scholarly journals Effects of anesthetic method on inflammatory response in patients with Parkinson’s disease: a randomized controlled study

2020 ◽  
Author(s):  
Won Jung Hwang ◽  
Min Ah Joo ◽  
Jin Joo
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
General Anesthesia ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Surgical Stress ◽  
Neutrophil Migration ◽  
Controlled Study ◽  
Group I ◽  
Tnf Α

Abstract BackgroundThe pathogenesis of Parkinson’s disease (PD) involves degeneration of dopaminergic neurons, which is influenced by innate and adaptive immunity. IL-17 is a characteristic cytokine secreted by Th17 cells, which acts as a powerful stimulator of neutrophil migration and infiltration and promotes the secretion of inflammatory cytokines. General anesthesia and surgical stress induce immune and inflammatory responses that activate the immunosuppressive mechanism in the perioperative period. The present study investigated changes in levels of inflammatory cytokines, such as IL-17, IL-1β, and TNF-α, in patients with PD undergoing general anesthesia with inhalational anesthetics or TIVA.MethodsAdult patients, aged 40–75 years, scheduled for cerebral stimulator implantation were enrolled. Upon arrival at the operating theater, patients were allocated to the inhalational (I) or TIVA (T) group using block randomization. In group I, anesthesia was induced by tracheal intubation 1–2 min after intravenous administration of propofol (1–2 mg/kg) and rocuronium (0.6–1 mg/kg). Thereafter, anesthesia was maintained with 1–2 vol% sevoflurane, 0.01–0.2 kg/min remifentanil, and O2/air (FiO2 0.4). In group T, propofol (3–6 µg/mL), remifentanil (2–6 ng/mL), and rocuronium (0.6–1 mg/kg) were administered using target controlled infusion (TCI) for induction of anesthesia. Blood samples were obtained preoperatively (T0), 2 h after induction of anesthesia (T1), and 24 h after surgery (T2). IL-17, IL-1β, and TNF-α levels were evaluated by ELISA.ResultsSerum levels of IL-17 were elevated at T2 in group I compared to group T but the difference was not statistically significant. IL-1β tended to be greater in group I compared to group T, but the differences were not significant. (Fig. 3). TNF-α was slightly higher at all time points in group T and showed a tendency to increase at T2 in both groups, but this was not statistically significant (Fig. 4).ConclusionsTIVA may be useful for inhibiting neuroinflammation by inhibiting the increase in serum levels of IL-17 24 h after implantation surgery. Serum IL-17 level may be used as a biomarker for PD progression.TRIAL REGISTRATION:Clinical Research Information Service of Korea National Institute of Health (CRIS) Identification number: KCT0002061. Registered 25 October 2019 - Retrospectively registered, https://cris.nih.go.kr/cris/search/search_result_st01.jsp?seq=15125

Spinal and general anesthesia produces differential effects on oxidative stress and inflammatory cytokines in orthopedic patients

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Peter A. Aremu ◽  
Abayomi M. Ajayi ◽  
Benneth Ben-Azu ◽  
Olayinka T. Orewole ◽  
Solomon Umukoro
Keyword(s):  
Oxidative Stress ◽  
General Anesthesia ◽  
Inflammatory Cytokines ◽  
Orthopedic Surgery ◽  
Interleukin 6 ◽  
Surgical Stress ◽  
Oxidative Stress Biomarkers ◽  
Differential Effects ◽  
Stress Biomarkers ◽  
Tnf Α

AbstractObjectivesThe contribution of anesthetic procedure to surgical stress and postoperative complications has been attributed to increased oxidative stress and release of inflammatory cytokines. Thus, the levels of oxidative stress biomarkers and inflammatory cytokines in patients with general anesthesia (GA) and spinal anesthesia (SA) that underwent open reduction and internal fixation (ORIF) in orthopedic surgery at Federal Teaching Hospital, Ido-Ekiti, Ekiti state, Nigeria were investigated.MethodsForty patients were randomly distributed into two groups (n = 20) namely GA and SA. Blood samples were collected before and after surgery for estimation of glucose, oxidative stress biomarkers (malondialdehyde [MDA], glutathione, catalase and nitrile) and inflammatory cytokines (tumor necrosis factor-α [TNF-α] and interleukin-6) levels.ResultsThe post-operative blood glucose level was higher than the pre-operative value (p<0.5) in the two groups. There were significant (p<0.05) changes in MDA concentration and catalase activity in patients with GA in the post-operative stage relative to preoperative phase. There were no significant differences in glutathione, nitrite and interleukin-6 contents between the two groups. The patients with SA had higher levels of TNF-α in the post-operative stage.ConclusionsThese findings suggest that anesthesia has differential effects on oxidative stress and inflammatory cytokines in patients with ORIF orthopedic surgery.

