Effects of tripterygium wilfordii Hook F extracts on induction of cyclooxygenase 2 activity and prostaglandin E2 production

Tao, Xiaochun; Schulze‐Koops, Hendrik; Ma, Li; Cai, Jian; Mao, Yan‐Ping; Lipsky, Peter E.

doi:10.1002/1529-0131(199801)41:1<130::aid-art16>3.0.co;2-4

Cited by 93 publications

(60 citation statements)

References 22 publications

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“…Production of COX-1 was not affected . Suppression of prostaglandin E 2 (PGE 2 ) synthesis was observed (Chang et al, 1997;Tao et al, 1998;Maekawa et al, 1999), but the mechanism of the suppression was not determined. Inhibition of lipoxygenase was also noted (Li et al, 2003a).…”

Section: Proinflammatory Enzymes-nitric Oxide Synthase (Nos) Catalyzementioning

confidence: 99%

Medicinal chemistry and pharmacology of genus Tripterygium (Celastraceae)

et al. 2007

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Plants in the genus Tripterygium, such as Tripterygium wilfordii Hook. f., have a long history of use in traditional Chinese medicine. In recent years there has been considerable interest in the use of Tripterygium extracts and of the main bioactive constituent, the diterpene triepoxide triptolide (1), to treat a variety of autoimmune and inflammation-related conditions. The main mode of action of the Tripterygium extracts and triptolide (1) is the inhibition of expression of proinflammatory genes such as those for interleukin-2 (IL-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2) and interferon-gamma (IFN-γ). The efficacy and safety of certain types of Tripterygium extracts were confirmed in human clinical trials in the US and abroad. Over 300 compounds have been identified in the genus Tripterygium, and many of these have been evaluated for biological activity. The overall activity of the extract is based on the interaction between its components. Therefore, the safety and efficacy of the extract cannot be fully mimicked by any individual constituent. This review discusses the biochemical composition and biological and pharmacological activities of Tripterygium extracts, and their main bioactive components.

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Section: Proinflammatory Enzymes-nitric Oxide Synthase (Nos) Catalyzementioning

confidence: 99%

Medicinal chemistry and pharmacology of genus Tripterygium (Celastraceae)

et al. 2007

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“…Meanwhile, many studies have been dedicated to elucidating the potential molecular mechanisms underlying the anti-inflammatory and immunosuppressive effects of TEs [18], including the inhibition of platelet activation [20], the induction of nitric oxide [21], and prostaglandin E 2 [22] production. Based on studies both in vitro and in vivo , it is easy to speculate that TEs are likely to be types of herbal DMARDs, which differ from synthetic DMARDs.…”

Section: Introductionmentioning

confidence: 99%

Extracts ofTripterygium wilfordiiHook F in the Treatment of Rheumatoid Arthritis: A Systemic Review and Meta-Analysis of Randomised Controlled Trials

Liu

Gao

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Clinical trials have reported the effects of Tripterygium wilfordii Hook F (TwHF) extracts (TEs) in the treatment of rheumatoid arthritis (RA); however, the results have been inconsistent. This meta-analysis is aimed to assess the safety of TEs and their effects on the treatment of RA. Randomised controlled trials (RCTs) comparing the effects of TEs and placebo (PBO) or disease-modifying antirheumatic drugs (DMARDs) in patients with RA were included. Weighted mean differences (MDs) were calculated for net changes by employing fixed-effect or random-effects models. After filtering, ten RCTs (involving 733 participants) were included in this study. The methodological quality of these studies was generally low. Compared with DMARDs, TEs alone produced a mild increase in grip strength (GS) (P = 0.02; standard mean difference (SMD) = 0.81; 95% confidence interval (CI): 0.14 to 1.48). The most common adverse effects (AEs) of TEs were gastrointestinal discomfort, menstruation disorders, and amenorrhea. In conclusion, TEs, as a sort of “herbal DMARD,” could be as effective as synthetic DMARDs in the treatment of RA. However, the efficacy of TEs in treating RA should be further estimated with better designed, fully powered, confirmatory RCTs that apply the American College of Rheumatology (ACR) improvement criteria to evaluate their outcomes.

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“…Triptolide inhibits LPS-stimulated COX-2 mRNA and synthesis of PGE 2 in LPS-stimulated monocytes. [22] In human synovial fibroblasts, triptolide suppresses the production and expression of prometalloproteinases 1 and 3 and inhibits the expression of COX-2 and IL-1-induced PGE 2 production. [23] Triptolide also inhibits vascular endothelial cell growth factor expression in phorbol 12-myristate 13-acetate (PMA)-activated endothelial cells [24] and attenuates the expression of IL-6, IL-8, and cell adhesion molecule ICAM-1 by PMA-stimulated human bronchial epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

Triptolide Attenuates Endotoxin- and Staphylococcal Exotoxin-Induced T-Cell Proliferation and Production of Cytokines and Chemokines

Krakauer

Chen

Howard³

et al. 2005

LIPI

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Proinflammatory cytokines mediate the toxic effects of superantigenic staphylococcal exotoxins (SE) and bacterial lipopolysaccharide (LPS). Triptolide, an oxygenated diterpene derived from a traditional Chinese medicinal herb, Tripterygium wilfordii, inhibited SE-stimulated T-cell proliferation (by 98%) and expression of interleukin 1b, interleukin 6, tumor necrosis factor, gamma interferon, monocyte chemotactic protein 1, macrophage inflammatory protein (MIP)-1a, and MIP-1b by human peripheral blood mononuclear cells (PBMC). It also blocked the production of these cytokines and chemokines by LPS-stimulated PBMC in a dose-dependent manner. These results suggest that triptolide has potent immunosuppressive effects even counteracting the effects of superantigens and LPS. It also may be therapeutically useful for mitigating the pathogenic effects of these microbial products by downregulating the signaling pathways activated by both bacterial exotoxins and endotoxins.

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Effects of tripterygium wilfordii Hook F extracts on induction of cyclooxygenase 2 activity and prostaglandin E2 production

Cited by 93 publications

References 22 publications

Medicinal chemistry and pharmacology of genus Tripterygium (Celastraceae)

Medicinal chemistry and pharmacology of genus Tripterygium (Celastraceae)

Extracts ofTripterygium wilfordiiHook F in the Treatment of Rheumatoid Arthritis: A Systemic Review and Meta-Analysis of Randomised Controlled Trials

Triptolide Attenuates Endotoxin- and Staphylococcal Exotoxin-Induced T-Cell Proliferation and Production of Cytokines and Chemokines

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