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Association Between Cox-2 and 15-Pgdh Polymorphisms and Sle Susceptibility Publisher Pubmed



Sandoughi M1 ; Saravani M2, 3 ; Rokni M4, 5 ; Nora M2 ; Mehrabani M6 ; Dehghan A7
Authors
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Authors Affiliations
  1. 1. Department of Internal Medicine, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran
  2. 2. Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran
  3. 3. Cellular and Molecular Research Center, Zahedan University of Medical Sciences, Zahedan, Iran
  4. 4. Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran
  7. 7. Noncommunicable Diseases Research Center, Fasa University of Medical Sciences, Fasa, Iran

Source: International Journal of Rheumatic Diseases Published:2020


Abstract

Aims: Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease. Prostaglandins E2 (PGE2), the product of the cyclo-oxygenase 2 (COX-2) enzyme, has critical roles in the etiology of autoimmune diseases. PGE2 level is controlled by a balance between its synthesis mediator (COX-2 enzyme) and its catabolic key enzyme (15-hydroxyprostaglandin dehydrogenase [15-PGDH] enzyme). In the present study, the associations of genotypic polymorphisms in COX-2 and 15-PGDH with SLE were investigated. Methods: One hundred and sixty SLE patients and 160 healthy controls participated in the study. The polymerase chain reaction - restriction fragments length polymorphism method was used for genotyping. The COX-2 rs2745557 G/A and 15-PGDH rs8752 G/A polymorphisms were investigated. Results: Regarding the COX-2 rs2745557 single nucleotide polymorphism, there was no significant association between COX-2 rs2745557 polymorphism and SLE. However, the dominant models showed a marginally significant relation (P =.048, odds ratio = 0.63, 95% CI = 0.4-1.0). Regarding GA genotype of 15-PGDH rd8752 polymorphism, there was a significant difference between two groups with a 4.5-fold increase in SLE development (P =.0001). The frequency of the A allele was higher in SLE patients than that in controls, showing a 1.4-fold increase in SLE development (P =.018). Conclusion: All results showed the protective effects of the dominant model of COX-2 rs2745557 polymorphism and risk factor of 15-PGDH rs8752 polymorphism on SLE development. © 2020 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd