子宫内膜蜕膜化中氧化应激的调控机制：SLC7A11和磷酸戊糖途径的协同作用

In this study, we investigated the regulatory mechanisms of oxidative stress during endometrial decidualization. We found that the intracellular reactive oxygen species (ROS) levels decreased while the expression of the transporter protein SLC7A11 significantly increased upon decidualization induction. We hypothesized that SLC7A11 promotes the generation of intracellular NADPH by transporting cysteine, which is then converted to the antioxidant glutathione, thereby reducing intracellular oxidative stress levels.

Furthermore, we also observed the activation of the pentose phosphate pathway (PPP) and a significant increase in the levels of glycolytic metabolites during decidualization. Further experiments confirmed that the inhibition of the rate-limiting enzyme G6PD in the PPP suppressed decidualization. This suggests that the PPP plays an important regulatory role in endometrial decidualization.

Interestingly, decidualization induction was hindered under conditions of glucose deprivation. However, the blockade of decidualization induction could be reversed by the addition of extra NADPH, cysteine, or glutathione. We speculated that glucose deprivation leads to insufficient NADPH synthesis, resulting in decreased intracellular antioxidant levels, increased oxidative stress, and thus inhibiting the process of decidualization. The addition of NADPH, cysteine, or glutathione partially reversed intracellular oxidative stress, thereby improving the impact of glucose deprivation on decidualization.

In conclusion, the novelty of this study lies in the discovery of the synergistic effect of SLC7A11-mediated cysteine transport and glucose-dependent PPP on NADPH. These mechanisms promote endometrial cell decidualization by increasing intracellular cysteine content and enhancing antioxidant levels. This finding is important for understanding the antioxidant mechanisms of endometrial cells during decidualization and provides a new theoretical basis for the study of related diseases.

Based on our research findings, we can further speculate that the production of glutathione during decidualization may play an important role in protecting endometrial cells from oxidative stress damage. Additionally, the activation of the PPP may also be related to the regulation of cellular energy metabolism, which requires further investigation. Moreover, our results provide a new therapeutic strategy, which involves improving the impact of glucose deprivation on endometrial decidualization by increasing the supply of cysteine and NADPH.

In summary, this study reveals the regulatory mechanisms of oxidative stress during endometrial decidualization and discovers the synergistic effect of SLC7A11-mediated cysteine transport and glucose-dependent PPP on NADPH. These findings provide new insights and treatment strategies for a deeper understanding of the physiological process of endometrial decidualization and the occurrence of related diseases.