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Continuous application of chemical fertilizers in plant cultivation can lead to the deterioration of the soil environment, resulting in reduced crop yield and quality. Currently, organic fertilizers, such as vermicompost, can partially replace chemical fertilizers and maximize yields while maintaining soil fertility. However, the effects of chemical fertilizers combined with vermicompost on watermelon (Citrullus lanatus) yield and quality are unclear. A field experiment was carried out on the watermelon cultivar Lihua No. 6. Six treatments were applied: no fertilizer (CK, control, 0N–0P–0K), 100% chemical fertilizer [CF, 5.4N–1P–5.4K (256, 47, and 255 kg·ha−1)], 75% chemical fertilizer + 25% organic fertilizer [A1, 5.4N–1P–5.4K (192, 35, and 191 kg·ha−1) + 2250 kg·ha−1 vermicompost], 50% chemical fertilizer + 50% organic fertilizer [A2, 5.4N–1P–5.4K (128, 24, and 127 kg·ha−1) + 4500 kg·ha−1 vermicompost], 25% chemical fertilizer + 75% organic fertilizer [A3, 5.4N–1P–5.4K (64, 12, and 64 kg·ha−1) + 6750 kg·ha−1 vermicompost], and 100% organic fertilizer (A4, 9000 kg·ha−1 vermicompost). Indices related to the growth, yield, and quality of watermelons were determined. Compared with CK, chemical fertilizer alone or in combination with organic fertilizers significantly increased growth parameters (plant height and leaf area) and chlorophyll content. The five fertilizer treatments enhanced the single fruit weight, yield, and biomass. In addition, the yield of reduced chemical fertilizer plus organic fertilizer was comparable to that of watermelons treated with CF. Compared with CF, the fertilizer treatments, especially the 1:1 mixture of chemical and organic fertilizer (A2) group, had elevated fruit-soluble solids and soluble sugar content, and reduced organic acid levels. Therefore, a combination of 50% chemical fertilizer and 50% organic fertilizer can effectively enhance the yield and quality of watermelons. These findings have important implications for guiding the management of watermelon fertilization and development of sustainable agriculture.

Dynamic changes in the endometrium are crucial for establishing early pregnancy in ruminants. Blastocyst elongation and implantation require hormones and nutrients to be secreted from the maternal endometrium. The fatty acid-binding protein FABP4 is a widely expressed fatty acid transport protein that promotes cell proliferation, migration, and invasion and is involved in conceptus implantation. However, the mechanism underlying the functional regulation of endometrial epithelial cells (EECs) by FABP4 during ovine peri-implantation remains unclear. We simulated hormonal changes in vitro in sheep EECs (SEECs) during the peri-implantation period and found that it elevated FABP4 expression. FABP4 inhibition significantly reduced cell migration, endoplasmic reticulum stress, and autophagy, suggesting that FABP4 regulates endometrial function in sheep. Moreover, the FABP4 inhibitor BMS309403 counteracted hormone-mediated functional changes in SEECs, and an endoplasmic reticulum stress activator and autophagy inhibitor reversed the abnormal secretion of prostaglandins induced by FABP4 inhibition. These results suggest that FABP4 affects ovine endometrial function during early gestation by regulating endoplasmic reticulum stress and autophagy in SEECs.

Peroxisome proliferator-activated receptor gamma (PPARγ) is a key nuclear receptor transcription factor that is highly expressed in trophoblastic cells during embryonic attachment and is accompanied by rapid cell proliferation and increased lipid accumulation. We previously showed that the autophagy pathway is activated in cells after activation of PPARγ, accompanied by increased lipid accumulation. In this study, we used PPARγ agonist rosiglitazone and inhibitor GW9662, as well as autophagy activator rapamycin and inhibitor 3-methyladenine, to unravel the probable mechanism of PPARγ engaged in lipid metabolism in sheep trophoblast cells (STCs). After 12 h, 24 h, and 48 h of drug treatment, the levels of autophagy-related proteins were detected by Western blot, the triglyceride content and MDA level of cells were detected by colorimetry, and the lipid droplets and lysosomes were localized by immunofluorescence. We found that PPARγ inhibited the activity of mammalian target of rapamycin (mTOR) pathway in STCs for a certain period of time, promoted the increase of autophagy and lysosome formation, and enhanced the accumulation of lipid droplets and triglycerides. Compared with cells whose PPARγ function is activated, blocking autophagy before activating PPARγ will hinder lipid accumulation in STCs. Pretreatment of cells with rapamycin promoted autophagy with results similar to rosiglitazone treatment, while inhibition of autophagy with 3-methyladenine reduced lysosome and lipid accumulation. Based on these observations, we conclude that PPARγ can induce autophagy by blocking the mTOR pathway, thereby promoting the accumulation of lipid droplets and lysosomal degradation, providing an energy basis for the rapid proliferation of trophoblast cells during embryo implantation. In brief, this study partially revealed the molecular regulatory mechanism of PPARγ, mTOR pathway, and autophagy on trophoblast cell lipid metabolism, which provides a theoretical basis for further exploring the functional regulatory network of trophoblast cells during the attachment of sheep embryos.

Trophoblast cells synthesize and secrete prostaglandins (PGs), which are essential for ruminants in early gestation to recognize pregnancy. Hormones in the intrauterine environment play an important role in regulating PGs synthesis during implantation, but the underlying mechanism remains unclear. In this study, co-treatment of sheep trophoblast cells (STCs) with progesterone (P4), estradiol (E2), and interferon-tau (IFN-τ) increased the ratio of prostaglandin E2 (PGE2) to prostaglandin F2α (PGF2α) and upregulated peroxisome proliferator-activated receptor γ (PPARγ) expression, while inhibiting the mechanistic target of rapamycin (mTOR) pathway and activating cellular autophagy. Under hormone treatment, inhibition of PPARγ activity decreased the ratio of PGE2/PGF2α and cellular activity, while activating expression of the mTOR downstream marker—the phosphorylation of p70S6K (p-p70S6K). We also found that the PPARγ/mTOR pathway played an important role in regulating trophoblast cell function. Inhibition of the mTOR pathway by rapamycin increased the ratio of PGE2/PGF2α and decreased the expression of apoptosis-related proteins after inhibiting PPARγ activity. In conclusion, our findings provide new insights into the molecular mechanism of prostaglandin regulation of trophoblast cells in sheep during early pregnancy, indicating that the PPARγ/mTOR pathway plays an important role in PGs secretion and cell viability.