Inflammatory response and matrix metalloproteinases in chronic kidney failure: Modulation by adropin and spexin

2021 ◽  
pp. 153537022110124
Author(s):  
Burak Yazgan ◽  
Filiz Avcı ◽  
Gülsün Memi ◽  
Ebru Tastekin
Keyword(s):  
Inflammatory Response ◽  
Kidney Failure ◽  
Renal Damage ◽  
Urine Volume ◽  
Kidney Tissue ◽  
Public Health Problem ◽  
Chronic Kidney Failure ◽  
Urine Protein ◽  
Cox 2 ◽  
Cox 1

Chronic kidney disease is a major global public health problem. The peptide hormones adropin and spexin modulate many physiological functions such as energy balance and glucose, lipid and protein metabolism. However, it is unclear whether these peptides may exert effects on renal damage, tissue remodeling, and inflammatory conditions. In view of the limited information, we aimed to investigate the effect of adropin and spexin on matrix metalloproteinase and inflammatory response genes a rat model of adenine-induced chronic kidney failure. Chronic kidney failure was induced in rats by administering adenine hemisulfate. Renal function was determined in an autoanalyzer. Histopathological modifications were assessed by H&E staining. mRNA expression levels of ALOX 15, COX 1, COX 2, IL-1β, IL-10, IL-17A, IL-18 IL-21, IL-33, KIM-1, MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MMP-13, NGAL, TGFβ1, TIMP-1, and TNFα in kidney tissue were measured by qPCR. Our results showed an increase of 24-h urine volume, serum creatinine, BUN, and urine protein levels in group with adenine-induced CKF. Adropin and spexin treatments decreased urine protein and 24-h urine volume. Renal damage, TIMP-1, IL-33, and MMP-2 increased after CKF induction, while COX 1, MMP-9, and MMP-13 levels were significantly reduced. Furthermore, KIM-1, TIMP-1, IL-33, and MMP-2 were downregulated by spexin treatment. Renal damage, NGAL, TIMP-1 IL-17A, IL-33, MMP-2, and MMP-3 decreased after adropin treatment, while MMP-13 levels were upregulated. Treatment with adropin+spexin decreased KIM-1, NGAL, TIMP-1, IL-1β, IL-17A, IL-18, IL-33, ALOX 15, COX 1, COX 2, TGFβ1, TNFα, MMP-2, MMP-3, and MMP-7, but increased MMP-13 levels. Our findings revealed that inflammatory response and MMP genes were modulated by adropin and spexin. These peptides may have protective effects on inflammation and chronic kidney damage progression.

scholarly journals Genetic Variations in Inflammatory Response Genes and Their Association with the Risk of Prostate Cancer

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Xin Cui ◽  
Hao Yan ◽  
Tong-Wen Ou ◽  
Chun-Song Jia ◽  
Qi Wang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Risk ◽  
Inflammatory Response ◽  
Prostate Cancer Risk ◽  
Genetic Variations ◽  
Odds Ratios ◽  
Comparison Model ◽  
Pcr Rflp ◽  
Cox 2 ◽  
Cox 1

Prostate cancer is a common cancer in men. Genetic variations in inflammatory response genes can potentially influence the risk of prostate cancer. We aimed to examine the association betweenPPARGPro12Ala,NFKB1-94 ins/del,NFKBIA-826C/T,COX-1(50C>T), andCOX-2(-1195G>A) polymorphisms on prostate cancer risk. The genotypes of the polymorphisms were ascertained in 543 prostate cancer patients and 753 controls through PCR-RFLP and the risk association was evaluated statistically using logistic regression analysis. TheNFKB1-94 polymorphism was shown to decrease prostate cancer risk in both heterozygous and homozygous comparison models (odds ratios of 0.74 (95% CI = 0.58–0.96) (P=0.02) and 0.57 (95% CI = 0.42–0.78) (P<0.01), resp.). An opposite finding was observed forCOX-2(-1195) polymorphism (odds ratios of 1.58 (95% CI = 1.15–2.18) (P<0.01) for heterozygous comparison model and 2.08 (95% CI = 1.48–2.92) (P<0.01) for homozygous comparison model). No association was observed for other polymorphisms. In conclusion,NFKB1-94 ins/del andCOX-2(-1195G>A) polymorphisms may be, respectively, associated with decreased and increased prostate cancer risk in the Chinese population.

