scholarly journals ONE-LUNG VENTILATION PATIENTS: CLINICAL CONTEXT OF ADMINISTRATION OF DIFFERENT DOSES OF DEXMEDETOMIDINE

Author(s):  
Hui Jiang ◽  
Yu Kang ◽  
Chunlin Ge ◽  
Zhengying Zhang ◽  
Yan Xie

Background: To investigate the effects of different doses of dexmedetomidine on inflammatory response, oxidative stress, cerebral tissue oxygen saturation (SctO2) and intrapulmonary shunt in patients undergoing one-lung ventilation (OLV). Methods: Sixty patients undergoing open pulmonary lobectomy in our hospital from January 2016 to December 2017 were enrolled and randomly divided into high-dose dexmedetomidine group (group D1, 1 μg/kg, n=20), low-dose dexmedetomidine group (group D2, 0.5 μg/kg, n=20) and control group (group C, n=20). Then, arterial blood and internal jugular venous blood were taken before anesthesia induction (T0) and at 15 min after two-lung ventilation (T1) and 5 min (T2) and 30 min (T3) after OLV for later use. Next, the changes in hemodynamic parameters [mean arterial pressure (MAP), heart rate (HR) and pulse oxygen saturation (SpO2)] of patients were observed in each group. Enzyme-linked immunosorbent assay (ELISA) was carried out to detect serum inflammatory factors such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) and oxidative stress indicators [superoxide dismutase (SOD) and malondialdehyde (MDA)]. The changes in SctO2, arterial partial pressure of oxygen (PaO2) and intrapulmonary shunt Qs/Qt were observed. Additionally, the changes in lung function indicators like lung dynamic compliance (Cdyn) and airway peak pressure (Ppeak) were determined. Results: There were no statistically significant differences in the MAP, HR and SpO2 among three groups at each observation time point (P>0.05). At T2 and T3, the levels of serum IL-6, TNF-α and IL-8 were obviously decreased in group D1 and D2 compared with those in group C (P<0.05), and the decreases in group D1 were overtly larger than those in group D2, and the decreases at T3 were markedly greater than those at T2 (P<0.05). In comparison with group C, group D1 and D2 had notably reduced levels of serum reactive oxygen species (ROS) and MDA (P<0.05) and remarkably increased SOD content (P<0.05) at T2 and T3, and the effects were markedly better in group D1 than those in group D2. Besides, they were significantly superior at T3 to those at T2 (P<0.05). The SctO2 in group D1 and D2 was evidently lowered at T2 and T3 compared with that at T0, and the decrease in group D1 was distinctly smaller than that in group D2 (P<0.05). The Qs/Qt was significantly lower in group D1 and D2 than that in group C at T2 and T3 (P<0.05), while the PaO2 content was notably raised (P<0.05), and the decrease and increase were significantly larger in group D1 than those in group D2, and they were obviously greater at T3 to those at T2 (P<0.05). At T0 and T1, no significant differences were detected in the Cdyn, Pplat and Ppeak among three groups. At T2 and T3, the Cdyn was significantly elevated, while the Pplat and Ppeak overtly declined (P<0.05), and group D1 had greater changes in comparison with group D2, and the changes were obviously more evident at T3 to those at T2 (P<0.05). Conclusions: Dexmedetomidine effectively ameliorates inflammatory response and oxidative stress, lowers oxygenation, Qs/Qt and the decrease in SctO2 and improves lung function during OLV, with good efficacy.

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Neuza Costa ◽  
Thaisa Verediano ◽  
Mirelle Viana ◽  
Maria Vaz-Tostes

