Autophagy attenuates the secondary senescence of endometrial stromal cells induced by Bisphenol S
- Chem Biol Interact. 2026 Jul 25:435:112138. doi: 10.1016/j.cbi.2026.112138.
- 1. Central Laboratory, Jilin Province People's Hospital, Changchun, China; Jilin Provincial Key Laboratory of Biotherapy and Gene Diagnosis, Jilin Province People's Hospital, Changchun, China.
- 2. Reproductive Medicine Center, Jilin Province People's Hospital, Changchun, China.
- 3. Central Laboratory, Jilin Province People's Hospital, Changchun, China.
- 4. School of Clinical Medicine, Changchun University of Chinese Medicine, Changchun, China.
- 5. Precision Molecular Medicine Center, Jilin Province People's Hospital, Changchun, China. Electronic address: [email protected].
- 6. Reproductive Medicine Center, Jilin Province People's Hospital, Changchun, China; Jilin Provincial Clinical Research Center for Reproductive Health, Jilin Province People's Hospital, Changchun, China. Electronic address: [email protected].
Bisphenol S (BPS), as an environmental pollutant, poses a potential threat to reproductive system health. In this study, we added BPS to primary human endometrial stromal cells (hEnSCs) to detect the acute injury it causes and its long-term effects on the endometrium. The results showed that short-term treatment with BPS can significantly promote oxidative stress and Apoptosis of hEnSCs, while long-term treatment can cause excessive senescence of hEnSCs and reduced receptivity. In addition, the culture medium of senescent cells treated with BPS can induce senescence of young hEnSCs. Studies have reported that secondary senescence can be alleviated, and we utilised the Autophagy activator Rapa to treat secondary senescence of hEnSCs. We found that Rapa can inhibit the senescence of young cells induced by the culture medium of senescent cells treated with BPS. Therefore, Autophagy activated by Rapa can attenuate the secondary senescence of hEnSCs induced by BPS-treated culture medium.
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Cat. No.Product NameDescriptionTargetResearch Area
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target: Endogenous Metabolite
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target: Progesterone Receptor
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target: mGluRResearch Areas: Neurological Disease