scholarly journals Myricetin Abrogates Cisplatin-Induced Oxidative Stress, Inflammatory Response, and Goblet Cell Disintegration in Colon of Wistar Rats

Plants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 28 ◽  
Author(s):  
Muneeb U. Rehman ◽  
Irfan A. Rather
Keyword(s):  
Body Weight ◽  
Phase Ii ◽  
Goblet Cell ◽  
Inflammatory Markers ◽  
Detoxification Enzymes ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Anti Oxidant ◽  
Oxidant Status ◽  
Cell Disintegration

Cisplatin [cis-diamminedichloroplatinum II] is an extensively prescribed drug in cancer chemotherapy; it is also useful for the treatment of diverse types of malignancies. Conversely, cisplatin is associated with a range of side effects such as nephrotoxicity, hepatotoxicity, gastrointestinal toxicity, and so on. Myricetin (3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-4chromenone) is a very common natural flavonoid found in fruits, tea, and plants. It has been found to have high-value pharmacological properties and strong health benefits. To examine the role of myricetin in colon toxicity induced by cisplatin, we conducted a concurrent prophylactic study in experimental animals that were treated orally with myricetin for 14 days at two doses—25 and 50 mg/kg of body weight. On the 14th day, a single intraperitoneal injection of cisplatin (7.5 mg/kg body weight) was administered in all groups except control. The effects of myricetin in cisplatin-induced toxicity in the colon were assessed in terms of antioxidant status, phase-II detoxification enzymes, the level of inflammatory markers, and goblet cell disintegration. Myricetin was found to restore the level of all the antioxidant enzymes analyzed in the study. In addition, the compound ameliorated cisplatin-induced lipid peroxidation, increase in xanthine oxidase activity, and phase-II detoxifying enzyme activity. Myricetin also attenuated deteriorative effects induced by cisplatin by regulating the level of molecular markers of inflammation (NF-κB, Nrf-2, IL-6, and TNF-α), restoring Nrf-2 levels, and controlling goblet cell disintegration. The current study reinforces the conclusion that myricetin exerts protection in colon toxicity via up-regulation of inflammatory markers, improving anti-oxidant status, and protecting tissue damage.

scholarly journals Effect of a Moderate Weight Loss on Serum Fetuin-A and Markers of Inflammation in Individuals With Obesity

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1232-1232
Author(s):  
Suresh Mathews ◽  
Kensie Grace ◽  
Amanda Reeder ◽  
G Tylicki
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Inflammatory Markers ◽  
Body Weight Loss ◽  
C Reactive Protein ◽  
Fetuin A ◽  
Reactive Protein ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Serum Crp

Abstract Objectives Elevated fetuin-A (Fet-A) has been shown to be a risk factor for several metabolic diseases and understanding the effects of moderate weight loss on changes in Fet-A and other inflammatory markers could allow for lifestyle intervention strategies. The association of inflammatory markers and Fet-A with incremental body weight loss is unknown. The objective of the study was to evaluate the association of inflammatory markers, including TNF-alpha (TNF-α), adiponectin, and C-reactive protein (CRP), Fet-A, and it's phosphorylated form, pFet-A, with incremental body weight loss. Methods Sixteen men achieved a targeted weight loss of 8% to 10% of initial body weight. In this study, we analyzed changes in serum TNF-α, adiponectin, and CRP inflammatory cytokines to changes in serum serum-Fet-A and pFet-A. We also examined the relationship of changes in cytokine profile to alterations in anthropometrics and other metabolic indices. All statistical analyses were performed using GraphPad Prism version 8.0. Results A moderate body weight loss of 8% to 10%, significantly decreased serum CRP, but did not affect TNF-α or adiponectin concentrations in individuals with obesity. Serum CRP started to decrease with 4% to 6% body weight loss, demonstrating a mean change in serum CRP concentrations of – 0.15 mg/L and – 0.10 mg/L, for 4%-6% and 8%-10% body weight loss, respectively, for each 1 kg of body weight loss. Weight-loss induced change in serum CRP concentrations were not significantly associated with a decrease in serum Fet-A or pFet-A, although a trend was observed for change in serum pFet-A (r = 0.44, P = 0.09). Conclusions A moderate weight loss improved serum inflammatory marker C-reactive protein but did not affect TNF-α or adiponectin concentrations in individuals with obesity. These changes were not significantly associated with a decrease in serum pFet-A although a trend was observed. Funding Sources This work was supported by the American Diabetes Association (ADA 7–04-JF-36); the Alabama Agricultural Experiment Station (ALA080–052).

