title: Acute nicotine treatment attenuates lipopolysaccharide-induced cognitive dysfunction by increasing BDNF expression and inhibiting neuroinflammation in the rat hippocampus.
abstract: Although nicotine has been shown to improve cognitive function in various studies, the mechanisms underlying acute nicotine treatment-induced neuroprotection remain incompletely understood. In this study, we evaluated the effect of acute nicotine treatment on the cognitive impairment induced by lipopolysaccharide (LPS) and explored the underlying mechanism. We found that acute nicotine injection markedly attenuated LPS-elicited cognitive deficits and suppressed the strong LPS-induced release of IL-1β, IL-6, and TNF-α into serum and the dorsal hippocampus at 4 and 24h after LPS injection. Western blot analysis indicated a clear increase in the levels of cleaved caspase-3 in LPS-treated animals but not in nicotine- or saline-treated animals. Furthermore, nicotine administration led to a significant increase in BDNF mRNA expression at 4 and 24h and in BDNF protein expression at 24h after LPS injection in the dorsal hippocampus. Taken together, acute nicotine administration attenuated LPS-induced cognitive dysfunction, and this neuroprotective effect may be related to the up-regulation of BDNF and the inhibition of neuroinflammation and apoptosis-related proteins in the dorsal hippocampus.
authors.affiliation: Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, PR China.
authors.forename: Penghui
authors.initials: P
authors.lastname: Wei
authors.affiliation: First Department of Surgery, Hospital affiliated with Shandong University of Traditional Chinese Medicine, Jinan, PR China.
authors.forename: Qingshen
authors.initials: Q
authors.lastname: Liu
authors.affiliation: Department of Cryomedicine, Qilu Hospital, Shandong University, Jinan, PR China.
authors.forename: Dong
authors.initials: D
authors.lastname: Li
authors.affiliation: Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, PR China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Zheng
authors.affiliation: Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, PR China.
authors.forename: Jinfeng
authors.initials: J
authors.lastname: Zhou
authors.affiliation: Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, PR China. Electronic address: ljj9573@163.com.
authors.forename: Jianjun
authors.initials: J
authors.lastname: Li
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D053148:Caspase 3 / Q000378:metabolism; D003072:Cognition Disorders / Q000188:drug therapy* / Q000378:metabolism / Q000523:psychology; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D009538:Nicotine / Q000494:pharmacology* / Q000627:therapeutic use; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D019208:Brain-Derived Neurotrophic Factor; D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D018696:Neuroprotective Agents; D014409:Tumor Necrosis Factor-alpha; D009538:Nicotine; D053148:Caspase 3
keywords: Acute nicotine treatment; Brain-derived neurotrophic factor (BDNF); Cognitive dysfunction; Lipopolysaccharide (LPS); Neuroinflammation