Role of prostaglandins in collecting duct-derived endothelin-1 regulation of blood pressure and water excretion

2007 ◽  
Vol 293 (6) ◽  
pp. F1805-F1810 ◽  
Author(s):  
Yuqiang Ge ◽  
Kevin A. Strait ◽  
Peter K. Stricklett ◽  
Tianxin Yang ◽  
Donald E. Kohan
Keyword(s):  
Blood Pressure ◽  
Collecting Duct ◽  
Urine Volume ◽  
Mrna Levels ◽  
Water Excretion ◽  
Salt Loading ◽  
Endothelin 1 ◽  
Cox 2 ◽  
Cox 1

Collecting duct (CD)-derived endothelin-1 (ET-1) exerts natriuretic, diuretic, and hypotensive effects. In vitro studies have implicated cyclooxygenase (COX) metabolites, and particularly PGE2, as important mediators of CD ET-1 effects. However, it is unknown whether PGE2 mediates CD-derived ET-1 actions in vivo. To test this, CD ET-1 knockout (KO) and control mice were studied. During normal salt and water intake, urinary PGE2 excretion was unexpectedly increased in CD ET-1 KO mice compared with controls. Salt loading markedly increased urinary PGE2 excretion in both groups of mice; however, the levels remained relatively higher in KO animals. Acutely isolated inner medullary collecting duct (IMCD) from KO mice also had increased PGE2 production. The increased IMCD PGE2 was COX-2 dependent, since NS-398 blocked all PGE2 production. However, increased CD ET-1 KO COX-2 protein or mRNA could not be detected in inner medulla or IMCD, respectively. Inner medullary COX-1 mRNA and protein levels and IMCD COX-1 mRNA levels were unaffected by Na intake or CD ET-1 KO. KO mice on a normal or high-Na diet had elevated blood pressure compared with controls; this difference was not altered by indomethacin or NS-398 treatment. However, indomethacin or NS-398 did increase urine osmolality and reduce urine volume in KO, but not control, animals. In summary, IMCD COX-2-dependent PGE2 production is increased in CD ET-1 KO mice, indicating that CD-derived ET-1 is not a primary regulator of IMCD PGE2. Furthermore, the increased PGE2 in CD ET-1 KO mice partly compensates for loss of ET-1 with respect to maintaining urinary water excretion, but not in blood pressure control.

scholarly journals Apolipoprotein c-iii (apo-c3) Metabolism in Patients with End Stage Renal Disease Treated with Long Term Hemodialysis

2018 ◽  
Vol 2 (2) ◽  
pp. 174-181
Author(s):  
Lutfi Zylbeari ◽  
Kastriot Haxhirexha ◽  
Nasir Behxheti ◽  
Ferizate Dika- Haxhirexha ◽  
Gazmend Zylbeari ◽  
...  
Keyword(s):  
Renal Disease ◽  
Kidney Failure ◽  
End Stage Renal Disease ◽  
Public Health Problem ◽  
Chronic Kidney Failure ◽  
The United States ◽  
Coronary Syndrome ◽  
Poor Outcomes ◽  
Stage Renal Disease ◽  
End Stage