scholarly journals Inflammatory markers in a randomised soya intervention among men

2008 ◽  
Vol 101 (12) ◽  
pp. 1740-1744 ◽  
Author(s):  
Gertraud Maskarinec ◽  
Robert Oum ◽  
Ann K. Chaptman ◽  
Simona Ognjanovic
Keyword(s):  
Body Weight ◽  
Inflammatory Markers ◽  
Serum Levels ◽  
Repeated Measurements ◽  
Intervention Effect ◽  
Reactive Protein ◽  
Markers Of Inflammation ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein ◽  
Multiplex Bead

The present analysis investigated the effect of soya foods on serum levels of six inflammatory markers, leptin, adiponectin, monocyte attractant protein 1 (MCP-1), macrophage inflammatory protein-1b (MIP-1b), IL-6 and C-reactive protein (CRP), and their relationship with BMI and lifetime soya intake. We randomised twenty-four men to a high- (two daily servings with 30–35 mg isoflavones per serving) or a low-soya diet for 3 months. After a 1-month washout period, the men crossed over to the other treatment. We used a multiplex bead immunoassay to measure leptin, adiponectin, MCP-1 and MIP-1b and ELISA assays for IL-6 and CRP. The statistical analysis applied mixed models that incorporated the four repeated measurements. The men had a mean age of 58·7 (sd 7·2) years and a mean BMI of 28·4 (sd 4·9) kg/m2. We observed no significant intervention effect of the soya treatment on any of the six markers. After adjustment for age and ethnicity, highly significant associations of BMI and body weight with leptin and MCP-1 emerged. Men with high soya intake early in life also had higher levels of leptin and MCP-1, whereas no association was seen for soya intake during adulthood. MIP-1b, adiponectin, IL-6 and CRP were not related to BMI, body weight or soya intake at any time in life. No intervention effect of soya foods on markers of inflammation was observed in this small study, but adiposity and early-life soya intake were related to higher leptin and MCP-1 levels.

scholarly journals Analysis of inflammatory markers in apparently healthy automobile vehicle drivers in response to exposure to traffic pollution fumes

2020 ◽  
Vol 36 (4) ◽  
Author(s):  
Hina Riaz Ahmed ◽  
Binafsha Manzoor Syed ◽  
Zulfiqar Laghari ◽  
Suleman Pirzada
Keyword(s):  
Inflammatory Markers ◽  
Cross Sectional Study ◽  
Traffic Pollution ◽  
Healthy Human ◽  
Cross Sectional ◽  
Positive Correlation ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Traffic Pollutants ◽  
Apparently Healthy

Objective: This study aimed to evaluate pattern of markers of inflammation in apparently healthy drivers who exposed to traffic fumes. Methods: This cross-sectional study was conducted from June 2016 to January 2017 at Liaquat University of Medical & Health Sciences (LUMHS), Jamshoro. It looked into the effects of traffic pollutants on markers of inflammation including CRP, Leukocytes count, IL-6, TNF-α, TNF-β of healthy human volunteers. Eighty-seven, apparently healthy, non-smoking automobile vehicle drivers, having daily contact of traffic exhaust for at least six hours, aged between 18-40 years recruited for this study. Levels of traffic-generated pollutants P.M2.5, P.M10, NOx were recorded in different areas of Hyderabad City. Results: P.M2.5 found to be positively correlated with markers of inflammation including IL-6 (rs = 0.99), TNF-α (rs = 0.41), CRP mg/dl (rs = 0.99) , neutrophils (rs = 0.29), lymphocytes (rs = 0.31), eosinophils (rs = 0.20), monocytes (rs = 0.42) and basophils (rs = 0.16). Positive correlation present among IL-6 (rs = 0.21), TNF-α (rs = 0.49) and CRP mg/dl (rs = 0.22) (rs = -0.31), Leukocytes (rs = 0.14) neutrophils (rs = 0.31), lymphocytes (rs = 0.21), monocytes (rs = 0.50), basophils (rs = 0.17) with P.M10. NOx showed positive correlation with IL-6 (rs = 0.22), TNF-α (rs = 0.48), CRP (rs = 0.22), neutrophils (rs = 0.31), lymphocytes (rs = 0.13), basophils (rs = 0.17) and monocytes (rs = 0.48). Conclusion: Findings of our study suggest that almost all markers of inflammation are positively correlated with traffic pollutants and this condition might raise the risk of systemic diseases. doi: https://doi.org/10.12669/pjms.36.4.2025 How to cite this:Riaz H, Syed BM, Laghari Z, Pirzada S. Analysis of inflammatory markers in apparently healthy automobile vehicle drivers in response to exposure to traffic pollution fumes. Pak J Med Sci. 2020;36(4):---------. doi: https://doi.org/10.12669/pjms.36.4.2025 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