scholarly journals Paroxetine suppresses reactive microglia-mediated but not lipopolysaccharide-induced inflammatory responses in primary astrocytes

2019 ◽  
Author(s):  
Xiong Zhang ◽  
Lan-Bing Zhu ◽  
Jia-Hui He ◽  
Hong-Qiu Zhang ◽  
Shu-Ya Ji ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Minor Amount ◽  
Reactive Microglia ◽  
Tnf Α ◽  
Primary Astrocytes ◽  
Underlying Mechanisms ◽  
The Impact

Abstract Background: Astrocytes are the most abundant glial cells in a brain that mediate inflammatory responses and provide trophic support for neurons. We have previously disclosed that paroxetine, a common selective serotonin reuptake inhibitor, ameliorates LPS-induced microglia activation. However, it remains elusive of the role of paroxetine in astrocytic responses. Methods: Isolated primary astrocytes were pretreated with paroxetine and stimulated with different stimuli, lipopolysaccharide (LPS) or microglia conditioned medium pre-activated with LPS (M/Lps). Inflammatory and neurotrophic responses, underlying mechanisms and the impact on neuronal survival were assessed. Results: Paroxetine had no impact on LPS-stimulated iNOS, TNF-α and IL-1β expression, but inhibited M/Lps-induced TNF-α and IL-1β expression in primary astrocytes. Paroxetine suppressed M/Lps- but not LPS-induced activation of NF-κB and had no impact on activation of MAPKs and STAT3. Incubation with the resulted astrocyte conditioned media caused no change in viability of SH-SY5Y cells. BDNF and MANF mRNA expressions were upregulated by M/Lps and paroxetine, respectively. However, M/Lps- or LPS-induced extracellular releases of NO, TNF-α and/or BDNF in astrocytes were in minor amount compared to those by microglia. Conclusions: Paroxetine ameliorates the reactive microglia-mediated inflammatory responses in astrocytes partially via inhibition of NF-κB pathway, but has no impact on LPS-stimulated astrocyte activation. While the effect of paroxetine on secondary astrocytic responses are not robust compared to its effect on the innate immune responses of microglia, the results together may implicate a therapeutic potential of paroxetine against neuroinflammation-associated neurological disorders such as Parkinson’s disease. Keywords: paroxetine, astrocytes, microglia, neuroinflammation, Parkinson’s disease

scholarly journals Punicalagin Prevents Inflammation in LPS-Induced RAW264.7 Macrophages by Inhibiting FoxO3a/Autophagy Signaling Pathway

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2794 ◽  
Author(s):  
Cao ◽  
Chen ◽  
Ren ◽  
Zhang ◽  
Tan ◽  
...  
Keyword(s):  
Western Blot ◽  
Signaling Pathway ◽  
Inflammatory Cytokines ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Inflammatory Responses ◽  
Raw264.7 Macrophages ◽  
Tnf Α ◽  
Autophagy Inhibition ◽  
Pro Inflammatory Cytokines

Punicalagin, a hydrolysable tannin of pomegranate juice, exhibits multiple biological effects, including inhibiting production of pro-inflammatory cytokines in macrophages. Autophagy, an intracellular self-digestion process, has been recently shown to regulate inflammatory responses. In this study, we investigated the anti-inflammatory potential of punicalagin in lipopolysaccharide (LPS) induced RAW264.7 macrophages and uncovered the underlying mechanisms. Punicalagin significantly attenuated, in a concentration-dependent manner, LPS-induced release of NO and decreased pro-inflammatory cytokines TNF-α and IL-6 release at the highest concentration. We found that punicalagin inhibited NF-κB and MAPK activation in LPS-induced RAW264.7 macrophages. Western blot analysis revealed that punicalagin pre-treatment enhanced LC3II, p62 expression, and decreased Beclin1 expression in LPS-induced macrophages. MDC assays were used to determine the autophagic process and the results worked in concert with Western blot analysis. In addition, our observations indicated that LPS-induced releases of NO, TNF-α, and IL-6 were attenuated by treatment with autophagy inhibitor chloroquine, suggesting that autophagy inhibition participated in anti-inflammatory effect. We also found that punicalagin downregulated FoxO3a expression, resulting in autophagy inhibition. Overall these results suggested that punicalagin played an important role in the attenuation of LPS-induced inflammatory responses in RAW264.7 macrophages and that the mechanisms involved downregulation of the FoxO3a/autophagy signaling pathway.

scholarly journals Relationships of gut microbiota, short-chain fatty acids, inflammation, and the gut barrier in Parkinson’s disease

