scholarly journals Neuroprotective effect of paeonol against isofluraneinduced neuroapoptosis and cognitive dysfunction

2016 ◽  
Vol 15 (10) ◽  
pp. 2173 ◽  
Author(s):  
Jian-Xin Zhang ◽  
Zhi-Ying Li ◽  
Liang Zhao ◽  
Gang Li ◽  
Gui-Lin Cao ◽  
...  
Keyword(s):  
Cognitive Dysfunction ◽  
Neuroprotective Effect

Curcumin Reduces Neuroinflammation and Improves the Impairments of Anesthetics on Learning and Memory by Regulating the Expression of miR-181a-5p

2021 ◽  
pp. 1-9
Author(s):  
Guizhen Liu ◽  
Yuchuan Sun ◽  
Fei Liu
Keyword(s):  
Cognitive Impairment ◽  
Protective Effect ◽  
Learning And Memory ◽  
Cognitive Dysfunction ◽  
Inflammatory Cytokines ◽  
Neuroprotective Effect ◽  
Morris Water Maze Test ◽  
Sprague Dawley ◽  
Protein Levels ◽  
Sprague Dawley Rats

<b><i>Objective:</i></b> The purpose of this study was to explore the role of curcumin (Cur) in isoflurane (ISO)-induced learning and memory dysfunction in Sprague-Dawley rats and further elucidate the mechanism of the protective effect produced by Cur. <b><i>Methods:</i></b> Rat models of cognitive impairment were established by inhaling 3% ISO. The Morris water maze test was used to assess the cognitive function of rats. ELISA and qRT-PCR were used to analyze the protein levels of pro-inflammatory cytokines and expression levels of miR-181a-5p, respectively. <b><i>Results:</i></b> Cur significantly improved the ISO-induced cognitive dysfunction in rats and alleviated the ISO-induced neuroinflammation. miR-181a-5p was overexpressed in ISO-induced rats, while Cur treatment significantly reduced the expression of miR-181a-5p. Overexpression of miR-181a-5p promoted the cognitive impairment and the release of inflammatory cytokines and reversed the neuroprotective effect of Cur. <b><i>Conclusion:</i></b> Cur has a protective effect on ISO-induced cognitive dysfunction, which may be achieved by regulating the expression of miR-181a-5p.

scholarly journals HDAC2 hyperexpression alters hippocampal neuronal transcription and microglial activity in neuroinflammation-induced cognitive dysfunction

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Xiao-Yu Sun ◽  
Teng Zheng ◽  
Xiu Yang ◽  
Le Liu ◽  
Shen-Shen Gao ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Histone Acetylation ◽  
Cognitive Dysfunction ◽  
Memory Impairment ◽  
Dorsal Hippocampus ◽  
Neuroprotective Effect ◽  
Memory Deficits ◽  
Peripheral Inflammation ◽  
Histone Deacetylase 2

Abstract Background Inflammation can induce cognitive dysfunction in patients who undergo surgery. Previous studies have demonstrated that both acute peripheral inflammation and anaesthetic insults, especially isoflurane (ISO), are risk factors for memory impairment. Few studies are currently investigating the role of ISO under acute peri-inflammatory conditions, and it is difficult to predict whether ISO can aggravate inflammation-induced cognitive deficits. HDACs, which are essential for learning, participate in the deacetylation of lysine residues and the regulation of gene transcription. However, the cell-specific mechanism of HDACs in inflammation-induced cognitive impairment remains unknown. Methods Three-month-old C57BL/6 mice were treated with single versus combined exposure to LPS injected intraperitoneally (i.p.) to simulate acute abdominal inflammation and isoflurane to investigate the role of anaesthesia and acute peripheral inflammation in cognitive impairment. Behavioural tests, Western blotting, ELISA, immunofluorescence, qRT-PCR, and ChIP assays were performed to detect memory, the expressions of inflammatory cytokines, HDAC2, BDNF, c-Fos, acetyl-H3, microglial activity, Bdnf mRNA, c-fos mRNA, and Bdnf and c-fos transcription in the hippocampus. Results LPS, but not isoflurane, induced neuroinflammation-induced memory impairment and reduced histone acetylation by upregulating histone deacetylase 2 (HDAC2) in dorsal hippocampal CaMKII+ neurons. The hyperexpression of HDAC2 in neurons was mediated by the activation of microglia. The decreased level of histone acetylation suppressed the transcription of Bdnf and c-fos and the expressions of BDNF and c-Fos, which subsequently impaired memory. The adeno-associated virus ShHdac2, which suppresses Hdac2 after injection into the dorsal hippocampus, reversed microglial activation, hippocampal glutamatergic BDNF and c-Fos expressions, and memory deficits. Conclusions Reversing HDAC2 in hippocampal CaMKII+ neurons exert a neuroprotective effect against neuroinflammation-induced memory deficits.

