Hyperoxia-induced BPD mouse model establishment

Fifty C57BL/6 J newborn mice (within 2 h of birth) with an average weight of 1.36 g ± 0.09 g were randomly divided into one litter (equal numbers of mice per litter). The mice for BPD modeling were exposed to 85% oxygen for postnatal day 1 (P1)—P14, while the control mice with normal lung development were exposed to 21% oxygen. Male and female animals were used because no gender bias was found in the study on perturbations to lung development of C57BL/6 J mice in response to hyperoxia. The normal hypoxia and hyperoxia was alternated every 24 h in order to limit oxygen toxicity. The mice were then randomly assigned into the control group (normal air-treated C57BL/6 J newborn mice), the BPD group (hyperoxia-induced BPD mice), the BPD + Hdac3 knockout (Hdac3^−/−) group (BPD mice treated with Hdac3 knockout) (Wang et al. 2016), the hyperoxia + Hdac3^−/− + antagomir negative control (NC) group (hyperoxia-induced BPD mice with Hdac3 knockout and injected with antagomir NC), and the hyperoxia + Hdac3^−/− + miR-17-antagomir group (hyperoxia-induced BPD mice with Hdac3 knockout and injected with miR-17-antagomir), with ten mice in each group. From the 5th day following grouping, mice were intraperitoneally injected with miR-17-antagomir and the corresponding antagomir NC (both were purchased from Shanghai GenePharma Co., Ltd., Shanghai, China) at a dose of 80 mg/kg body weight, after which the weight was measured every three days. Mice in P14 (the stage of massive alveolarization) were euthanized by intraperitoneal injection of excessive pentobarbital (500 mg/kg), and the lungs of mice were then extracted for further analyses (Zhu et al., 2020).