Abstract Objectives To investigate the prebiotic effect of yacon, source of fructooligosaccharides (FOS), on the integrity of the intestinal barrier, inflammatory response and oxidative stress in rats with induced colon cancer. Methods 44 adult Wistar rats were distributed into 4 groups: S (without colon cancer and yacon; n = 10); C (with colon cancer without yacon; n = 12); Y (without colon cancer with yacon; n = 10); and CY (with colon cancer and yacon; n = 12). Animals of groups S and C received AIN-93 M diet and animals of groups Y and CY received the same diet but added with yacon flour containing 28.95% FOS, to provide 5% FOS in the diet, for 16 weeks. From week 4 to 8, the animals of C and CY groups received an intraperitoneal dose of 25 mg/kg body weight of 1.2-dimethylhydrazine (DMH-Sigma®) once a week. In the last week, 24h-urine collection was performed for intestinal permeability analysis using lactulose and mannitol. Blood sample was collected for the analysis of IL-10 and IL-12 cytokines (Milliplex® Map, Luminex®) and total antioxidant capacity - TAC (Elabscience®). Large intestine was collected for intraluminal pH, short chain fatty acids - SCFA (HPLC) and immunoglobulin A – sIgA (Cloud-Clone®) analysis. Normal distributed data were analyzed by Two-way ANOVA, followed by Newman-Keuls (p < 0.05), using GraphPad Prism®, version 7. Results Cancer-induced animals showed higher TNF-α, SCFA (acetate, propionate and butirate), and lower TAC. Yacon reduced intraluminal pH and lactulose/mannitol ratio, increased propionic acid in the feces, but showed no effect on IL-10, IL-12, TNF-α, and IL-10/IL-12 ratio. The levels of sIgA were increased only in the group fed yacon without cancer (group Y). Mannitol and TAC were higher in CY group, showing a significant interaction of yacon and colon cancer. Conclusions Yacon reduced pH, intestinal permeability and the oxidative stress associated with colon cancer. The local immunity (sIgA) was raised, although no effect was observed on cytokines with yacon consumption. Yacon is a rich source of FOS wich improves the intestinal barrier and mucosal immunity, particularly in healthy animals. Funding Sources CNPq, FAPES.


Author(s):  
Rukiye Nalan Tiftik ◽  
Meryem Temiz-Reşitoğlu ◽  
Demet Sinem Güden ◽  
Gülsen Bayrak ◽  
İsmail Ün ◽  
...  

It has been clearly indicated that osteoarthritis (OA) is an inflammatory and degenerative disease that could be promoted by Rho-kinase (ROCK); however, little is known about the role of ROCK/inhibitor κB alpha (IκB-α)/nuclear factor-κB (NF-κB) p65 pathway activation in interleukin-1β (IL-1β) induced inflammatory response and oxidative stress in primary human chondrocytes. To test this hypothesis, we focused on determining ROCK-II, IκB-α, p-IκB-α, NF-κB p65, p-NF-κB p65, IL-6, tumor necrosis factor alpha (TNF-α), cyclooxygenase-2 (COX-2), p22phox, and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subtype 4 (NOX4) protein expression, ROCK-II activity, NADPH oxidase levels, and total antioxidant capacity (TAC) in the presence and absence of ROCK-inhibitor fasudil. IL-1β (2 ng·mL–1, 24 h) increased the expression of ROCK-II, p-IκB-α, NF-κB p65, p-NF-κB p65, IL-6, TNF-α, COX-2, and p22phox proteins, and decreased the expression of IκB-α, and the NOX4 protein level did not alter. ROCK activity and NADPH oxidase levels were increased, whereas the TAC was decreased by IL-1β. Fasudil (10−5–10−7 M) reversed all these changes induced by IL-1β. These results demonstrate that ROCK/IκB-α/NF-κB p65 pathway activation contributes to the IL-1β-induced inflammatory response and oxidative stress, and thus, ROCK inhibition might be a beneficial treatment option for OA patients mainly based on its anti-inflammatory and antioxidant effects.


2010 ◽  
Vol 58 (20) ◽  
pp. 10840-10846 ◽  
Author(s):  
Wuyang Huang ◽  
Subhadeep Chakrabarti ◽  
Kaustav Majumder ◽  
Yanyan Jiang ◽  
Sandra T. Davidge ◽  
...  

2021 ◽  
Author(s):  
Hui-Ting Li ◽  
Fang Tan ◽  
Tian-Hua Zhang ◽  
Long-Hui Cao ◽  
Hong-ying Tan ◽  
...  

Abstract Background: Curcumin has attracted much attention due to its wide range of therapeutic effects. In this study, we used serum collected from patients undergoing one-lung ventilation (OLV) to establish an in vitro acute lung injury (ALI) model to explore the potential protective mechanism of curcumin on ALI to provide a new reference for the prevention and treatment of ALI induced by OLV.Methods: A549 cells were treated with 20% serum from patients undergoing OLV to establish an in vitro ALI model. Curcumin, at a dose of 40 μg/ml, was administered two hours prior to this model. The levels of inflammation and oxidative stress markers were observed by Western blot, qRT–PCR, ELISA and reactive oxygen species assay. Additionally, the expression of peroxiredoxin 6 (Prdx6) and proteins involved in the NF-κB signaling pathway were evaluated.Results: Twenty percent of serum collected from patients undergoing OLV downregulated the expression of Prdx6, leading to the activation of the NF-κB signaling pathway, which was associated with the subsequent overproduction of inflammatory cytokines and reactive oxygen species. Pretreatment with curcumin restored Prdx6 downregulation and inhibited NF-κB pathway activation by suppressing the nuclear translocation of P65, eventually reducing inflammation and oxidative stress damage in A549 cells.Conclusions: Prdx6 mediated the protective function of curcumin by inhibiting the activation of the NF-κB pathway in ALI in vitro.


