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Alpha7 nicotinic acetylcholine receptor activation attenuated intestine-derived acute lung injury.
J Surg Res. 2016 Apr; 201(2):258-65.JS

Abstract

BACKGROUND

Intestinal ischemia-reperfusion (IIR) could lead to acute lung injury, associated with severe alveolar epithelial cells inflammatory and oxidative injury. Alpha7 nicotinic acetylcholine receptor (α7nAChR) is an essential component of the cholinergic anti-inflammatory pathway. The aim of this study was to investigate the important role of α7nAChR on the lung subjected to IIR.

METHODS

Thirty-two Sprague-Dawley rats were randomly divided into four groups (n = 8 in each): sham group (group S), model group (group M), α7nAChR agonist PNU-282987-treated group (group PNU), and specific α7nAChR antagonist methyllycaconitine-treated group (group MLA). Intestinal IR damage was induced by clamping the superior mesenteric artery for 75 min, followed by a 120-min reperfusion. All rats were killed at 2 h after release of the clamps. The histologic examination of lungs was made, and lung water content was detected. Expression levels of malondialdehyde, tumor necrosis factor alpha, interleukin-6, and superoxide dismutase activity of the lungs were detected. Additionally, expression level of toll-like receptor (TLR)4 and nuclear factor-kappaB (NF-κB p65) in the nucleus of lung tissue and apoptosis-related protein (Bax, Bcl-2, and cleaved-caspase3) were detected using Western blot.

RESULTS

Lungs were damaged after intestine IR, manifested by higher lung water content, histologic score, concentrations of interleukin-6, tumor necrosis factor alpha, and malondialdehyde of group M than those of group S, accompanied with decreased superoxide dismutase activity (P < 0.05). PNU treatment could significantly improve the pulmonary function of rats subjected to IIR. These effects of activation of α7nAChR were associated with suppression of TLR4/NF-κB pathway and subsequent reduction of apoptosis-related protein. However, MLA treatment aggravated lung injury.

CONCLUSIONS

α7nAChR plays a role in acute lung injury induced by IIR via attenuating lung oxidative stress and inflammation through suppression of TLR4/NF-κB pathway, resulting in reduction of apoptosis in the lung.

Authors+Show Affiliations

Department of Anesthesiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.Department of Emergency, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.Department of Anesthesiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.Department of Anesthesiology, Henan Provincal People's Hospital, Zhengzhou, China.Department of Anesthesiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.Department of Anesthesiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Electronic address: yaoweifeng881205@163.com.Department of Anesthesiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Electronic address: 18922102871@163.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27020805

Citation

He, Ye, et al. "Alpha7 Nicotinic Acetylcholine Receptor Activation Attenuated Intestine-derived Acute Lung Injury." The Journal of Surgical Research, vol. 201, no. 2, 2016, pp. 258-65.
He Y, Ye ZQ, Li X, et al. Alpha7 nicotinic acetylcholine receptor activation attenuated intestine-derived acute lung injury. J Surg Res. 2016;201(2):258-65.
He, Y., Ye, Z. Q., Li, X., Zhu, G. S., Liu, Y., Yao, W. F., & Luo, G. J. (2016). Alpha7 nicotinic acetylcholine receptor activation attenuated intestine-derived acute lung injury. The Journal of Surgical Research, 201(2), 258-65. https://doi.org/10.1016/j.jss.2015.10.046
He Y, et al. Alpha7 Nicotinic Acetylcholine Receptor Activation Attenuated Intestine-derived Acute Lung Injury. J Surg Res. 2016;201(2):258-65. PubMed PMID: 27020805.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Alpha7 nicotinic acetylcholine receptor activation attenuated intestine-derived acute lung injury. AU - He,Ye, AU - Ye,Zhi-Qiang, AU - Li,Xiang, AU - Zhu,Guo-Song, AU - Liu,Yue, AU - Yao,Wei-Feng, AU - Luo,Gang-Jian, Y1 - 2015/11/06/ PY - 2015/08/23/received PY - 2015/10/07/revised PY - 2015/10/30/accepted PY - 2016/3/30/entrez PY - 2016/3/30/pubmed PY - 2016/8/23/medline KW - Acute lung injury KW - Apoptosis KW - Intestinal ischemia–reperfusion KW - TLR4/NF-κB KW - α7nAChR SP - 258 EP - 65 JF - The Journal of surgical research JO - J. Surg. Res. VL - 201 IS - 2 N2 - BACKGROUND: Intestinal ischemia-reperfusion (IIR) could lead to acute lung injury, associated with severe alveolar epithelial cells inflammatory and oxidative injury. Alpha7 nicotinic acetylcholine receptor (α7nAChR) is an essential component of the cholinergic anti-inflammatory pathway. The aim of this study was to investigate the important role of α7nAChR on the lung subjected to IIR. METHODS: Thirty-two Sprague-Dawley rats were randomly divided into four groups (n = 8 in each): sham group (group S), model group (group M), α7nAChR agonist PNU-282987-treated group (group PNU), and specific α7nAChR antagonist methyllycaconitine-treated group (group MLA). Intestinal IR damage was induced by clamping the superior mesenteric artery for 75 min, followed by a 120-min reperfusion. All rats were killed at 2 h after release of the clamps. The histologic examination of lungs was made, and lung water content was detected. Expression levels of malondialdehyde, tumor necrosis factor alpha, interleukin-6, and superoxide dismutase activity of the lungs were detected. Additionally, expression level of toll-like receptor (TLR)4 and nuclear factor-kappaB (NF-κB p65) in the nucleus of lung tissue and apoptosis-related protein (Bax, Bcl-2, and cleaved-caspase3) were detected using Western blot. RESULTS: Lungs were damaged after intestine IR, manifested by higher lung water content, histologic score, concentrations of interleukin-6, tumor necrosis factor alpha, and malondialdehyde of group M than those of group S, accompanied with decreased superoxide dismutase activity (P < 0.05). PNU treatment could significantly improve the pulmonary function of rats subjected to IIR. These effects of activation of α7nAChR were associated with suppression of TLR4/NF-κB pathway and subsequent reduction of apoptosis-related protein. However, MLA treatment aggravated lung injury. CONCLUSIONS: α7nAChR plays a role in acute lung injury induced by IIR via attenuating lung oxidative stress and inflammation through suppression of TLR4/NF-κB pathway, resulting in reduction of apoptosis in the lung. SN - 1095-8673 UR - https://www.unboundmedicine.com/medline/citation/27020805/Alpha7_nicotinic_acetylcholine_receptor_activation_attenuated_intestine_derived_acute_lung_injury_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-4804(15)01080-X DB - PRIME DP - Unbound Medicine ER -