Background: End Stage Renal disease (ESRD) as it was historically termed is a term that encompasses all degrees of decreased renal function, from damaged–at risk through mild, moderate, and severe chronic kidney failure. ESRD is a worldwide public health problem. In the United States, there is a rising incidence and prevalence of kidney failure, with poor outcomes and high cost (see Epidemiology).Material and Methods: The blood sample for routine analysis (lipidogram) and specific analysis was taken at 08o'clock in the morning with the room temperature that variated from 19 to 24°C, before the hemodialysis session, minimum 12 hours of fasting - with tendency to avoid the absorption effect of food by the intestine as well as avoid absorption of lipids and formation of chilomicrones. In all samples regardless of their group, the concentration of ApoC-II and lipids were analyzed in a period of 12 months in a period of 12 months (the measurements were made every three months, it means we totally made 3 measurements in 9 months).Results: The results from patients and controlling group for Apo-C3 and lipid profile (ChT, TG, HDL-ch, LDL-ch) are given in table number 3. A significant statistical difference with p<0.0001 is found from the results of the lipidic profile and ApoC-III of patients with ESRD treated with HD compared with the results of the controlling group for the same parameters.Conclusion: In this study patients with ESRD treated with HD have high parameters of ApoC-III, TG, LDL-ch but low concentrations of HDL-ch due to impaired catabolism of apolipoproteins in this specific group of patients. In all patients symptoms of CDV (myocardial infarction, angina pectoris, ischemia), acute coronary syndrome were noticed.

scholarly journals Apolipoprotein c-iii (apo-c3) Metabolism in Patients with End Stage Renal Disease Treated with Long Term Hemodialysis.

2018 ◽  
Vol 2 (2) ◽  
Author(s):  
Lutfi Zylbeari ◽  
Kastriot Haxhirexha ◽  
Nasir Behxheti ◽  
Ferizate Dika Haxhirexha ◽  
Gazmend Zylbeari ◽  
...  
Keyword(s):  
Renal Disease ◽  
Kidney Failure ◽  
End Stage Renal Disease ◽  
Public Health Problem ◽  
Chronic Kidney Failure ◽  
The United States ◽  
Coronary Syndrome ◽  
Poor Outcomes ◽  
Stage Renal Disease ◽  
End Stage

Background: End Stage Renal disease (ESRD) as it was historically termed is a term that encompasses all degrees of decreased renal function, from damaged–at risk through mild, moderate, and severe chronic kidney failure. ESRD is a worldwide public health problem. In the United States, there is a rising incidence and prevalence of kidney failure, with poor outcomes and high cost (see Epidemiology).Material and Methods: The blood sample for routine analysis (lipidogram) and specific analysis was taken at 08o'clock in the morning with the room temperature that variated from 19 to 24°C, before the hemodialysis session, minimum 12 hours of fasting - with tendency to avoid the absorption effect of food by the intestine as well as avoid absorption of lipids and formation of chilomicrones. In all samples regardless of their group, the concentration of ApoC-II and lipids were analyzed in a period of 12 months in a period of 12 months (the measurements were made every three months, it means we totally made 3 measurements in 9 months).Results: The results from patients and controlling group for Apo-C3 and lipid profile (ChT, TG, HDL-ch, LDL-ch) are given in table number 3. A significant statistical difference with p<0.0001 is found from the results of the lipidic profile and ApoC-III of patients with ESRD treated with HD compared with the results of the controlling group for the same parameters.Conclusion: In this study patients with ESRD treated with HD have high parameters of ApoC-III, TG, LDL-ch but low concentrations of HDL-ch due to impaired catabolism of apolipoproteins in this specific group of patients. In all patients symptoms of CDV (myocardial infarction, angina pectoris, ischemia), acute coronary syndrome were noticed.

scholarly journals Protective effect of ganoderan on renal damage in rats with chronic glomerulonephritis

2008 ◽  
Vol 31 (4) ◽  
pp. 212 ◽  
Author(s):  
Wei-De Zhong ◽  
Hui-Chan He ◽  
Ru-Biao Ou ◽  
Xue-Cheng Bi ◽  
Qi-Shan Dai ◽  
...  
Keyword(s):  
Serum Creatinine ◽  
Protective Effect ◽  
Renal Damage ◽  
Light And Electron Microscopy ◽  
Kidney Tissue ◽  
Chronic Glomerulonephritis ◽  
Protective Effects ◽  
Model Group ◽  
Sprague Dawley ◽  
Urine Protein

