https://www.selleckchem.com/products/Tanshinone-I.html Bronchopulmonary dysplasia (BPD), also known as chronic lung disease, is one of the most common respiratory diseases in premature new‑born humans. Mitochondria are not only the main source of reactive oxygen species but are also critical for the maintenance of homeostasis and a wide range of biological activities, such as producing energy, buffering cytosolic calcium and regulating signal transduction. However, as a critical quality control method for mitochondria, little is known about the role of mitophagy in BPD. The present study assessed mitochondrial function in hyperoxia‑exposed alveolar type II (AT‑II) cells of rats during lung development. New‑born Sprague‑Dawley rats were divided into hyperoxia (85% oxygen) and control (21% oxygen) groups. Histopathological and morphological properties of the lung tissues were assessed at postnatal days 1, 3, 7 and 14. Ultrastructural mitochondrial alteration was observed using transmission electron microscopy and the expression of the mitophagy proteins putative kiat the accumulation of dysfunctional mitochondria may be a key factor in the pathogenesis of BPD and result in attenuated alveolar development.Breast cancer is the most common type of cancer with the highest morbidity and mortality rates in women worldwide. Recent efforts to improve the current antitumor therapies have led to the development of novel treatment approaches based on the delivery of therapeutic non‑coding RNAs (ncRNAs) using nanotechnology. Treatment methods using lipid‑based nanoparticles (LBNPs) have greatly improved the delivery efficiency of ncRNAs into tumor cells and tissues. This type of delivery approach has provided significant advantages, such as reduced therapeutic doses, lower cytotoxicity to normal cells and the ability to reverse resistance to chemotherapy. LBNPs have demonstrated the ability to deliver therapeutic ncRNAs, more specifically microRNAs (miRNAs) and small interfering