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

Wei, Penghui; Zheng, Qiang; Liu, Hui; Zhou, Jinfeng; Dong, Li; Zhou, Huixia; Li, Jing; Ji, Fucheng; Tang, Wenxi; Li, Jianjun

doi:10.1093/ntr/ntx157

Cited by 34 publications

(30 citation statements)

References 26 publications

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“…BDNF-TrkB signaling modulates the pain process by regulating neuroinflammation which has been reported in other pathological pain models as well [16,17]. Glial cells play an important role in the development of neuroinflammatory and neuropathic pain.…”

Section: Discussionmentioning

confidence: 81%

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BDNF promotes activation of astrocytes and microglia contributing to neuroinflammation and mechanical allodynia in cyclophosphamide-induced cystitis

Ding

Chen

et al. 2020

J Neuroinflammation

107

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Background: Patients with interstitial cystitis/bladder pain syndrome (IC/BPS) often grieve over a low quality of life brought about by chronic pain. In our previous studies, we determined that neuroinflammation of the spinal dorsal horn (SDH) was associated with mechanisms of interstitial cystitis. Moreover, it has been shown that brain-derived neurotrophic factor (BDNF) participates in the regulation of neuroinflammation and pathological pain through BDNF-TrkB signaling; however, whether it plays a role in cyclophosphamide (CYP)-induced cystitis remains unclear. This study aimed to confirm whether BDNF-TrkB signaling modulates neuroinflammation and mechanical allodynia in CYP-induced cystitis and determine how it occurs. Methods: Systemic intraperitoneal injection of CYP was performed to establish a rat cystitis model. BDNF-TrkB signaling was modulated by intraperitoneal injection of the TrkB receptor antagonist, ANA-12, or intrathecal injection of exogenous BDNF. Mechanical allodynia in the suprapubic region was assessed using the von Frey filaments test. The expression of BDNF, TrkB, p-TrkB, Iba1, GFAP, p-p38, p-JNK, IL-1β, and TNF-α in the L6-S1 SDH was measured by Western blotting and immunofluorescence analysis. Results: BDNF-TrkB signaling was upregulated significantly in the SDH after CYP was injected. Similarly, the expressions of Iba1, GFAP, p-p38, p-JNK, IL-1β, and TNF-α in the SDH were all upregulated. Treatment with ANA-12 could attenuate mechanical allodynia, restrain activation of astrocytes and microglia and alleviate neuroinflammation. Besides, the intrathecal injection of exogenous BDNF further decreased the mechanical withdrawal threshold, promoted activation of astrocytes and microglia, and increased the release of TNF-α and IL-1β in the SDH of our CYP-induced cystitis model. Conclusions: In our CYP-induced cystitis model, BDNF promoted the activation of astrocytes and microglia to release TNF-α and IL-1β, aggravating neuroinflammation and leading to mechanical allodynia through BDNF-TrkB-p38/JNK signaling.

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Section: Discussionmentioning

confidence: 81%

“…A large amount of evidence suggests that neuroinflammation can lead to and aggravate pathological pain [15]. Previous studies have reported that BDNF-TrkB signaling can affect pain modulation by regulating neuroinflammation in some pathological pain models [16,17].…”

Section: Introductionmentioning

confidence: 99%

BDNF promotes activation of astrocytes and microglia contributing to neuroinflammation and mechanical allodynia in cyclophosphamide-induced cystitis

Ding

Chen

et al. 2020

J Neuroinflammation

107

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“…BDNF was an important neurotrophic factor, regulating not only learning and memory, but also stress and motivation (Li and Wolf, 2015 ). Previous studies have shown that surgery in aged rodents largely reduced the expression of BDNF in the hippocampus of brain, leading to the decrease of synaptic plasticity and neuronal loss (Fan et al, 2016 ; Wei et al, 2018 ). In this study, A10E was shown to prevent surgery-induced decrease of BDNF in the hippocampus of aged mice, indicating that A10E might act on BDNF to enhance cognitive performance.…”

Section: Discussionmentioning

confidence: 99%

Tacrine(10)-Hupyridone Prevents Post-operative Cognitive Dysfunction via the Activation of BDNF Pathway and the Inhibition of AChE in Aged Mice

Chen

et al. 2018

Front. Cell. Neurosci.

