Effect of Pregabalin and Diclofenac on tactile allodynia, mechanical hyperalgesia and pro inflammatory cytokine levels (IL-6, IL-1β) induced by chronic constriction injury of the infraorbital nerve in rats

Cytokine ◽  
2018 ◽  
Vol 104 ◽  
pp. 124-129 ◽  
Author(s):  
Junad Khan ◽  
Noma Noboru ◽  
Yoshiki Imamura ◽  
Eli Eliav
Author(s):  
P. F. Zabrodskii ◽  
V. V. Maslyakov ◽  
M. S. Gromov

In experiments on outbred albino rats, it was established that subacute intoxication with ethylene chlorohydrin (0.2 LD50 daily for 4 days) causes a decrease in Th1 and Th2 lymphocytes function to the same extent, diminishes parameters of humoral and cellular immune responses and the content of immunoregulatory cytokines IFN- , IL-2, IL-4 in blood, increases concentrations of pro-inflammatory cytokine IL-6 and anti-inflammatory cytokine IL-10.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lidan Liu ◽  
Chaim Z. Aron ◽  
Cullen M. Grable ◽  
Adrian Robles ◽  
Xiangli Liu ◽  
...  

AbstractLevels of intestinal toll-like receptor 4 (TLR4) impact inflammation in the neonatal gastrointestinal tract. While surfactant protein A (SP-A) is known to regulate TLR4 in the lung, it also reduces intestinal damage, TLR4 and inflammation in an experimental model of necrotizing enterocolitis (NEC) in neonatal rats. We hypothesized that SP-A-deficient (SP-A−/−) mice have increased ileal TLR4 and inflammatory cytokine levels compared to wild type mice, impacting intestinal physiology. We found that ileal TLR4 and proinflammatory cytokine levels were significantly higher in infant SP-A−/− mice compared to wild type mice. Gavage of neonatal SP-A−/− mice with purified SP-A reduced ileal TLR4 protein levels. SP-A reduced expression of TLR4 and proinflammatory cytokines in normal human intestinal epithelial cells (FHs74int), suggesting a direct effect. However, incubation of gastrointestinal cell lines with proteasome inhibitors did not abrogate the effect of SP-A on TLR4 protein levels, suggesting that proteasomal degradation is not involved. In a mouse model of experimental NEC, SP-A−/− mice were more susceptible to intestinal stress resembling NEC, while gavage with SP-A significantly decreased ileal damage, TLR4 and proinflammatory cytokine mRNA levels. Our data suggests that SP-A has an extrapulmonary role in the intestinal health of neonatal mice by modulating TLR4 and proinflammatory cytokines mRNA expression in intestinal epithelium.


2019 ◽  
Vol 317 (5) ◽  
pp. G557-G568 ◽  
Author(s):  
Rose A. Willemze ◽  
David J. Brinkman ◽  
Olaf Welting ◽  
Patricia H. P. van Hamersveld ◽  
Caroline Verseijden ◽  
...  

Clinical trials suggest that vagus nerve stimulation presents an alternative approach to classical immune suppression in Crohn's disease. T cells capable of producing acetylcholine (ChAT+ T cells) in the spleen are essential mediators of the anti-inflammatory effect of vagus nerve stimulation. Besides the spleen, ChAT+ T cells are found abundantly in Peyer’s patches of the small intestine. However, the role of ChAT+ T cells in colitis pathogenesis is unknown. Here, we made use of CD4creChATfl/fl mice (CD4ChAT−/− mice) lacking ChAT expression specifically in CD4+ T cells. Littermates (ChATfl/fl mice) served as controls. In acute dextran sulfate sodium (DSS)-induced colitis (7 days of 2% DSS in drinking water), CD4ChAT−/− mice showed attenuated colitis and lower intestinal inflammatory cytokine levels compared with ChATfl/fl mice. In contrast, in a resolution model of DSS-induced colitis (5 days of 2% DSS followed by 7 days without DSS), CD4ChAT−/− mice demonstrated a worsened colitis recovery and augmented colonic histological inflammation scores and inflammatory cytokine levels as compared with ChATfl/fl mice. In a transfer colitis model using CD4+CD45RBhigh T cells, T cells from CD4ChAT−/− mice induced a similar level of colitis compared with ChATfl/fl T cells. Together, our results indicate that ChAT+ T cells aggravate the acute innate immune response upon mucosal barrier disruption in an acute DSS-induced colitis model, whereas they are supporting the later resolution process of this innate immune-driven colitis. Surprisingly, ChAT expression in T cells seems redundant in the context of T cell-driven colitis. NEW & NOTEWORTHY By using different mouse models of experimental colitis, we provide evidence that in dextran sulfate sodium-induced colitis, ChAT+ T cells capable of producing acetylcholine worsen the acute immune response, whereas they support the later healing phase of this innate immune-driven colitis.


Author(s):  
Sergei G. Levin ◽  
Ekaterina V. Pershina ◽  
Nickolay A. Bugaev-Makarovskiy ◽  
Irina Yu. Chernomorets ◽  
Maxim V. Konakov ◽  
...  

