致死性肺病 z-bo 2020-10-20 298

　　Recently, researchers at the University of Georgia discovered that the anti-tumor drug tricilibine can slow down or reverse the development of pulmonary fibrosis and pulmonary hypertension. Both of these are almost fatal. Related research results have been published in the "British Journal of Pharmacology".

　　When lung fibroblasts are chemically or physically damaged, they secrete collagen to repair the lung interstitial tissue, which leads to lung fibrosis. Pulmonary hypertension is a hemodynamic and pathophysiological disease in which pulmonary artery pressure rises above a certain critical value, and disability and mortality are high. In this study, researchers used mouse models to simulate human pulmonary fibrosis and pulmonary hypertension, and studied the effects of triselenium on these two diseases.

　　In previous studies, triselenoprotein produced akt1 protein. Akt1 has a partial effect on the development of myofibroblasts. It can move to tissue damage sites and help tissue repair damage. However, the imbalance of these cells can cause scarring, leading to lung fibrosis and loss of functional vasculature. The researchers waited until the mice began to develop a disease phenotype, and then injected tricycline once a day for 3 weeks. The results showed that the lung scar formation characteristics of each mouse were reduced, and the pulmonary vascular system was lost. After that, the lungs of some mice began to return to normal. The researchers also used mice lacking the akt1 pathway and found that none of the knockout mice exhibited pathological features of pulmonary fibrosis and pulmonary hypertension. They further tested their hypothesis and akt1, which proved to be an important factor in the development of these two diseases. .

　　Finally, the researchers are only relatively preliminary results, more to evaluate whether tricilibine has similar effects in patients with pulmonary fibrosis and pulmonary hypertension.