FK506 (tacrolimus) improves lung injury through inhibition of Fas-mediated inflammation

Koshika, Tadatsura; Masunaga, Taro; Hirayama, Yoshitaka

doi:10.1007/s00011-006-0077-x

Cited by 1 publication

(1 citation statement)

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“…However, long-term use of tacrolimus has been reported to affect organ transplant survival adversely because its chronic administration has been associated with nephrotoxicity, diabetes, neurotoxicity, and gastrointestinal disturbances [7,8,9]. In this regard, several studies have shown tacrolimus is toxic to renal proximal tubular epithelial cells, insulin-secreting cells, and gastric and lung epithelial cells [10,11,12]. Furthermore, the excessive production of inflammatory regulators such as cyclooxygenase-2 and transforming growth factor-β has been reported to promote tacrolimus-induced glomerular and tubular cell damage [13,14].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Nargenicin A1 against Tacrolimus-Induced Oxidative Stress in Hirame Natural Embryo Cells

Park

Kwon

Hwang

et al. 2019

IJERPH

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Tacrolimus is widely used as an immunosuppressant to reduce the risk of rejection after organ transplantation, but its cytotoxicity is problematic. Nargenicin A1 is an antibiotic extracted from Nocardia argentinensis and is known to have antioxidant activity, though its mode of action is unknown. The present study was undertaken to evaluate the protective effects of nargenicin A1 on DNA damage and apoptosis induced by tacrolimus in hirame natural embryo (HINAE) cells. We found that reduced HINAE cell survival by tacrolimus was due to the induction of DNA damage and apoptosis, both of which were prevented by co-treating nargenicin A1 or N-acetyl-l-cysteine, a reactive oxygen species (ROS) scavenger, with tacrolimus. In addition, apoptosis induction by tacrolimus was accompanied by increases in ROS generation and decreases in adenosine triphosphate (ATP) levels caused by mitochondrial dysfunction, and these changes were significantly attenuated in the presence of nargenicin A1, which further indicated tacrolimus-induced apoptosis involved an oxidative stress-associated mechanism. Furthermore, nargenicin A1 suppressed tacrolimus-induced B-cell lymphoma-2 (Bcl-2) down-regulation, Bax up-regulation, and caspase-3 activation. Collectively, these results demonstrate that nargenicin A1 protects HINAE cells against tacrolimus-induced DNA damage and apoptosis, at least in part, by scavenging ROS and thus suppressing the mitochondrial-dependent apoptotic pathway.

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Section: Introductionmentioning

confidence: 99%

Protective Effects of Nargenicin A1 against Tacrolimus-Induced Oxidative Stress in Hirame Natural Embryo Cells

Park

Kwon

Hwang

et al. 2019

IJERPH

View full text Add to dashboard Cite

show abstract

FK506 (tacrolimus) improves lung injury through inhibition of Fas-mediated inflammation

Abstract: Tacrolimus serves as a therapeutic option for improving lung injury through inhibition of Fas-mediated inflammation.

Cited by 1 publication

References 39 publications

Protective Effects of Nargenicin A1 against Tacrolimus-Induced Oxidative Stress in Hirame Natural Embryo Cells

Protective Effects of Nargenicin A1 against Tacrolimus-Induced Oxidative Stress in Hirame Natural Embryo Cells

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