2001 ◽  
Vol 101 (2) ◽  
pp. 185 ◽  
Author(s):  
Andrew STEPTOE ◽  
Gonneke WILLEMSEN ◽  
Natalie OWEN ◽  
Louise FLOWER ◽  
Vidya MOHAMED-ALI

2021 ◽  
Author(s):  
Tingmei Wu ◽  
Haiwen Li ◽  
Huixia Zhou ◽  
Xuemei Hao ◽  
Xiaojun Wang ◽  
...  

Abstract Objective: Enhanced recovery after surgery (ERAS) protocols are established in adults but not fully evaluated in children. This study investigated whether an ERAS protocol improved recovery and influenced postoperative inflammatory cytokine levels in children undergoing surgery for hydronephrosis. Methods: This randomized controlled study included patients who underwent robot-assisted laparoscopic surgery for hydronephrosis at Bayi Children's Hospital (Beijing, China) between October 2018 and September 2019. Patients were randomized to an ERAS group (perioperative ERAS protocol) or control group (standard perioperative management). Outcomes related to postoperative recovery and inflammatory cytokine levels were evaluated. Results: The final analysis included 18 patients in each group. Five patients (27.78%) in each group experienced postoperative complications (abdominal pain, nausea and vomiting, subcutaneous emphysema or fever). The ERAS group had a shorter time to first postoperative flatus than the control group (25 vs. 49 hours; P =0.009), although the time for abdominal drainage flow to reach ≤20 mL/day, time to urinary catheter removal and length of hospital stay did not differ significantly between groups. Preoperative plasma cytokine levels were comparable between groups. Compared with the control group, the ERAS group had a higher IL-6 level on postoperative day 2 ( P <0.05) and a lower concentration of IL-1β on postoperative days 1 and 2 ( P <0.05). Postoperative levels of CRP, TNFα and IL-10 did not differ significantly between groups. Conclusions: ERAS may accelerate postoperative recovery and modulate the postoperative inflammatory response in pediatric patients undergoing robot-assisted laparoscopic pyeloplasty for hydronephrosis.


2017 ◽  
Vol 45 (1) ◽  
pp. 5
Author(s):  
Deniz Uluisik ◽  
Ercan Keskin

Background: Coenzyme Q10 is a well-known cofactor in the mitochondrial electron transport chain required for ATP production. Coenzyme Q10 is recognized as an intracellular antioxidant that protects cell membrane phospholipids, mitochondrial membrane protein, and plasma low-density lipoprotein against oxidative damage caused by free radicals. Diabetes and its complications have been related to increased levels of free radicals and systemic proinflammatory cytokines and to an abnormal lipid profile. The aim of this study was to investigate the effects of coenzyme Q10 supplementation on some cytokine levels in streptozotocin-induced diabetic rats.Materials, Methods & Results: In this study, 38 healthy, adult male rats were used. The rats were divided into 5 groups. All animals were housed in separated cages during the four weeks. The animals in group 1 was fed standard rat pellets for 4 weeks. It was administered at 0.3 mL corn oil intraperitoneally daily for four weeks in group 2 animals. The animals in group 3 was injected intraperitoneally with 10 mg/kg CoQ10 daily for 4 weeks. Group 4 was made diabetic by subcutaneous injections of streptozotocin at dose of 40 mg/kg in 0.1 M citrate buffer (pH 4.5) single daily dose for two days and group 5 was made diabetic by subcutaneous injections of streptozotocin at dose of 40 mg/kg in 0.1 M citrate buffer (pH 4.5) single daily dose for two days and then was injected intraperitoneally with 10 mg/kg CoQ10 daily for 4 weeks. During the experiment, three animals from group 4 and one animals from group 5 were died due to streptozotocin-induced hypoglycemia. At the end of the study, blood samples were taken from all animals. In these blood samples, IL-4, IL-6, IL-10 and TNF-α plasma levels were determined with ELISA using sandwich enzyme-linked immunosorbent method via commercial kits. In this study, IL-4 level as an anti-inflammatory cytokine significantly decreased (P < 0.05) with diabetes induction compared to control group level. IL-10 level in diabetic group was statistically different (P < 0.05) from control group level. CoQ10 application to diabetic animals improved the falling in IL-10 level of diabetic group (P < 0.05). IL-6 and TNF-α levels in diabetic group significantly increased (P < 0.05) in parallel with each other compared to control group levels. The same parameters were reduced (P < 0.05) by CoQ10 application in diabetic animals.Discussion: In this study, the occurred changes in pro- and anti-inflammatory cytokines with experimentally induced diabetes are expected results and these results are consistent with some studies related diabetes. These results may be considered to hazardous effects and inflammation caused by diabetes on liver, pancreas and other tissues. CoQ10 suppressed the increments in plasma pro-inflammatory cytokine levels, whereas it restored the reducing in anti-inflammatory cytokine levels arising due to diabetes. The obtained results from this study after CoQ10 application supported similar studies used CoQ10 application against deleterious effects of diabetes in animals and humans. Therefore, it is possible to say that CoQ10 may play important role in regulation of imbalance between inflammation markers in diabetes conditions and further studies are needed to clear the beneficial effects of CoQ10 treatment on the other inflammation markers in diabetes status.


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