To investigate soybean responses to drought stress and growth through metabolism compensation after rehydration, and for the establishment of an optimal water-saving irrigation model, we used the soybean variety Suinong 14 as experimental material and adopted a weighing method for water control in potted plants. We exposed soybean plants to stress treatments at different growth stages using different stress levels and durations. We then studied the effects of drought stress and rehydration on soybean growth and development, osmoregulation, and endogenous hormonal regulations, as well as antioxidant systems. The results showed that drought stress inhibited increases in the soybean plant height and leaf area. This inhibition became more significant as the level, duration, and frequency of the drought stress increased. After rehydration, the soybean plant heights and leaf areas exhibited rapid increases and partial compensation for their decreased sizes. As the level, duration, and frequency of drought stress increased, the compensation effect decreased, but it did not return to the control level. Drought stress reduced the chlorophyll content and relative water content in the soybean leaves and increased the osmolyte contents, antioxidant potential, and peroxidation of the membrane lipids. In addition, the changes mentioned above became more dramatic as the drought stress level, duration, and frequency increased. Upon rehydration, various levels of growth compensation were observed in each physio-biochemical parameter. As the drought stress level, duration, and frequency increased, the compensation effect also increased. Overall, the compensation effect for drought stress that occurred at the early growth stages was higher than that at the later growth stages. Drought stress led to decreases in the ZR/IAA and ZR/ABA ratios in soybean leaves and an increase in the ABA/(IAA + GA + ZR) ratio; thus, the plant growth was inhibited. These hormone ratios exhibited more dramatic changes when the drought stress level became more severe and the stress duration was prolonged. After rehydration, these hormone ratios produced equal compensation effects. Therefore, the compensatory effect of rewatering after drought stress is conditional. Severe stress, especially long-term severe stress, will reduce the compensatory effect. At the same time, drought resistance treatment at seedling stage can improve the adaptability and compensatory effect of re-drought at grain filling stage.

No abstract

No abstract

Although estrogen has crucial functions for endometrium growth, the specific dose and underlying molecular mechanism in intrauterine adhesion (IUA) remain unclear. In this study, we aimed to investigate the effects of estrogen on epithelial-mesenchymal transition (EMT) in normal and fibrotic endometrium, and the role of estrogen and Wnt/β-catenin signaling in the formation of endometrial fibrosis. CCK-8 and immunofluorescence assay were performed to access the proliferation of different concentrations of estrogen on normal human endometrial epithelial cells (hEECs). qRT-PCR and western blot assay were utilized to explore the effect of estrogen on EMT in normal and fibrotic endometrium, and main components of Wnt/β-catenin signaling pathway in vitro . Hematoxylin and eosin and Masson staining were used to evaluate the effect of estrogen on endometrial morphology and fibrosis in vivo . Our results indicated that the proliferation of normal hEECs was inhibited by estrogen at a concentration of 30 nM accompanied by upregulation of mesenchymal markers and downregulation of epithelial markers. Interestingly, in the model of transforming growth factor β1 (TGF-β1)-induced endometrial fibrosis, the same concentration of estrogen inhibited the process of EMT, which might be partially mediated by regulation of the Wnt/β-catenin pathway. In addition, relatively high doses of estrogen efficiently increased the number of endometrial glands and reduced the area of fibrosis as determined by the reduction of EMT in IUA animal models. Taken together, our results demonstrated that an appropriate concentration of estrogen may prevent the occurrence and development of IUA by inhibiting the TGF-β1-induced EMT and activating the Wnt/β-catenin pathway.

No abstract