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Nicotine-Induced Neuroprotection against Cognitive Dysfunction after Partial Hepatectomy Involves Activation of BDNF/TrkB Signaling Pathway and Inhibition of NF-κB Signaling Pathway in Aged Rats.
Nicotine Tob Res. 2018 03 06; 20(4):515-522.NT

Abstract

Introduction

The main purpose of this study was to investigate the effects and possible mechanisms of nicotine pre-treatment on postoperative cognitive dysfunction (POCD) in aged rats.

Methods

Nicotine (0.5 mg/kg) was given i.p. immediately after anesthesia induction. After the Morris water maze test was used to evaluate the rats' spatial learning and memory, serum and hippocampal tissues were harvested 1 and 3 days after intervention. Inflammatory cytokines in the serum were evaluated by Enzyme-linked Immunosorbent Assay (ELISA). Brain-derived neurotrophic factor (BDNF), p-TrkB, neuroinflammation cytokines, NF-κB p65, and cleaved caspase-3 were measured by western blotting; neuronal apoptosis in the hippocampal CA1 region was also evaluated by TUNEL staining.

Results

We found that nicotine markedly attenuated the POCD and reduced the elevated levels of inflammatory cytokines in the serum, including IL-1β and high mobility group box-1 (HMGB1), on postoperative day 1. Additionally, nicotine suppressed the surgery-induced release of IL-1β, TNF-ɑ, HMGB1, and NF-κB p65 in the hippocampus on postoperative day 1 and day 3. In addition, operated rats displayed lower BDNF and p-TrkB in the hippocampus on postoperative day 1, returning to baseline by postoperative day 3. However, nicotine pre-treatment clearly reversed the surgical stress-induced decrease in both BDNF and p-TrkB expression in the hippocampus. Furthermore, nicotine pre-treatment significantly alleviated the surgery-induced increase in the neuronal apoptosis in the hippocampus on postoperative day 1 and day 3.

Conclusions

Our results showed that nicotine-induced neuroprotection against POCD may involve activation of the BDNF/TrkB signaling pathway and inhibition of the NF-κB signaling pathway.

Implications

Nicotine has long been considered a potent therapeutic agent for neuroprotection. This study reported the positive effect of nicotine treatment on cognitive dysfunction after partial hepatectomy in aged rats. Furthermore, the underlying mechanism may involve activation of the BDNF/TrkB signaling pathway and inhibition of the NF-κB signaling pathway in the hippocampus.

Authors+Show Affiliations

Department of Anesthesiology, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China.Department of Anesthesiology, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China.Department of Anesthesiology, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China. Department of Anesthesiology, Shandong Univeristy School of Medicine, Jinan, Shandong, P.R. China.Department of Anesthesiology, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China. Department of Anesthesiology, Shandong Univeristy School of Medicine, Jinan, Shandong, P.R. China.Department of Anesthesiology, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China.Department of Cryomedicine, Qilu Hospital, Shandong University, Jinan, Shandong, P.R. China.Department of Anesthesiology, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China.Department of Anesthesiology, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China.Department of Anesthesiology, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China.Department of Anesthesiology, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China.Department of Anesthesiology, Qilu Hospital of Shandong University (Qingdao), Qingdao, P.R. China.

Pub Type(s)