scholarly journals Resveratrol ameliorates neuronal apoptosis and cognitive impairment by activating the SIRT1/RhoA pathway in rats after anesthesia with sevoflurane

2021 ◽  
Author(s):  
Qiaoyun Zhou ◽  
Yingfeng Deng ◽  
Xuelian Hu ◽  
Yinye Xu
Keyword(s):  
Signaling Pathway ◽  
Cognitive Dysfunction ◽  
Neuronal Apoptosis ◽  
Neuroprotective Effect ◽  
Postoperative Cognitive Dysfunction ◽  
Male Rats ◽  
Vehicle Group ◽  
Rhoa Signaling ◽  
Bcl2 Expression

Studies have shown that long-term exposure to sevoflurane (SEV) may cause postoperative cognitive dysfunction. This study aimed to investigate the effects of resveratrol (RES) treatment on the changes in the cognitive function of rats after prolonged anesthesia with SEV. Seventy-six adult male rats were used in this study. The SEV model was established under continuous anesthesia for 6 h. Rats were randomly classified into four groups as follows: control, SEV+vehicle, SEV+pre-RES (RES was administered 24 h before establishing the SEV model), and SEV+post-RES (RES was administered 1 h after establishing the SEV model) groups. Neurobehavioral outcomes and the potential mechanism underlying RES-mediated neuroprotection through the SIRT1/RhoA signaling pathway were evaluated. The water maze test showed that long-term exposure to SEV may lead to loss of learning and memory ability in rats (p<0.05). Compared with the SEV+vehicle group, the RES treatment groups showed significantly improved neurobehavioral scores (p<0.05). Additionally, the SEV+pre-RES group had a better outcome than the SEV+vehicle group on days 1 or 2 (p<0.05), unlike the SEV+post-RES group (p>0.05). Western blotting showed that SIRT1, RhoA, and cleaved Caspase-3 (CC3) expression significantly increased in the SEV+vehicle group (p<0.05), while Bcl2 expression decreased (p < 0.05). RES treatment further upregulated SIRT1 and Bcl2 expression and downregulated the expression of RhoA and CC3 (p<0.05). In conclusion, RES treatment improved cognitive dysfunction by reducing neuronal apoptosis in adult rats exposed to SEV. RES partly exerted a neuroprotective effect through the activation of the SIRT1/RhoA signaling pathway.

Neuroprotective effect of SSRI among 781 cancer patients receiving chemotherapy: A URCC CCOP Study

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 9512-9512
Author(s):  
P. Jean-Pierre ◽  
S. Mohile ◽  
G. Morrow ◽  
C. Figueroa-Moseley ◽  
J. Berenberg ◽  
...  
Keyword(s):  
Cancer Patients ◽  
Cognitive Dysfunction ◽  
Psychosocial Functioning ◽  
Neuroprotective Effect ◽  
Repeated Measure ◽  
Attention And Memory ◽  
Component Structure ◽  
Significant Difference ◽  
Wilks Lambda ◽  
Paroxetine Hydrochloride

9512 Background: Cancer and its treatment impact important areas of cognitive function such as attention and memory, which are essential to patients effective psychosocial functioning and quality of life. Previous studies reported that 17% to 75% of cancer patients reported cognitive dysfunction during and after treatment. Few studies, however, have examined the effectiveness of pharmacological interventions to control cancer-related cognitive dysfunction (CRCD). The present study examines the effect of paroxetine hydrochloride (Paxil, P) on CRCD. Methods: The sample included 574 female and 207 male cancer patients between 22 and 87 years. Memory Problems was assessed using a Self-Reported Memory Problem (SRMP) measures derived from the Fatigue Symptom Checklist that relate to memory dysfunction. Cronbach coefficient alpha (α) and a principal components analysis (PCA) were conducted to determine reliability and appropriateness of the SRMP for this sample. A repeated measure ANOVA (r-ANOVA) and t-tests were used to assess changes in mean scores on the SRMP and the effect of P versus placebo. Depression was assessed using the CESD. Results: Scale reliability assessment showed α = .90, supporting the reliability of the SRMP. The PCA revealed a one-component structure that explained 72% of the variance. The r-ANOVA showed a significant difference between scores on the SRMP at baseline (after first chemotherapy cycle, and before P) and follow-up (after four cycles of chemotherapy, after P) (Wilks' Lambda = .99, F (1, 583) = 5.52, p = 0.02). The t-tests also showed a significant effect of P on CRMP (p < 0.05). P had a significant effect after controlling for depression (p < 0.001) Conclusions: CRCD is a serious problem for patients that can be alleviated by P. Future studies should examine the usefulness of other psychotropic agents and combined behavioral and pharmacologic interventions to control CRCD. Supported by NCI Grants U10CA37420, R25CA102618, and 3U01CA116924–04S1. No significant financial relationships to disclose.

Sign in / Sign up

Export Citation Format

Share Document