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KMID : 0338420210360061437
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The Korean Journal of Internal Medicine
2021 Volume.36 No. 6 p.1437 ~ p.1449
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Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death
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Jiang Yu Ji
Cui Sheng
Luo Kang
Ding Jun
Nan Qi Yan
Piao Shang Guo
Xuan Mei Ying
Zheng Hai Lan
Jin Yong Jie
Jin Ji Zhe
Lee Jung-Pyo
Chung Byung-Ha
Choi Bum-Soon
Yang Chul-Woo
Li Can
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Abstract
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Background/Aims: Cigarette smoking is an important modifiable risk factor in kidney disease progression. However, the underlying mechanisms for this are lacking. This study aimed to assess whether nicotine (NIC), a major toxic component of cigarette smoking, would exacerbates tacrolimus (TAC)-induced renal injury.
Methods: Sprague-Dawley rats were treated daily with NIC, TAC, or both drugs for 4 weeks. The influence of NIC on TAC-caused renal injury was examined via renal function, histopathology, oxidative stress, mitochondria, endoplasmic reticulum (ER) stress, and programmed cell death (apoptosis and autophagy).
Results: Both NIC and TAC significantly impaired renal function and histopathology, while combined NIC and TAC treatment aggravated these parameters beyond the effects of either alone. Increased oxidative stress, ER stress, mitochondrial dysfunction, proinf lammatory and profibrotic cytokine expressions, and programmed cell death from either NIC or TAC were also aggravated by the two combined.
Conclusions: Our observations suggest that NIC exacerbates chronic TAC nephrotoxicity, implying that smoking cessation may be beneficial for transplant smokers taking TAC.
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KEYWORD
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Nicotine , Tacrolimus , Apoptosis , Autophagy , Mitochondria
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