scholarly journals Dipeptidyl-peptidase-4 (DPP-4) inhibitor ameliorates 5-flurouracil induced intestinal mucositis

BMC Cancer ◽  
2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Jung Min Lee ◽  
In Kyung Yoo ◽  
Jae Min Lee ◽  
Seung Han Kim ◽  
Hyuk Soon Choi ◽  
...  
Keyword(s):  
Body Weight ◽  
Cell Count ◽  
Mrna Expression ◽  
Goblet Cell ◽  
Weight Change ◽  
Body Weight Change ◽  
Epithelial Lining ◽  
Villus Height ◽  
Tnf Α ◽  
Significant Difference

Abstract Background Chemotherapy-induced alimentary mucositis (AM) is difficult to prevent and treatment is rarely effective. Recent study have been showed that glucagon-like peptide (GLP)-1 and GLP-2 has protective in chemotherapy-induced AM. While the DPP-4 enzyme degrades this GLP-1, the DPP-4 inhibitor blocks the degradation process and raises the concentration of GLP-1. This study aimed to assess the role of DPP-4 inhibitor, a well-known hypoglycemic agent, on chemotherapy-induced AM. Methods Twenty-four 6-week-old male C57BL/6 mice were divided into 4 groups: control, 5-fluorouracil (5-FU), DPP-4 inhibitor, and saline (DPP-4i), and DPP-4 inhibitor and 5-FU (DPP-4i + 5-FU). Mucositis was induced by intraperitoneal injection of 5-FU (400 mg/kg). DPP-4 inhibitor (50 mg/kg) was administered orally for four days starting the day before 5-FU administration. Post 72 h of 5-FU injection, mice were sacrificed and body weight change, diarrhea score, villus height, villus/crypt ratio, histologic characteristics including goblet cell count, and mRNA expression of inflammatory cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6, were assessed. Results Daily body weight change was not statistically significant between the 5-FU and the DPP-4i + 5-FU group (P = 0.571). Diarrhea score was significantly different between these two groups (P = 0.033). In the 5-FU group, the villus height was not maintained well, the epithelial lining was irregular, and inflammatory cell infiltration was observed. Goblet cell count in the DPP-4i + 5-FU group was significantly higher than in the 5-FU group (P = 0.007). However, in the DPP-4i + 5-FU group, the villus height, epithelial lining, and crypt structure were better maintained than in the 5-FU group. Compared with the control group, mRNA expression of TNF-α was significantly up-regulated in the 5-FU group. Moreover, mRNA expression of TNF-α in the DPP-4i + 5-FU group was down-regulated compared to the 5-FU group. However, IL-6 in the 5-FU group was significantly down-regulated compared to the control, there was no significant difference in expression of IL-6 between the 5-FU and DPP4i + 5-FU group. Conclusion DPP-4 inhibitor can improve 5-FU induced AM and, therefore, has potential as an alternative treatment for chemotherapy-induced AM.

scholarly journals Mangosteen (Garcinia mangostana) flesh supplementation attenuates biochemical and morphological changes in the liver and kidney of high fat diet-induced obese rats

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Noratirah Shazlin Muhamad Adyab ◽  
Asmah Rahmat ◽  
Noor Atiqah Aizan Abdul Kadir ◽  
Hawa Jaafar ◽  
Radhiah Shukri ◽  
...  
Keyword(s):  
Body Weight ◽  
Glutathione Peroxidase ◽  
High Fat Diet ◽  
Inflammatory Markers ◽  
Morphological Changes ◽  
High Fat ◽  
Garcinia Mangostana ◽  
Tnf Α ◽  
Obese Rats ◽  
Liver And Kidney

