Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death

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...

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Autores principales:	Yu Ji Jiang, Sheng Cui, Kang Luo, Jun Ding, Qi Yan Nan, Shang Guo Piao, Mei Ying Xuan, Hai Lan Zheng, Yong Jie Jin, Ji Zhe Jin, Jung Pyo Lee, Byung Ha Chung, Bum Soon Choi, Chul Woo Yang, Can Li
Formato:	article
Lenguaje:	EN
Publicado:	The Korean Association of Internal Medicine 2021
Materias:	nicotine tacrolimus apoptosis autophagy mitochondria Medicine R
Acceso en línea:	https://doaj.org/article/8f4db247e3324446ad59a322ddc478e4
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spelling	oai:doaj.org-article:8f4db247e3324446ad59a322ddc478e42021-11-08T00:59:06ZNicotine exacerbates tacrolimus-induced renal injury by programmed cell death1226-33032005-664810.3904/kjim.2021.326https://doaj.org/article/8f4db247e3324446ad59a322ddc478e42021-11-01T00:00:00Zhttp://www.kjim.org/upload/pdf/kjim-2021-326.pdfhttps://doaj.org/toc/1226-3303https://doaj.org/toc/2005-6648Background/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, proinflammatory 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.Yu Ji JiangSheng CuiKang LuoJun DingQi Yan NanShang Guo PiaoMei Ying XuanHai Lan ZhengYong Jie JinJi Zhe JinJung Pyo LeeByung Ha ChungBum Soon ChoiChul Woo YangCan LiThe Korean Association of Internal MedicinearticlenicotinetacrolimusapoptosisautophagymitochondriaMedicineRENThe Korean Journal of Internal Medicine, Vol 36, Iss 6, Pp 1437-1449 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	nicotine tacrolimus apoptosis autophagy mitochondria Medicine R
spellingShingle	nicotine tacrolimus apoptosis autophagy mitochondria Medicine R Yu Ji Jiang Sheng Cui Kang Luo Jun Ding Qi Yan Nan Shang Guo Piao Mei Ying Xuan Hai Lan Zheng Yong Jie Jin Ji Zhe Jin Jung Pyo Lee Byung Ha Chung Bum Soon Choi Chul Woo Yang Can Li Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death
description	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, proinflammatory 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.
format	article
author	Yu Ji Jiang Sheng Cui Kang Luo Jun Ding Qi Yan Nan Shang Guo Piao Mei Ying Xuan Hai Lan Zheng Yong Jie Jin Ji Zhe Jin Jung Pyo Lee Byung Ha Chung Bum Soon Choi Chul Woo Yang Can Li
author_facet	Yu Ji Jiang Sheng Cui Kang Luo Jun Ding Qi Yan Nan Shang Guo Piao Mei Ying Xuan Hai Lan Zheng Yong Jie Jin Ji Zhe Jin Jung Pyo Lee Byung Ha Chung Bum Soon Choi Chul Woo Yang Can Li
author_sort	Yu Ji Jiang
title	Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death
title_short	Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death
title_full	Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death
title_fullStr	Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death
title_full_unstemmed	Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death
title_sort	nicotine exacerbates tacrolimus-induced renal injury by programmed cell death
publisher	The Korean Association of Internal Medicine
publishDate	2021
url	https://doaj.org/article/8f4db247e3324446ad59a322ddc478e4
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Nicotine exacerbates tacrolimus-induced renal injury by programmed cell death

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