Background: Premature ovarian insufficiency (POI) is characterized by abnormal ovarian function before the age of 40. POI showed that primordial follicles developed in disorder. mTOR signaling plays a vital role in the process of follicle development. It has been verified that the mTOR signaling pathway activator, MHY1485, can promote primordial follicle development in mice. We considered that MHY1485 would be a promising fertility preservation method for POI patients.
Methods: The fragmented ovarian tissues of normal woman was cultured with activator MHY1485 , and then the control and activated ovaries were transplanted into the kidney capsules of ovariectomized mice. We then used the Infinium Human Methylation EPIC BeadChip to verify the DNA methylation level of ovarian tissues, thus exploring the effectiveness of them.
Results: MHY1485 stimulated mTOR, S6K1, and rpS6 phosphorylation. Cultured with MHY1485, ovarian weights increased and endocrine function was restored. The number of growing follicles was increased. The activation process did not induce histological changes or abnormal DNA methylation occurrence.
Conclusion: MHY1485 for activation (IVA) is effective for ovarian rejuvenation and is a potential therapeutic treatment for POI patients.
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http://dx.doi.org/10.3389/fgene.2020.603683 | DOI Listing |
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Department of Medicine, Section of Pulmonary and Critical Care Medicine, The University of Chicago, Chicago, IL 60637.
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Neonatal hypoxic-ischemic encephalopathy (HIE) is the most common cause of death and long-term disabilities in term neonates. Caffeine exerts anti-inflammatory effects and has been used in neonatal intensive care units in recent decades. In our neonatal rat model of hypoxic-ischemic (HI) brain injury, we demonstrated that a single daily dose of caffeine (40 mg/kg) for 3 days post-HI reduced brain tissue loss and microgliosis compared to the vehicle group.
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Department of Medical Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, Sichuan, China, 610041.
The EGFR-TKIs (epidermal growth factor receptor-tyrosine kinases inhibitors) offer significant benefits to lung cancer patients with sensitive EGFR mutations; however, the development of acquired resistance poses a significant challenge and leads to poor prognosis. Thus, exploring novel therapeutic strategies to overcome EGFR-TKI resistance is urgently needed. This study introduces an innovative approach utilizing folic acid-modified milk exosomes loaded with c-kit siRNA (FA-mExo-siRNA-c-kit) to target EGFR-TKI resistance in lung cancer.
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