Abstract Background Mangosteen is a native fruit from Southeast Asia. It is rich in phenolic compounds such as xanthones, anthocyanins and phenolic acids. Mangosteen pericarp extract showed inhibitory activity towards pancreatic lipase and may have potential use for obesity treatment. However, there is limited study on the beneficial effects of mangosteen flesh against obesity. This study aimed to investigate the effects of Garcinia mangostana flesh (GMF) on biochemical and morphological changes in the liver and kidney of high-fat diet-induced obese rats. Methods Forty healthy Sprague-Dawley rats were randomised into five groups (n = 8) with four groups were fed with high-fat diet (HFD) for 10 weeks and a control group was fed with rat chow diet. Supplementation with GMF in obese rats was continued for 7 weeks starting from week 10th after the initiation of HFD at different doses (200 mg/kg, 400 mg/kg and 600 mg/kg). The positive and negative control rats were given distilled water via oral gavage. Plasma lipid profile, antioxidant enzymes and pro-inflammatory markers were determined using commercial kits. Liver and kidney structure were defined by histology. Results The rats fed with HFD for 10 weeks increased plasma LDL-cholesterol, reduced plasma glutathione peroxidase level and had significantly higher body weight compared to normal control rats (p < 0.05). Obese rats also showed elevated level of TNF-α and IL-6 after 17 weeks of HFD. Supplementation with GMF for 7 weeks in obese rats reduced their body weight, improved lipid profile, increased total antioxidant capacity and glutathione peroxidase level and lowered plasma pro-inflammatory markers (TNF-α and IL-6) (p < 0.05). In addition, GMF supplementation attenuated the abnormalities of the liver and kidney tissue caused by high fat diet. Conclusion Taken together, the findings suggest that supplementation of Garcinia mangostana flesh may help in reducing body weight and has the potential to ameliorate the biochemical changes of the high fat diet-induced obesity in rats. Further studies on pharmacodynamic and pharmacokinetic are required before the results are translated to human.

scholarly journals Nerolidol: a potential approach in rheumatoid arthritis through reduction of TNF-α, IL-1β, IL-6, NF-Kβ, COX-2 and anti-oxidant effect in CFA-induced arthritic model

2021 ◽  
Author(s):  
Shanila Akhter ◽  
Hafiz Muhammad Irfan ◽  
Alamgeer Yuchi ◽  
Shah Jahan ◽  
Muhammad Shahzad ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Body Weight ◽  
Inflammatory Cytokines ◽  
The Body ◽  
Primary Study ◽  
Tnf Α ◽  
Ankle Joints ◽  
Anti Oxidant ◽  
Cox 2 ◽  
Anti Inflammatory

Abstract Rheumatoid arthritis an autoimmune infectious disorder, is categorized by inflammation and increased level of pro-inflammatory cytokines which are released by immune cells, macrophages or activation of arachidonic acid metabolism. The expression of these cytokines, oxidative free radicals and the activation of COX-2 enzymes are crucial targets for chronic inflammation. On the basis of established anti-inflammatory efficacy of Nerolidol, the primary study was further appraised to determine its efficacy against Freund’s complete adjuvant (CFA) rheumatoid model. Arthritis was persuaded by inoculation of 0.1mL CFA injection into left hind footpad of rats. Anti-arthritic potential of nerolidol (at 200, 400 and 800mg/kg doses) was assessed by measuring the paw volume, body weight, serum analysis, histopathological and radio-graphics of ankle joints. Expressions of cytokine’s panels like IL-10, IL-4, COX-2, NF-Kβ, TNF-α, IL-6, PGE-2 and IL-1β were determined by real time qPCR. Antioxidant enzyme analyses was calculated by measuring the SOD, POD and catalase activity from serum and equated with arthritic control group. Nerolidol prevented the body weight loss, stabilized the biochemical and haematological homeostasis and significantly reduced the paw volume. Furthermore, X-ray and histopathological assessment of ankle joints showed an improvement in the joint structure of rats treated with nerolidol. Besides that, over expression of gene pointers like TNF-α, IL-1β, IL-6, NF-Kβ, PGE-2 and COX-2 in CFA treated control rats were also reversed with nerolidol. This anti-arthritic mechanism was further supported by the increased level of IL-10, IL-4 and serum anti-oxidant activity. The present findings demonstrate that nerolidol reduce the adjuvant arthritis by down-regulating the proinflammatory cytokines and up-regulating the aforementioned anti-inflammatory cytokines and may be used as a therapeutic substance for the management of human rheumatoid arthritis.