Purpose: To investigate the protective effect of ganoderan on renal damage in rat models with chronic glomerulonephritis induced by adriamycin. Methods: 48 healthy Sprague-Dawley rats were randomly divided into three groups: control, nephritic model and ganoderan treatment groups. Changes of the following indices in the three groups were observed 6 weeks after treatment: 24-hour urine protein, albumen, serum creatinine, cholesterol. Histopathological observations of the renal cortex were made by light and electron microscopy. Results: Compared with controls, levels of 24-hour urine protein (9.60±0.57mg/d vs. 82.50±3.18mg/d), serum creatinine (35.25±2.63?mol/L vs. 44.75±8.06?mol/L) and cholesterol (1.15±0.10mmol/L vs. 4.02±0.25mmol/L) of rats in the nephritic model group were increased (P < 0.05), and the concentration of albumen was decreased (35.98±1.34g/L vs. 19.05±0.62g/L, P < 0.05). Ganoderan administration decreased 24-hour urine protein (82.50±3.18mg/d vs. 45.01±3.94mg/d, P < 0.05). Following ganoderan, the pathological changes in kidney tissue were improved compared with those in the nephritic model group. Conclusion: Ganoderan exerts protective effects in rats with chronic glomerulonephritis induced by ADR. Ganoderan reduced 24-hour urine protein, serum creatinine, cholesterol, improving renal function and reducing the severity of renal injury.

scholarly journals Inhibition of Cyclooxygenase-1 and Cyclooxygenase-2 Impairs Trypanosoma cruzi Entry into Cardiac Cells and Promotes Differential Modulation of the Inflammatory Response

2014 ◽  
Vol 58 (10) ◽  
pp. 6157-6164 ◽  
Author(s):  
Aparecida D. Malvezi ◽  
Carolina Panis ◽  
Rosiane V. da Silva ◽  
Rafael Carvalho de Freitas ◽  
Maria I. Lovo-Martins ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Trypanosoma Cruzi ◽  
Chagas Disease ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Etiologic Agent ◽  
Cardiac Cells ◽  
Content Type ◽  
Cox 2 ◽  
Cox 1

ABSTRACTThe intracellular protozoan parasiteTrypanosoma cruziis the etiologic agent of Chagas disease, a serious disorder that affects millions of people in Latin America. Cell invasion byT. cruziand its intracellular replication are essential to the parasite's life cycle and for the development of Chagas disease. Here, we present evidence suggesting the involvement of the host's cyclooxygenase (COX) enzymes duringT. cruziinvasion. Pharmacological antagonists for COX-1 (aspirin) and COX-2 (celecoxib) caused marked inhibition ofT. cruziinfection when rat cardiac cells were pretreated with these nonsteroidal anti-inflammatory drugs (NSAIDs) for 60 min at 37°C before inoculation. This inhibition was associated with an increase in the production of NO and interleukin-1β and decreased production of transforming growth factor β (TGF-β) by cells. Taken together, these results indicate that COX-1 more than COX-2 is involved in the regulation of anti-T. cruziactivity in cardiac cells, and they provide a better understanding of the influence of TGF-β-interfering therapies on the innate inflammatory response toT. cruziinfection and may represent a very pertinent target for new therapeutic treatments of Chagas disease.

scholarly journals Anti-Inflammatory Activity of Miodesin™: Modulation of Inflammatory Markers and Epigenetic Evidence

2020 ◽  
Vol 2020 ◽  
pp. 1-11 ◽  
Author(s):  
Carlos Rocha Oliveira ◽  
Rodolfo Paula Vieira
Keyword(s):  
Dna Methylation ◽  
Transcription Factor ◽  
Inflammatory Response ◽  
Inflammatory Markers ◽  
Epigenetic Mechanism ◽  
Macrophage Cell ◽  
Inflammatory Processes ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Cox 1

