool characteristics were recorded daily. Mice were sacrificed by cervical dislocation on day 8, and disease activity indices, colon tissue histological scores and colonic histopathological scores were subsequently calculated. Serum levels of IL-1β were evaluated by enzyme-linked immunosorbent assay, and IL-1β expression levels were examined by reverse transcription-quantitative polymerase chain reaction with colonic mucosa specimen at the gene level and western blot analysis at the protein level. The IL-1β mRNA and protein expression levels were significantly elevated in the normal saline injection and propylene glycol injection groups compared with the blank control group and (P<0.01). In TL (TL2 and TL3)- and dexamethasone-treated mice, IL-1β expression levels were significantly decreased, as compared with the normal saline and propylene glycol injection groups (P<0.05). No significant difference was detected between TL (TL2 and TL3) and dexamethasone treatments. The results of the present study indicated that IL-1β expression was upregulated in the UC mouse model, which may be associated with the development and progression of UC. Furthermore, TL inhibited IL-1β expression, suggesting that TL may be a novel therapeutic target for the treatment of UC.

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“…Serum TNF-α is upregulated in patients with active CD activity compared with healthy control [23]. Triptolide, an active ingredient derived from TWH, could significantly reduce the production of TNF-α, IFN-γ and IL-4 in the colon [24]. In addition, it could ameliorate Th1-mediated chronic colitis and disordered immune state in IL-10(−/−) mice by inhibiting TNF-alpha/TNFR2 signal pathway [25].…”

Section: Discussionmentioning

confidence: 99%

A network pharmacology study on the Tripteryguim wilfordii Hook for treatment of Crohn’s disease

Zhang

Huang

Zhao

et al. 2020

BMC Complement Med Ther

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Background: To explore the mechanism of action of Tripterygium wilfordii Hook (TWH) in the treatment of Crohn's disease (CD) by network pharmacology. Methods: Traditional Chinese Medicine Systems Pharmacology database and analysis platform (TCMSP) was used to obtain the active constituents and targets of TWH. "Crohn's disease" was used as a search term to search for related targets of CD from GeneCards database and OMIM database, thereby obtaining the targets of TWH against CD. The Cytoscape 3.7.1 software was used to construct a Chinese medicine compound-target network and STRING database to construct a protein-protein interaction network (PPI). The DAVID 6.8 online tool was used to perform gene ontology (GO) and kyoto encyclopedia of genes and genome (KEGG) pathway enrichment analysis of overlapping targets. Results: The database results showed that there were 30 active ingredients (14 key active ingredients) in TWH and 36 targets were screened out for CD treatment. Network analysis indicated that main targets of main active components of TWH were target genes such as VEGFA, MAPK8 and CASP3, which are involved in the regulation of cancer pathway, TNF signal pathway, hepatitis B pathway, apoptosis pathway, NF-kappa B signal pathway and so forth. Conclusions: TWH can play a multi-target and multi-channel synergistic treatment of CD by anti-angiogenesis, antiapoptosis, anti-inflammation and immune regulation.

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Therapeutic effects of triptolide on interleukin-10 gene-deficient mice with colitis

Cited by 24 publications

References 26 publications

Triptolide markedly attenuates albuminuria and podocyte injury in an animal model of diabetic nephropathy

Triptolide markedly attenuates albuminuria and podocyte injury in an animal model of diabetic nephropathy

Therapeutic effects of triptolide via the inhibition of IL-1β expression in a mouse model of ulcerative colitis

A network pharmacology study on the Tripteryguim wilfordii Hook for treatment of Crohn’s disease

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