scholarly journals Galectin-1 reduces the severity of ulcerative colitis induced by dextran sulfate sodium via suppressing inflammatory and oxidative mediators

2020 ◽  
Author(s):  
Pelin Arda-Pirincci ◽  
Guliz Aykol-Celik
Keyword(s):  
Ulcerative Colitis ◽  
Cell Proliferation ◽  
Body Weight ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Proliferation Index ◽  
Tnf Α ◽  
Anti Oxidant ◽  
Anti Inflammatory

Ulcerative colitis is an inflammatory bowel disease and many people suffers from this disease across the word. Dextran sulfate sodium (DSS) is a synthetic sulfated polysaccharide that is used to produce ulcerative colitis in rodents. Galectin-1 is a β-galactoside binding animal lectin which plays key roles in many biological events. In this study, we investigated the role of galectin-1 on colon morphology, cell proliferation, oxidative stress, anti-oxidant system, inflammatory and anti-inflammatory mediators in the model of experimental ulcerative colitis induced by DSS in mice. C57BL/6  mice were fed orally 3% DSS in their drinking water for 5 days for acute colitis induction. Animals were injected with 1 mg/kg recombinant human galectin-1 for 7 consecutive days. Oral DSS application resulted in colitis injury by causing histopathological changes; an increase in disease activity index (DAI), lipid peroxidation (MDA), myeloperoxidase (MPO) and TNF-α levels; a decrease in body weight, colon length, cell proliferation index, catalase (CAT), glutahione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities, gluathione (GSH) and IL-10 levels. However, treatment with galectin-1 prevented DSS-induced colitis injury through the reduction of DAI, MDA, MPO and TNF-α levels, and the increase of body weight, colon length, cell proliferation, antioxidant enzymes activities, GSH and IL-10 levels. As a result, this study showed that galectin-1 has proliferative, anti-oxidant, anti-inflammatory, and cytoprotective effects against DSS-induced colitis in mice. In addition, galectin-1 reduces the severity of ulcerative colitis via suppressing inflammatory and oxidative mediators.

scholarly journals Kaempferol Attenuates the Development of Diabetic Neuropathic Pain in Mice: Possible Anti-Inflammatory and Anti-Oxidant Mechanisms

2014 ◽  
Vol 2 (3) ◽  
pp. 424-430 ◽  
Author(s):  
Osama M. Abo-Salem
Keyword(s):  
Neuropathic Pain ◽  
Body Weight Gain ◽  
Thermal Hyperalgesia ◽  
Pain Sensation ◽  
Diabetic Neuropathic Pain ◽  
Reduced Body ◽  
Markers Of Inflammation ◽  
Tnf Α ◽  
Anti Oxidant ◽  
Factor Α

BACKGROUND: Diabetic neuropathic pain (DNP) is one of the most difficult types of pain to treat.  Many studies emphasized on the role of microglial cells, oxidative stress (OS) and inflammatory cytokines (IC) in the development of diabetic neuropathy (DN).AIM: Present study was designed to evaluate the effect of kaempferol in attenuation of DN in mice. METHODS: Diabetes was induced in mice by i.p. injection of a single dose of streptozotocin (STZ) (200 mg/kg). Cold allodynia, thermal hyperalgesia and chemical hyperalgesia were assessed, as well as markers of inflammation and OS.RESULTS: Diabetic mice (DM) showed an increased pain sensation, IC and OS accompanied with reduced body weigh gain. Treatment of DM with kaempferol (25, 50 and 100 mg/kg/day/orally) attenuated the development of DN and reduced pain sensation. Moreover, it reduced interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), lipid peroxidation and nitrite, concomitant with the improvement of antioxidant defense and body weight gain. In contrast, kaempferol (100 mg/kg) had no effects on the behavioral and biochemical parameters. Our results strongly suggest that activated microglia, IC and OS are involved in the development of DN.CONCLUSIONS: Kaempferol attenuates the development of DNP in mice probably by inhibition of neuroimmune activation of microglia and, partly mediated by reducing IC and OS.

