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异丙酚通过刺激沉默调节蛋白 1 并抑制细胞焦亡减轻肾缺血/再灌注诱导的急性肺损伤。

Propofol reduces renal ischemia/reperfusion-induced acute lung injury by stimulating sirtuin 1 and inhibiting pyroptosis.

机构信息

Department of Anesthesiology, Cangzhou Central Hospital, Cangzhou, Hebei, China.

Department of Gastroenterology, Cangzhou Central Hospital, Cangzhou, Hebei, China.

出版信息

Aging (Albany NY). 2020 Dec 1;13(1):865-876. doi: 10.18632/aging.202191.

DOI:10.18632/aging.202191
PMID:33260147
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7834996/
Abstract

The activation of pyroptosis is an important feature of renal ischemia/reperfusion (rI/R)-induced acute lung injury (ALI). Propofol, a general anesthetic, is known to inhibit inflammation in I/R-induced ALI. We investigated whether propofol could suppress pyroptosis during rI/R-induced ALI by upregulating sirtuin 1 (SIRT1). We generated an model of rI/R-induced ALI by applying microvascular clamps to the renal pedicles of rats for 45 min. Pathological studies revealed that rI/R provoked substantial lung injury and inflammatory cell infiltration. The rI/R stimulus markedly activated pyroptotic proteins such as NLRP3, ASC, caspase 1, interleukin-1β and interleukin-18 in the lungs, but reduced the mRNA and protein levels of SIRT1. Propofol treatment greatly inhibited rI/R-induced lung injury and pyroptosis, whereas it elevated SIRT1 expression. Treatment with the selective SIRT1 inhibitor nicotinamide reversed the protective effects of propofol during rI/R-induced ALI. Analogous defensive properties of propofol were detected in rat alveolar macrophages incubated with serum from the rI/R rat model. These findings indicate that propofol attenuates rI/R-induced ALI by suppressing pyroptosis, possibly by upregulating SIRT1 in the lungs.

摘要

细胞焦亡的激活是肾缺血/再灌注（rI/R）诱导的急性肺损伤（ALI）的一个重要特征。丙泊酚是一种全身麻醉剂，已知能抑制 I/R 诱导的 ALI 中的炎症。我们研究了丙泊酚是否可以通过上调沉默调节蛋白 1（SIRT1）来抑制 rI/R 诱导的 ALI 中的细胞焦亡。我们通过对大鼠肾蒂施加微血管夹 45 分钟来建立 rI/R 诱导的 ALI 模型。病理研究表明，rI/R 引起了大量的肺损伤和炎症细胞浸润。rI/R 刺激在肺部显著激活了细胞焦亡蛋白，如 NLRP3、ASC、半胱天冬酶 1、白细胞介素-1β和白细胞介素-18，但降低了 SIRT1 的 mRNA 和蛋白水平。丙泊酚治疗极大地抑制了 rI/R 诱导的肺损伤和细胞焦亡，同时提高了 SIRT1 的表达。用选择性 SIRT1 抑制剂烟酰胺处理逆转了丙泊酚在 rI/R 诱导的 ALI 中的保护作用。在与来自 rI/R 大鼠模型的血清孵育的大鼠肺泡巨噬细胞中检测到丙泊酚的类似防御特性。这些发现表明，丙泊酚通过抑制肺组织中的细胞焦亡来减轻 rI/R 诱导的 ALI，这可能是通过上调 SIRT1 实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/9675d28b2da6/aging-13-202191-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/e84e5e31d310/aging-13-202191-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/fd67f756fc4a/aging-13-202191-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/b3a752f47b2f/aging-13-202191-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/480a9881e4d1/aging-13-202191-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/edc52f019361/aging-13-202191-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/97dfcad142bf/aging-13-202191-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/9675d28b2da6/aging-13-202191-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/e84e5e31d310/aging-13-202191-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/fd67f756fc4a/aging-13-202191-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/b3a752f47b2f/aging-13-202191-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/480a9881e4d1/aging-13-202191-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/edc52f019361/aging-13-202191-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/97dfcad142bf/aging-13-202191-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef47/7834996/9675d28b2da6/aging-13-202191-g007.jpg

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