Non-infectious prenatal mortality severely affects the porcine industry, with pathological placentation as a likely key reason. Previous studies have demonstrated that peroxisome proliferator-activated receptor gamma (PPARγ) deficiency causes defects in the uteroplacental vasculature and induces embryonic losses in mice. However, its role in porcine placental angiogenesis remains unclear. In the present study, PPARγ expression was investigated in porcine uteroplacental tissues at gestational day (GD) 25, GD40 and GD70 via quantitative polymerase chain reaction (qPCR), Western blot and immunohistochemistry (IHC). Moreover, the roles of PPARγ in porcine placental angiogenesis were investigated using a cell model of porcine umbilical vein endothelial cells (PUVECs) to conduct proliferation, migration and tube formation assays in vitro and a mouse xenograft model to assess capillary formation in vivo. The results showed that PPARγ was mainly located in the glandular epithelium, trophoblast, amniotic chorion epithelium and vascular endothelium, as indicated by the higher expression levels at GD25 and GD40 than at GD70 in endometrium and by higher expression levels at GD40 and GD70 than at GD25 in placenta. Moreover, PPARγ expression was significantly downregulated in placenta with dead foetus. In PUVECs, knocking out PPARγ significantly inhibited proliferation, migration and tube formation in vitro and inhibited capillary formation in mouse xenografts in vivo by blocking S-phase, promoting apoptosis and downregulating the angiogenic factors of VEGF and its receptors. Overall, the spatiotemporal heterogeneity of PPARγ expression in porcine uteroplacental tissue suggests its vital role in endometrial remodelling and placental angiogenesis, and PPARγ regulates placental angiogenesis through VEGFmediated signalling.

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Perillae Fructus oil has an important function in relieving cold stress. However, its application in this aspect has still been restricted because of instability and low bioavailability. In this study, Perillae Fructus oil was extracted through Soxhlet extraction, analyzed through gas chromatography–mass spectrometry (GC–MS), and nanopackaged into a yeast shell for the preparation of nanoparticles for oral administration. The characteristics of the nanoparticles were investigated using a Malvern zeta‐size nanoinstrument, scanning electron microscopy (SEM), and high‐performance liquid chromatography (HPLC). Then, the roles of orally administered nanoparticles in relieving cold stress were evaluated by investigating blood physiological and biochemical indexes in mice. The results showed that the oil yield from Perillae Fructus and shell yield from yeast cells were ~48.37% and ~16.87%, respectively. Approximately 89.21% of the added oil was packaged into the yeast shell to form nanoparticles with an average diameter of 316.74 nm and a surface charge of +2.9 mV. The nanoparticles were stable in simulated gastric acid and could be effectively released in simulated intestinal fluid with an efficiency of ~91.34%. After oral administration of nanoparticles, the mouse blood indexes of white blood cells (WBCs), superoxide dismutase (SOD) activity, and malonaldehyde (MDA) content were recovered compared to those in model mice, with a more remarkable effect than oral administration of free Perillae Fructus oil. Overall, the stability and bioavailability were improved by packaging Perillae Fructus oil into a yeast shell. These nanoparticles are a new agent for the prevention of cold stress.