Abstract
Enhanced Airway Hyperresponsiveness by Up-Regulation of Tumor Necrosis Factor Αlpha Pathway in Long-Term High-Fat and Sucrose Diet in Bama Mini Pigs
Department of Histology and Embryology, School of Basic Medical Sciences, Inner Mongolia Medical University, 1Department of Gastroenterology, TCM hospital of Mongolian Medicine, Hohhot, Inner Mongolia 010110, China
Correspondence Address:
Nashunbayaer, Department of Histology and Embryology, School of Basic Medical Sciences, Inner Mongolia Medical University, Hohhot, Inner Mongolia 010110, China, E-mail: nashunbayaer@163.com
Obesity can lead to an elevated risk of asthma, however, the associated mechanism between them remains largely unclear. The present work analyzed how diet-induced obesity affects tumor necrosis factor alpha expression and its protein expression in the lungs of Bama mini pigs following ovalbumin treatment. Altogether 20 mini pigs were randomized into 4 groups (5 pigs in each group) namely, control with normal diet, ovalbumin-sensitization with normal diet, control with high-fat diet and ovalbumin-sensitization with high-fat diet. Mini pigs were raised using high-fat diet or standard pellets for 23 mo; in the final month, they were sensitized and challenged with saline or ovalbumin. After these treatments, lungs were collected to detect tumor necrosis factor-alpha messenger ribonucleic acid through real-time polymerase chain reaction assay. Body weight, lipid profiles and obesity indices were elevated in diet-induced obesity groups. Additionally, tumor necrosis factor-alpha and messenger ribonucleic acid expression significantly elevated in ovalbuminsensitization groups compared with the remaining groups (p<0.001). Besides, tumor necrosis factor-alpha and messenger ribonucleic acid expression of sensitization+high-fat diet group evidently elevated relative to remaining groups (p<0.001). According to our findings, high-fat diet upregulated tumor necrosis factoralpha, messenger ribonucleic acid and tumor necrosis factor-alpha protein expression within the experimental asthma model. Moreover, obesity-related asthma probably results in local pro-inflammatory factor activation and release.
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