Inhibitory effect of triptolide on platelet derived growth factor-A and coronary arteriosclerosis after heart transplantation

Hachida, M; Lü, Hua; Zhang, X; Saitô, Satoshi; Furutani, Yoshiyuki; Matsuoka, Rumiko; Hoshi, H; Koyanagi, Hitoshi

doi:10.1016/s0041-1345(99)00539-4

Cited by 14 publications

(10 citation statements)

References 15 publications

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“…In addition, Trip shows antiproliferative effect and anti‐inflammatory effects 19–21 . It blocks fibroblast maturation/proliferation and inhibits TGF‐β mRNA production in vitro and blocks both inflammation and fibrosis in the bleomycin model of mouse lung fibrosis, attenuates airway obliteration in a tracheal allograft model of obliterative airway disease and attenuates coronary arteriosclerosis in a rat cardiac transplant model 20,22,23 …”

Section: Discussionmentioning

confidence: 99%

Triptolide attenuates renal interstitial fibrosis in rats with unilateral ureteral obstruction

Yuan¹,

He²,

Wang³

et al. 2011

Nephrology

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Section: Discussionmentioning

confidence: 99%

Triptolide attenuates renal interstitial fibrosis in rats with unilateral ureteral obstruction

Yuan¹,

He²,

Wang³

et al. 2011

Nephrology

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“…Triptolide and its prodrugs and derivatives have the potential for establishing a new class of potent immunosuppressive agents, which work by a unique mechanism of action. This class of compounds has not only demonstrated activity in animal models of acute rejection but also has been shown to attenuate airway obliteration in a murine model of bronchiolitis obliterans and to decrease coronary graft arteriosclerosis in a rat model of heart transplantation (44,45).…”

Section: Collaborations With Pharmagenesis and Atherogenicsmentioning

confidence: 99%

New Drugs to Improve Transplant Outcomes

First¹,

Fitzsimmons²

2004

Transplantation

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Fujisawa is committed to improving the outcomes of transplant patients worldwide. Research and development programs are underway for a new modified release dosage form of tacrolimus (MR-4), a new analog of leflunomide (FK 778), and several novel compounds (PG 490-88, AGI 1096) in collaboration with other companies. These programs are targeted to address many of the unmet medical needs in transplantation including (1) improving compliance, (2) reducing chronic rejection, and (3) improving long-term safety by reducing infectious and cardiovascular risk.

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“…Several studies have shown that triptolide has various activities and can function as an immunosuppressor, an anti-cancer drug, and a contraceptive (1)(2)(3). In many types of tumor cells, triptolide has been shown to induce apoptosis by promoting the release of cytochrome c as a result of mitochondrial damage and by decreasing the expression of anti-apoptotic proteins (4).…”

Section: Introductionmentioning

confidence: 99%

Triptolide inactivates Akt and induces caspase-dependent death in cervical cancer cells via the mitochondrial pathway

Kim¹,

Lee²,

Kim³

et al. 2010

Int J Oncol

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Abstract. Triptolide, the main active component of the traditional Chinese herbal medicine Tripterygium wilfordii Hook F, has been shown to have potent immunosuppressive and anti-inflammatory properties. Here, we investigated the pro-apoptotic effect of triptolide in human cervical cancer cells and its underlying mechanisms. Exposure of cervical cancer cells to triptolide induced apoptosis, which was accompanied by loss of mitochondrial membrane potential, caspase processing (caspase-8, -9 and -3), and cleavage of the caspase substrate, poly(ADP-ribose) polymerase. The cytotoxic effects of triptolide were significantly inhibited by the caspase inhibitor, z-VAD-fmk. Triptolide-induced apoptosis was associated with a marked reduction in Akt phosphorylation and was exacerbated by LY294002 (phosphatidylinositol-3'-kinase inhibitor). Conversely, it was attenuated by Akt overexpression. Triptolide-induced apoptosis was also associated with downregulation of Mcl-1 and was significantly inhibited by Mcl-1 overexpression. These findings show that triptolide induces caspase-dependent, mitochondria-mediated apoptosis in cervical cancer cells, in part, by negatively regulating Akt and Mcl-1.

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Inhibitory effect of triptolide on platelet derived growth factor-A and coronary arteriosclerosis after heart transplantation

Cited by 14 publications

References 15 publications

Triptolide attenuates renal interstitial fibrosis in rats with unilateral ureteral obstruction

Triptolide attenuates renal interstitial fibrosis in rats with unilateral ureteral obstruction

New Drugs to Improve Transplant Outcomes

Triptolide inactivates Akt and induces caspase-dependent death in cervical cancer cells via the mitochondrial pathway

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