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HEI‑OC1 cells that were pretreated with PNS exhibited significantly increased cell viability compared with that noted in cells treated only with cisplatin. In addition, PNS suppressed the induction of apoptosis and ROS production following cisplatin treatment. The upregulation of NQO1, HO‑1 and GCLC expression in PNS‑pretreated cells was associated with p‑AKT levels and the activation of Nrf2. These findings suggested that PNS protected auditory cells against ototoxicity induced by cisplatin by activating AKT/Nrf2 signaling. PNS may serve as a potential candidate in regulating cisplatin‑induced cytotoxicity.Astronauts are inevitably exposed to two major risks during space flight, microgravity and radiation. Exposure to microgravity has been discovered to lead to rapid and vigorous bone loss due to elevated osteoclastic activity. In addition, long‑term exposure to low‑dose‑rate space radiation was identified to promote DNA damage accumulation that triggered chronic inflammation, resulting in an increased risk for bone marrow suppression and carcinogenesis. In our previous study, melatonin, a hormone known to regulate the sleep‑wake cycle, upregulated calcitonin expression levels and downregulated receptor activator of nuclear factor‑κB ligand expression levels, leading to improved osteoclastic activity in a fish scale model. These results indicated that melatonin may represent a potential drug or lead compound for the prevention of bone loss under microgravity conditions. However, it is unclear whether melatonin affects the biological response induced by space radiation. The aim of the present study was to evaluaiation.Vascular smooth muscle cell (VSMC) hyperplasia is a common cause of carotid restenosis. In the present study, the potential protective effects of docosahexaenoic acid (DHA) in carotid restenosis and the underlying mechanism of its effects were examined. VSMCs were treated with DHA, a polyunsaturated ω‑3 fatty acid. Cell migration and proliferation were assessed using wound healing and Cell Counting Kit‑8 assays and by measuring Ki‑67 protein levels. Additionally, the expression levels of microRNA‑155 were determined by reverse transcription‑quantitative PCR (RT‑qPCR). The involvement of microRNA‑155 in the regulation of migration and proliferation was evaluated by transfecting VSMCs with microRNA mimics and inhibitors. Moreover, the reversal of migration and proliferation after transfection of VSMCs with the microRNA mimics and subsequent treatment with DHA was investigated. A target gene of microRNA‑155 was identified using RT‑qPCR and luciferase assays. The migration and proliferation of VSMCs, as well as the expression of microRNA‑155 was inhibited by DHA stimulation. MicroRNA‑155 regulated the migration and proliferation of VSMCs. Finally, proliferation and migration of VSMCs were reduced following DHA treatment, which was mediated by an increase in the expression levels of microRNA‑155. Suppressor of cytokine signalling 1 (Socs1) was the target gene of microRNA‑155. In conclusion, DHA inhibited VSMC migration and proliferation by reducing microRNA‑155 expression. This effect may be caused by the microRNA‑155 target gene Socs1.The scavenger receptor class B type I (SR‑BI) is a multi‑ligand membrane protein receptor that binds to high‑density lipoprotein (HDL) under physiological conditions, promoting the selective uptake of cholesterol esters from HDL into cells. SR‑BI also promotes the reverse transport of excess cholesterol from peripheral tissues to the liver, contributing to the synthesis of bile acids for excretion and the removal of excess cholesterol from the body, thereby lowering the cholesterol load and exerting anti‑atherosclerotic effects. Studies in mice and humans have demonstrated that a functional defect of SR‑BI can cause atherosclerotic lesions and cardiovascular diseases, such as myocardial infarction and stroke. Additionally, SR‑BI in vascular endothelial cells promoted the deposition of low‑density lipoprotein under the endothelium. Although SR‑BI is widely expressed in various tissues and cell types throughout the body, its expression level and function vary accordingly. The present review focuses on the biological functions and mechanisms of SR‑BI in regulating atherosclerosis.Interleukin 17D (IL‑17D) plays an important role in host defense against inflammation and infection. In the present study, the role of nuclear factor erythroid 2‑related factor 2 (Nrf2) in regulating the production of IL‑17D was investigated under hyperoxia. For this purpose, neonatal rats were randomized into two groups; the model group was exposed to hyperoxia (80‑85% O2), while the control group was maintained under normoxic conditions (21% O2). Small intestine tissue was collected on postnatal days 3, 7, 10 and 14. IL‑17D expression was detected by immunofluorescence, immunohistochemistry and western blotting. The levels of Nrf2 and kelch‑like ECH‑associated protein 1 (keap1) were detected by immunohistochemistry and western blotting. Results showed that IL‑17D expression in intestine epithelial cells increased steadily, reaching a peak on day 7, and decreased gradually on days 10 and 14 under hyperoxia. Nrf2 expression was consistent with IL‑17D, and it was positively correlated with IL‑17D. However, on postnatal days 10 and 14, the number of CD4+ T cells and CD19+ B cells expressing IL‑17D was increased, and positive cells of the model group were significantly more than that of the control group. Keap1 levels were lower at the early stage. In conclusion, the expression levels of intestinal IL‑17D and Nrf2 were altered simultaneously following neonatal rat development in hyperoxia, indicating that Nrf2 may be involved in regulating the expression of IL‑17D in intestinal epithelial cells. learn more Moreover, IL‑17D in intestinal epithelial cells may play a unique immunological role during hyperoxia.Esophageal squamous cell carcinoma (ESCC) is a type of digestive tract malignant tumor that severely threatens human health. The long non‑coding RNA BRAF activated non‑coding RNA (BANCR) and insulin‑like growth factor 1 receptor (IGF1R) are associated with various types of cancer; however, it remains unclear whether BANCR can regulate IGF1R expression in ESCC. In the present study, the expression levels of BANCR, IGF1R mRNA and microRNA‑338‑3p (miRNA/miR‑338‑3p) in ESCC tissues or cells were detected by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). The levels of IGF1R, E‑cadherin, N‑cadherin, Vimentin, p‑Raf‑1, p‑MEK1/2 and p‑ERK1/2 were measured by western blot analysis. The proliferation, migration and invasion of ESCC cells were determined by 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide (MTT) or Transwell assays. The relationship between miR‑338‑3p and BANCR or IGF1R was predicted using starBase2.0 and confirmed by dual‑luciferase reporter assay. The role of BANCR in ESCC in vivo was confirmed through a tumor xenograft assay.