Protective effect of dexpanthenol (vitamin B5) in a rat model of LPS-induced endotoxic shock

2018 ◽  
Vol 43 (6) ◽  
pp. 632-637
Author(s):  
Buket Demirci ◽  
Mustafa Yilmaz ◽  
Hilal Bektas Uysal
Keyword(s):  
Protective Effect ◽  
Intraperitoneal Injection ◽  
Endotoxic Shock ◽  
Sepsis Group ◽  
Tissue Samples ◽  
Treatment Groups ◽  
Single Intraperitoneal Injection ◽  
Tnf Α ◽  
Anti Oxidant ◽  
Oxidant Status

Abstract Objectives This study investigated the protective effect of dexpanthenol (DEX) in the septic shock model of rats with biochemical parameters. Methods 12–15 weeks old male 32 Wistar rats has been used for this study. Sepsis was induced by a single intraperitoneal injection of lipopolysaccharide (LPS) (5 mg/kg) and treatment groups received single intraperitoneal injection of DEX (500 mg/kg) just 30-min before. The blood and tissue samples were obtained 16 h later of LPS intervention under the ketamine and xylasine (50 and 5 mg/kg, respectively) anesthesia. Results Giving alone DEX did not alter any physiologic levels of biochemical markers. Induction of sepsis resulted in a marked increase in ALT, AST, urea, creatinine, lactate, procalcitonin, TNF-α, IL-1β levels to show the tissue damage. In all serum parameters, liver’s GSH, CAT levels and kidney’s CAT, GSH, MDA and NO levels have ameliorated by DEX treatment in sepsis group. Conclusion Along with the standard therapy of sepsis, DEX can be used as a safe way of restoring (anti)oxidant status of kidney and liver tissues. It can be effective to control cytokine pathway, to decrease procalcitonin and regulate the metabolic process of sepsis, such as lactate.

scholarly journals Higher anticholinergic burden from medications is associated with significant increase in markers of inflammation in the EPIC-Norfolk prospective population-based cohort study

2021 ◽  
Author(s):  
RIA SANGHAVI ◽  
Tiberiu Pana ◽  
Hulkar Mamayusuppova ◽  
Ian Maidment ◽  
Chris Fox ◽  
...  
Keyword(s):  
Inflammatory Markers ◽  
Population Based ◽  
Adverse Outcomes ◽  
Necrosis Factor Alpha ◽  
Cross Sectional ◽  
Anticholinergic Medications ◽  
Markers Of Inflammation ◽  
Increased Risk ◽  
Tnf Α ◽  
Anticholinergic Burden

Background: Higher anticholinergic burden from medications is associated with increased risk of cardiovascular disease and cognitive function decline. A mechanistic pathway has never been established. We aimed to determine whether chronic inflammation may mediate these associations. Methods: Participants were drawn from the European Prospective Investigation into Cancer, Norfolk cohort (40-79 years at baseline). The anticholinergic cognitive burden score (ACB) was calculated at baseline/first (1HC) (1993/97) and second (2HC) (1998/2000) health checks. Plasma fibrinogen and C-reactive protein (CRP) were measured during 1HC and Tumour Necrosis Factor alpha (TNF-α) and interleukin 6 (IL-6) during 2HC. Cross-sectional associations between ACB and inflammatory markers were examined for 1HC and 2HC, respectively. The prospective association was also examined between 1HC ACB and 2HC inflammatory markers. All models adjusted for age, sex, lifestyle factors, co-morbidities and medications. Results: 17,678 and 22,051 participants were included in cross-sectional analyses for CRP, and fibrinogen, respectively. A total of 5,101 participants with available data for TNF-α and IL-6 were included in the longitudinal analyses. Cross-sectionally, a point increase in the ACB was associated with a significant increase in all inflammatory markers (beta (standard error): fibrinogen – 0.035g/l (0.006), p<0.001; CRP 0.284mg/l (0.044), p<0.001; TNF-α 0.031pg/ml (0.010), p=0.002; and IL-6 0.112pg/ml (0.033), p=0.001. Longitudinally, a unit increase in the ACB was associated with a significant increase in TNF-α 0.028pg/ml (0.011), p=0.013 and IL-6 0.076 pg/ml (0.035), p=0.029. Conclusion: Higher anticholinergic burden was significantly associated with higher inflammatory markers. Inflammation may mediate the relationship between exposure to anticholinergic medications and adverse outcomes

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