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

Language

eng

PubMed ID

29065194

Citation

Wei, Penghui, et al. "Nicotine-Induced Neuroprotection Against Cognitive Dysfunction After Partial Hepatectomy Involves Activation of BDNF/TrkB Signaling Pathway and Inhibition of NF-κB Signaling Pathway in Aged Rats." Nicotine & Tobacco Research : Official Journal of the Society for Research On Nicotine and Tobacco, vol. 20, no. 4, 2018, pp. 515-522.
Wei P, Zheng Q, Liu H, et al. Nicotine-Induced Neuroprotection against Cognitive Dysfunction after Partial Hepatectomy Involves Activation of BDNF/TrkB Signaling Pathway and Inhibition of NF-κB Signaling Pathway in Aged Rats. Nicotine Tob Res. 2018;20(4):515-522.
Wei, P., Zheng, Q., Liu, H., Wan, T., Zhou, J., Li, D., Zhou, H., Li, J., Ji, F., Tang, W., & Li, J. (2018). Nicotine-Induced Neuroprotection against Cognitive Dysfunction after Partial Hepatectomy Involves Activation of BDNF/TrkB Signaling Pathway and Inhibition of NF-κB Signaling Pathway in Aged Rats. Nicotine & Tobacco Research : Official Journal of the Society for Research On Nicotine and Tobacco, 20(4), 515-522. https://doi.org/10.1093/ntr/ntx157
Wei P, et al. Nicotine-Induced Neuroprotection Against Cognitive Dysfunction After Partial Hepatectomy Involves Activation of BDNF/TrkB Signaling Pathway and Inhibition of NF-κB Signaling Pathway in Aged Rats. Nicotine Tob Res. 2018 03 6;20(4):515-522. PubMed PMID: 29065194.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nicotine-Induced Neuroprotection against Cognitive Dysfunction after Partial Hepatectomy Involves Activation of BDNF/TrkB Signaling Pathway and Inhibition of NF-κB Signaling Pathway in Aged Rats. AU - Wei,Penghui, AU - Zheng,Qiang, AU - Liu,Hui, AU - Wan,Tiantian, AU - Zhou,Jinfeng, AU - Li,Dong, AU - Zhou,Haipeng, AU - Li,Jing, AU - Ji,Fucheng, AU - Tang,Wenxi, AU - Li,Jianjun, PY - 2016/12/20/received PY - 2017/07/10/accepted PY - 2017/10/25/pubmed PY - 2019/7/26/medline PY - 2017/10/25/entrez SP - 515 EP - 522 JF - Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco JO - Nicotine Tob. Res. VL - 20 IS - 4 N2 - Introduction: The main purpose of this study was to investigate the effects and possible mechanisms of nicotine pre-treatment on postoperative cognitive dysfunction (POCD) in aged rats. Methods: Nicotine (0.5 mg/kg) was given i.p. immediately after anesthesia induction. After the Morris water maze test was used to evaluate the rats' spatial learning and memory, serum and hippocampal tissues were harvested 1 and 3 days after intervention. Inflammatory cytokines in the serum were evaluated by Enzyme-linked Immunosorbent Assay (ELISA). Brain-derived neurotrophic factor (BDNF), p-TrkB, neuroinflammation cytokines, NF-κB p65, and cleaved caspase-3 were measured by western blotting; neuronal apoptosis in the hippocampal CA1 region was also evaluated by TUNEL staining. Results: We found that nicotine markedly attenuated the POCD and reduced the elevated levels of inflammatory cytokines in the serum, including IL-1β and high mobility group box-1 (HMGB1), on postoperative day 1. Additionally, nicotine suppressed the surgery-induced release of IL-1β, TNF-ɑ, HMGB1, and NF-κB p65 in the hippocampus on postoperative day 1 and day 3. In addition, operated rats displayed lower BDNF and p-TrkB in the hippocampus on postoperative day 1, returning to baseline by postoperative day 3. However, nicotine pre-treatment clearly reversed the surgical stress-induced decrease in both BDNF and p-TrkB expression in the hippocampus. Furthermore, nicotine pre-treatment significantly alleviated the surgery-induced increase in the neuronal apoptosis in the hippocampus on postoperative day 1 and day 3. Conclusions: Our results showed that nicotine-induced neuroprotection against POCD may involve activation of the BDNF/TrkB signaling pathway and inhibition of the NF-κB signaling pathway. Implications: Nicotine has long been considered a potent therapeutic agent for neuroprotection. This study reported the positive effect of nicotine treatment on cognitive dysfunction after partial hepatectomy in aged rats. Furthermore, the underlying mechanism may involve activation of the BDNF/TrkB signaling pathway and inhibition of the NF-κB signaling pathway in the hippocampus. SN - 1469-994X UR - https://www.unboundmedicine.com/medline/citation/29065194/Nicotine_Induced_Neuroprotection_against_Cognitive_Dysfunction_after_Partial_Hepatectomy_Involves_Activation_of_BDNF/TrkB_Signaling_Pathway_and_Inhibition_of_NF_κB_Signaling_Pathway_in_Aged_Rats_ L2 - https://academic.oup.com/ntr/article-lookup/doi/10.1093/ntr/ntx157 DB - PRIME DP - Unbound Medicine ER -