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Post-operative cognitive dysfunction (POCD) could cause short-term or long-term cognitive disruption lasting weeks or months after anesthesia and surgery in elderly. However, no effective treatment of POCD is currently available. Previous studies indicated that the enhancement of brain-derived neurotrophic factor (BDNF) expression, and the elevation the cholinergic system, might be effective to prevent POCD. In this study, we have discovered that tacrine(10)-hupyridone (A10E), a novel acetylcholinesterase (AChE) inhibitor derived from tacrine and huperzine A, could prevent surgery-induced short-term and long-term impairments of recognition and spatial cognition, as evidenced by the novel object recognition test and Morris water maze (MWM) tests, in aged mice. Moreover, A10E significantly increased the expression of BDNF and activated the downstream Akt and extracellular regulated kinase (ERK) signaling in the surgery-treated mice. Furthermore, A10E substantially enhanced choline acetyltransferase (ChAT)-positive area and decreased AChE activity, in the hippocampus regions of surgery-treated mice, indicating that A10E could prevent surgery-induced dysfunction of cholinergic system, possibly via increasing the synthesis of acetylcholine and the inhibition of AChE. In conclusion, our results suggested that A10E might prevent POCD via the activation of BDNF pathway and the inhibition of AChE, concurrently, in aged mice. These findings also provided a support that A10E might be developed as a potential drug lead for POCD.

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“…It is reported that nicotine is able to treat cognitive dysfunction after partial hepatectomy in aged mice. The underlying mechanism might be activation of BDNF/TrkB signalling pathway and inhibition of NF‐κB signalling pathway in hippocampus . In addition, BDNF/TrkB pathway can modulate several signalling pathways in breast cancer, including Akt/PI3K, Jak/STAT, NF‐κB, UPAR/UPA and Wnt/β‐catenin, and BDNF promotes neurite growth primarily by activating the JAK/STAT pathway .…”

Section: Discussionmentioning

confidence: 99%

“…The underlying mechanism might be activation of BDNF/TrkB signalling pathway and inhibition of NF-jB signalling pathway in hippocampus. [33] In addition, BDNF/TrkB pathway can modulate several signalling pathways in breast cancer, including Akt/PI3K, Jak/STAT, NF-jB, UPAR/UPA and Wnt/b-catenin, [34] and BDNF promotes neurite growth primarily by activating the JAK/STAT pathway. [35] These studies suggest that activation of BDNF/TrkB signalling pathway leads to inhibition of NF-jB signalling pathway by activating STAT signalling, and ultimately regulating the expression of inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

Brain-derived neurotrophic factor fused with a collagen-binding domain inhibits neuroinflammation and promotes neurological recovery of traumatic brain injury mice via TrkB signalling

Yin

Zhao

Qiu

2020

Journal of Pharmacy and Pharmacology

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Objectives As one of the vital nutrient factors in central nervous system (CNS), brain‐derived neurotrophic factor (BDNF) can significantly attenuate neuron damage and promote neurogenesis. Nevertheless, little research has been conducted on regulating the effect of BDNF on the inflammatory response after traumatic brain injury (TBI). Methods In this study, we used BDNF fused with a collagen‐binding domain (CBD‐BDNF) to maintain a sufficient concentration of BDNF in the TBI hemisphere, and then, the regulatory effects of BDNF and CBD‐BDNF on the inflammatory response of microglia were investigated both on a TBI mice model in vivo and LPS‐stimulated microglia experiment in vitro. Key findings The results revealed that BDNF and CBD‐BDNF had similar effects on attenuating the pro‐inflammatory reactions but promoting anti‐inflammatory responses of microglia induced by LPS in vitro. Furthermore, CBD‐BDNF significantly improved the neurological behaviours of TBI mice and alleviated the inflammatory reaction after TBI, while BDNF had weaker effects compared with those of CBD‐BDNF. Additionally, the TrkB inhibitor K252a significantly inhibited the above effects of CBD‐BDNF. Conclusions In conclusion, CBD‐BDNF can promote the anti‐inflammatory function of microglia and neurological recovery of TBI mice through TrkB signalling.

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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

Cited by 34 publications

References 26 publications

BDNF promotes activation of astrocytes and microglia contributing to neuroinflammation and mechanical allodynia in cyclophosphamide-induced cystitis

BDNF promotes activation of astrocytes and microglia contributing to neuroinflammation and mechanical allodynia in cyclophosphamide-induced cystitis

Tacrine(10)-Hupyridone Prevents Post-operative Cognitive Dysfunction via the Activation of BDNF Pathway and the Inhibition of AChE in Aged Mice

Brain-derived neurotrophic factor fused with a collagen-binding domain inhibits neuroinflammation and promotes neurological recovery of traumatic brain injury mice via TrkB signalling

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