Purpose. To investigate the effects of a combined herbal medicine Miodesin™ on the inflammatory response of key cells involved in the acute and chronic inflammatory processes as well as the possible epigenetic involvement. Methods. After the establishment of the IC50 dose, the chondrocyte, keratinocyte, and macrophage cell lines were pretreated for 2 hours with Miodesin™ (200 μg/mL) and stimulated with LPS (1 μg/mL) for 24 hours. The supernatant was used to measure the levels of cytokines (IL-1β, IL-6, IL-8, and TNF-α) and chemokines (CCL2, CCL3, and CCL5), and the cells were used to extract the mRNA for the transcription factor (NF-κβ), inflammatory enzymes (COX-1, COX-2, PLA2, and iNOS), and chemokines (CCL2, CCL3, and CCL5). Results. Miodesin™ inhibited the release of LPS-induced cytokines (IL-1β, IL-6, IL-8, and TNF-α; p<0.01) and chemokines (CCL2, CCL3, and CCL5; p<0.01) and the expression of the transcription factor (NF-κβ; p<0.01), inflammatory enzymes (COX-1, COX-2, PLA2, iNOS; p<0.01), and chemokines (CCL2, CCL3, and CCL5; p<0.01). In addition, the evaluation of epigenetic mechanism revealed that Miodesin™ did not induce changes in DNA methylation, assuring the genetic safeness of the compound in terms of the inflammatory response. Conclusions. Miodesin™ presents anti-inflammatory properties, inhibiting hyperactivation of chondrocytes, keratinocytes, and macrophages, involving epigenetics in such effects.

Mucosal damage induced by preferential COX-1 and COX-2 inhibitors: Role of prostaglandins and inflammatory response

Life Sciences ◽  
2004 ◽  
Vol 74 (7) ◽  
pp. 873-884 ◽  
Author(s):  
Isabel Villegas ◽  
Carmen La Casa ◽  
Catalina Alarcón de la Lastra ◽  
Virginia Motilva ◽  
Juan Manuel Herrerı́as ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mucosal Damage ◽  
Cox 2 ◽  
Cox 2 Inhibitors ◽  
Cox 1

Persistent accumulation of cyclooxygenase-1—expressing microglial cells and macrophages and transient upregulation by endothelium in human brain injury

2002 ◽  
Vol 96 (5) ◽  
pp. 892-899 ◽  
Author(s):  
Jan M. Schwab ◽  
Rudi Beschorner ◽  
Richard Meyermann ◽  
Fatma Gözalan ◽  
Hermann J. Schluesener
Keyword(s):  
Smooth Muscle ◽  
Brain Injury ◽  
Inflammatory Response ◽  
Protein Expression ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Content Type ◽  
Cox 2 ◽  
Cox 1 ◽  
Fine Print

Object. Secondary damage after central nervous system (CNS) injury is driven in part by oxidative stress and CNS inflammation and is substantially mediated by cyclooxygenases (COXs). To date, the rapidly inducible COX-2 isoform has been primarily linked to inflammatory processes, whereas expression of COX-1 is confined to physiological functions. The authors report the differential localization of COX-1 in human traumatic brain injury (TBI). Methods. Differential cellular COX-1 protein expression profiles were analyzed following TBI in 31 patients and compared with neuropathologically unaltered control brains by using immunohistochemistry. In these patients with TBI, a significant increase of COX-1 protein expression by vessel endothelial and smooth-muscle cells and CD68+ microglia/macrophages was observed to be strictly confined to the lesion. Accumulation of COX-1+ microglia/macrophages in the lesion was already evident 6 hours postinjury, reaching maximal levels after several weeks and remaining elevated at submaximal levels for several months after injury. Furthermore, COX-1+ cell clusters were located in the Virchow—Robin space during the leukocyte infiltration period from Days 4 to 8 after TBI. Double-labeling experiments confirmed coexpression of COX-1 by CD68+ microglia/macrophages. The numbers of COX-1+ vessel endothelial and smooth-muscle cells increased from Day 1, remaining at submaximal levels for months after injury. Conclusions. The prolonged accumulation of COX-1+ microglia/macrophages that were restricted to perilesional areas affected by the acute inflammatory response points to a role of COX-1 in secondary injury. The authors have identified localized, accumulated COX-1 expression as a potential pharmacological target following TBI. Their results challenge the current paradigms of a selective COX-2 role in the postinjury inflammatory response.

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