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Velma T. E. Aho ◽  
Madelyn C. Houser ◽  
Pedro A. B. Pereira ◽  
Jianjun Chang ◽  
Knut Rudi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Fatty Acids ◽  
Parkinson's Disease ◽  
Gut Microbiota ◽  
Inflammatory Responses ◽  
Disease Onset ◽  
Short Chain Fatty Acids ◽  
Short Chain ◽  
Dependent Manner ◽  
Chain Fatty Acids

Abstract Background Previous studies have reported that gut microbiota, permeability, short-chain fatty acids (SCFAs), and inflammation are altered in Parkinson’s disease (PD), but how these factors are linked and how they contribute to disease processes and symptoms remains uncertain. This study sought to compare and identify associations among these factors in PD patients and controls to elucidate their interrelations and links to clinical manifestations of PD. Methods Stool and plasma samples and clinical data were collected from 55 PD patients and 56 controls. Levels of stool SCFAs and stool and plasma inflammatory and permeability markers were compared between patients and controls and related to one another and to the gut microbiota. Results Calprotectin was increased and SCFAs decreased in stool in PD in a sex-dependent manner. Inflammatory markers in plasma and stool were neither intercorrelated nor strongly associated with SCFA levels. Age at PD onset was positively correlated with SCFAs and negatively correlated with CXCL8 and IL-1β in stool. Fecal zonulin correlated positively with fecal NGAL and negatively with PD motor and non-motor symptoms. Microbiota diversity and composition were linked to levels of SCFAs, inflammatory factors, and zonulin in stool. Certain relationships differed between patients and controls and by sex. Conclusions Intestinal inflammatory responses and reductions in fecal SCFAs occur in PD, are related to the microbiota and to disease onset, and are not reflected in plasma inflammatory profiles. Some of these relationships are distinct in PD and are sex-dependent. This study revealed potential alterations in microbiota-host interactions and links between earlier PD onset and intestinal inflammatory responses and reduced SCFA levels, highlighting candidate molecules and pathways which may contribute to PD pathogenesis and clinical presentation and which warrant further investigation.

Regulation of astrocyte inflammatory responses by the Parkinson's disease‐associated gene DJ–1

2009 ◽  
Vol 23 (8) ◽  
pp. 2478-2489 ◽  
Author(s):  
Jens Waak ◽  
Stephanie S. Weber ◽  
Andrea Waldenmaier ◽  
Karin Görner ◽  
Marianna Alunni‐Fabbroni ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inflammatory Responses

A crossover, controlled study comparing pergolide with bromocriptine as an adjunct to levodopa for the treatment of Parkinson's disease

Neurology ◽  
1995 ◽  
Vol 45 (Issue 3, Supplement 3) ◽  
pp. S22-S27 ◽  
Author(s):  
G. Pezzoli ◽  
E. Martignoni ◽  
C. Pacchetti ◽  
V. Angeleri ◽  
P. Lamberti ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Controlled Study

To Compare Frequency of Sore Throat in Early Postop period in General Anesthesia and Endotracheal Intubation for Abdominal Surgeries who are given Dexamethasone and Normal Saline

2021 ◽  
Vol 15 (6) ◽  
pp. 1227-1229
Author(s):  
R. Farooqi ◽  
T. Iqbal ◽  
M. S. Mehmood ◽  
Z. Y. Bhatti ◽  
F. Liaquat
Keyword(s):  
General Anesthesia ◽  
Sore Throat ◽  
Endotracheal Intubation ◽  
Normal Saline ◽  
Controlled Study ◽  
Control Group ◽  
Chi Square ◽  
Group I ◽  
Chi Square Test ◽  
Group Ii

Aim: To Compare frequency of sore throat in early post operative period among patients undergoing general anaesthesia and endotracheal intubation for abdominal surgeries who are given dexamethasone and normal saline. Study Design: Randomized controlled study Setting: Department of Anesthesia/ ICU, Sheikh Zayed Hospital, Lahore Duration of study: Six months i.e. 25-09-2009 to 25-03-2010. Methodology: 120 patients undergoing elective general surgery on abdomen were selected. They were divided into two groups. Group I received dexamethasone 8mg (2ml) I/V pre-operatively and group II received 2ml normal saline I/V pre-operatively. Chi square test was used. Visual analogue (VAS) scale was used for recording sore throat. The VAS score ≤4 was considered as no sore throat and VAS scores>4 were considered as the sore throat. Results: Frequency of post-operative sore throat after the first 24 hours following GA and endotracheal intubation was lower in group (I) as compared to the control group (II). Eleven (20%) patients with dexamethasone had post-operative sore throat compared to thirty one (56.3%) patients in control group. (p<0.01). Conclusion: Pre-operative use of dexamethasone was associated with decreased incidence of post-operative sore throat. Keywords: Visual analogue scale (VAS), Post-operative sore throat, general anesthesia

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