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Showing 2 results for Tumor Necrosis Factor Alpha
Effects of Eight Weeks of Core Stability Training on Serum level of Progranulin and Tumor Necrosis Factor Alpha in Women with Multiple Sclerosis
Maryam Karimi, Mahtab Moazzami, Najmeh Rezaeian,
Volume 15, Issue 1 (1-2021)
Abstract

Background and objectives: Multiple sclerosis (MS) is a common debilitating neurodegenerative disease caused by inflammatory demyelinating processes in the central nervous system. The present study aimed to evaluate the effects of core stability training on serum levels of progranulin and tumor necrosis factor alpha (TNF-α) in women with MS.

Methods: The study population consisted of 24 women with MS (aged 25 to 40 years) in Bojnourd (Iran) with expanded disability status scale score of 2-5. Patients were randomly divided into two groups of core stability training (n=12) and control (n=12). The training group performed 30-40 minutes of core stability training, three sessions a week for eight weeks. Blood sampling was done 24 hours before the first session and 48 hours after the last training session. Serum levels of progranulin and TNF-α were measured using commercial ELISA kits. Analysis of covariance was used to assess data at a significance level of 0.05 . 
Results: The eight-week core stability training was associated with a significant increase in serum level of progranulin (P=0.037) and a significant decrease in the level of TNF-α (P=0.000).
Conclusion: The findings indicate that the eight-week core stability training could significantly change serum levels of progranulin and TNF-α and improve the condition of women with MS. Therefore, this type of training could be applied as a complementary therapy for MS patients.

Upregulated A20 (TNFAIP3) expression during respiratory syncytial virus infection in mice
Bahman Aghcheli , Romina Yavarinamini , Alireza Tahamtan ,
Volume 20, Issue 1 (1-2026)
Abstract
Background: Severe lower respiratory tract infections in infants and young children are frequently caused by respiratory syncytial virus (RSV), with the degree of illness strongly associated with disproportionate inflammatory activity. The signaling protein A20 (TNFAIP3) functions to inhibit NF-κB pathway activation, suggesting a possible role in tempering RSV-triggered lung inflammation. In this study, we assessed how RSV infection alters A20 gene expression in the lungs using a mouse model system.
Methods: Of the twelve female BALB/c mice allocated for the study, half were administered RSV intranasally at a concentration of 3 × 106 plaque-forming units (PFU), while the remaining six served as uninfected controls. All animals were humanely euthanized five days post-infection. Upon collection, lung tissue samples were immediately processed. The relative expression levels of messenger RNA (mRNA) for the TNFAIP3 gene, which encodes the A20 protein, were subsequently quantified using real-time reverse transcription polymerase chain reaction (RT-PCR).
Results: Analysis by quantitative PCR revealed that A20 expression was significantly higher in the lungs of RSV-infected mice compared with uninfected controls at day 5 post-infection (P = 0.0048).
Conclusion: The upregulation of A20 in RSV-infected mice suggests its potential role in modulating post-viral pulmonary inflammation.
 

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