2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Feng Sun ◽  
Haiwei Zhang ◽  
Tianwen Huang ◽  
Jianhui Shi ◽  
Tianli Wei ◽  
...  

Objectives. To investigate the roles of miR-221 in spinal cord injury (SCI) as well as the underlying mechanism. Methods. A mouse model of SCI was generated and used to examine dynamic changes in grip strength of the mouse upper and lower limbs. The expression of miR-221 and tumor necrosis factor-α (TNF-α) was detected by RT-qPCR and Western blot. Levels of inflammation and oxidative stress in microglia cells of the injured mice overexpressing miR-221 were then measured by ELISA. Bioinformatics analysis and dual-luciferase reporter assay were conducted to identify the miR-221 target. Results. We successfully constructed SCI mouse model. The results of qRT-PCR showed that miR-221 was gradually upregulated in the spinal cord tissue of mice in the SCI group with the prolonged injury time. At the same time, the mRNA and protein of TNF-α gradually decreased. We further confirmed through cell experiments that the inflammatory factors TNF-α and IL-6, as well as iNOS and eROS, were upregulated in spinal cord microglia cells of SCI mice, and upregulation of miR-122 can inhibit their expression. Finally, the luciferase reporter experiment confirmed that miR-122 targeted TNF-α. Conclusions. We present evidence that miR-221 promotes functional recovery of the injured spinal cord through targeting TNF-α, while alleviating inflammatory response and oxidative stress.


2019 ◽  
Vol 20 (7) ◽  
pp. 1800 ◽  
Author(s):  
Yueqin Qiu ◽  
Xuefen Yang ◽  
Li Wang ◽  
Kaiguo Gao ◽  
Zongyong Jiang

This study aimed to explore the effect of L-arginine on lipopolysaccharide (LPS)-induced inflammatory response and oxidative stress in IPEC-2 cells. We found that the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), cluster of differentiation 14 (CD14), nuclear factor-kappaBp65 (NF-κBp65), chemokine-8 (IL-8), tumor necrosis factor (TNF-α) and chemokine-6 (IL-6) mRNA were significantly increased by LPS. Exposure to LPS induced oxidative stress as reactive oxygen species (ROS) and malonaldehyde (MDA) production were increased while glutathione peroxidase (GSH-Px) were decreased in LPS-treated cells compared to those in the control. LPS administration also effectively induced cell growth inhibition through induction of G0/G1 cell cycle arrest. However, compared with the LPS group, cells co-treatment with L-arginine effectively increased cell viability and promoted the cell cycle into the S phase; L-arginine exhibited an anti-inflammatory effect in alleviating inflammation induced by LPS by reducing the abundance of TLR4, MyD88, CD14, NF-κBp65, and IL-8 transcripts. Cells treated with LPS+L-arginine significantly enhanced the content of GSH-Px, while they decreased the production of ROS and MDA compared with the LPS group. Furthermore, L-arginine increased the activity of arginase-1 (Arg-1), while Arg-1 inhibitor abolished the protection of arginine against LPS-induced inflammation and oxidative stress. Taken together, these results suggested that L-arginine exerted its anti-inflammatory and antioxidant effects to protect IPEC-J2 cells from inflammatory response and oxidative stress challenged by LPS at least partly via the Arg-1 signaling pathway.


2020 ◽  
Author(s):  
Fangcheng Fan ◽  
Yangwen Ai ◽  
Qingshan Liu ◽  
Yong Cheng

Abstract It remains unclear whether acute unpleasant exercise (AUE) caused by foot shocks leads to gastrointestinal (GI) mucosal injury and bleeding. In this study, we investigated the involvement of inflammatory cytokines in AUE-induced GI mucosal injury/bleeding and oxidative stress by analyzing the expressions of pro-inflammatory (IL-1β, IL-6, TNF-α, and iNOS) and anti-inflammatory (IL-10) cytokines in the hypothalamus and duodenum after foot shocks using PCR. Results showed that the expressions of IL-1β, IL-6, TNF-α, and iNOS were significantly increased following the process, while IL-10 was not activated. These findings suggest that the activation of inflammatory response system (IRS) is closely related to GI mucosal injury/bleeding and oxidative stress induced by AUE caused by foot shocks.


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