Regulation of autophagy-related gene expressions by Trans-chalcone in the lungs of adult male rats

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Abstract
Background. Autophagy is responsible for maintaining cellular homeostasis by degrading and recycling macromolecules and unwanted intracellular components, such as damaged organelles. Trans-chalcone is a compound with anti-cancer and anti-inflammatory properties. However, its impact on autophagy in lung tissue has not been investigated yet. Therefore, this study evaluated the effects of trans-chalcone on autophagy-related Gene Expressions in the lung. Methods. Twelve male rats were randomly divided into control and chalcone groups. In the control group, rats were orally gavaged with Tween 80(10%), while in the chalcone group, rats were orally gavaged with trans-chalcone once a day for six weeks. Blood and lung samples were collected from overnight fasted rats. Serum insulin and glucose levels were used to estimate the fasting glucose-to-insulin ratio. Further, a real-time polymerase chain reaction was performed to assess the levels of p62, LC3, and Beclin-1 gene expression in the lungs of rats. Results. Trans-chalcone significantly increased the fasting glucose-to-insulin ratio (insulin sensitivity). In addition, this compound significantly increased Beclin-1 mRNA expression levels and decreased p62 expression levels in the lungs of rats. Nevertheless, the upregulatory effect of this compound on LC3 expression was not statistically significant. Conclusion. Based on the findings, trans-chalcone increases insulin sensitivity and has a regulatory effect on autophagy in the lungs of healthy rats. Changes in Beclin-1 and p62 mRNA levels reflect this issue. Practical Implications. The ability of trans-chalcone to up-regulate Beclin-1, a key marker of autophagy, and down-regulate p62 mRNA expression indicates its regulatory effect on autophagy. Further studies are required to validate the potential of this chalcone as a promising treatment for autophagy-related lung diseases.

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