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The Effects of Soluble Epoxide Hydrolase Inhibitor (sEHi) in a Murine Model of Asthma

Undergraduate #161
Discipline: Biological Sciences
Subcategory: Pollution/Toxic Substances/Waste

Jontravious Wallace - Fort Valley State University
Co-Author(s): Savannah Mack, Ciara Fulgar, Emilia Laing, and Kent Pinkerton, Ph.D. University of California, Davis, CA



Asthma is a chronic lung disease that inflames and narrows the airways. According to the CDC 18.4 million adults currently have asthma. In previous studies it has been demonstrated that inhibition of soluble epoxide hydrolase attenuates allergic airway inflammation and airway responsiveness in a murine model. Therefore, sEH inhibitors may have potential as a novel therapeutic strategy for allergic asthma. An asthma model was used to test the efficacy of 4 different delivery methods. We hypothesize that treatment with the sEHi would reduce the degree of inflammation in an asthmatic lung. `A murine model of asthma was created by administering Ovalbumin (OVA). Following, the Soluble Epoxide Hydrolase Inhibitor (sEHi) (1-Trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea, TPPU) was given via 4 different methods of delivery. The results are based on airway (bronchiole) inflammation scores. Statistical significance is seen between the control and OVA + PEG group (*p-value = 0.026031) and between the control and OVA + TPPU (S.C.) group (#p-value = 0.026031).The 2 HR group compared to the Vehicle group showed that inhalation was more effective , but it does not show a level of significant difference. The p-value for the difference in means between the two is 0.15684. Based on the results my hypothesis was rejected.

Not Submitted

Funder Acknowledgement(s): This work was supported by NSF HRD (#1238789) HBCU-UP Targeted Infusion grant to Prof. Seema Dhir at Fort Valley State University, Fort Valley, GA.

Faculty Advisor: Prof. Seema Dhir, dhirs@fvsu.edu

Role: I tested the effect of four different delivery methods by treating lung tissue samples with TPPU an inhibitor of sEHi. I measured the degree of inflammation in the asthmatic lung tissue.

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This material is based upon work supported by the National Science Foundation (NSF) under Grant No. DUE-1930047. Any opinions, findings, interpretations, conclusions or recommendations expressed in this material are those of its authors and do not represent the views of the AAAS Board of Directors, the Council of AAAS, AAAS’ membership or the National Science Foundation.

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