Volume 33, Issue 223 (8-2023)                   J Mazandaran Univ Med Sci 2023, 33(223): 125-131 | Back to browse issues page

XML Persian Abstract Print

Abstract:   (649 Views)
 Background and purpose: Disturbance in the immune system is one of the main causes of endometriosis. Previous studies have shown the role of physical activity and antioxidant supplements on regulating the expression of genes related to improving the immune system, and reducing inflammation and infection. The present study examines the effect of swimming and vitamin E supplementation on the expression of NFKβ1 and P65 genes in endometriosis model rats.
Materials and methods: Thirty female rats were divided into six groups (n=5 per group); healthy, endometriosis, without exercise-saline-endometriosis, exercise-saline-endometriosis, without exercise supplement-endometriosis, and exercise-supplement-endometriosis. Endometriosis was surgically induced. Physical activity included swimming for eight weeks, five sessions/week and 30 minutes/session, and supplement was provided by daily gavage of 200 mg of vitamin E/kg for eight weeks. Twenty four hours after the last swimming session, the animals were sacrificed and the endometriosis tissue was removed. Relative expression levels of NFKB1 and P65 genes were measured using Real-Time PCR. Data were analyzed using one-way and two-way ANOVA.
Results: Induction of endometriosis caused a significant increase in the expression of genes studied (P<0.05). Exercise and vitamin E independently caused a significant decrease in the genes expression in rats (P<0.05). No synergistic effect was observed regarding the effect of exercise and vitamin E on the dependent variables (P>0.05).
Conclusion: According to this study, swimming and vitamin E supplement can be considered in improving endometriosis.
Full-Text [PDF 349 kb]   (288 Downloads)    
Type of Study: Brief Report | Subject: physiology

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.