1.Extracellular vesicles: Roles in oocytes and emerging therapeutic opportunities.
Zhongyu ZHAO ; Yinrui SUN ; Renhao GUO ; Junzhi LIANG ; Wanlin DAI ; Yutao JIANG ; Yafan YU ; Yuexin YU ; Lixia HE ; Da LI
Chinese Medical Journal 2025;138(9):1050-1060
The production of high-quality oocytes requires precisely orchestrated intercellular communication. Extracellular vesicles (EVs) are cell-derived nanoparticles that play a vital role in the transfer of bioactive molecules, which has gained much attention in the field of diagnosis and treatment. Over the past ten years, the participation of EVs in the reproductive processes of oocytes has been broadly studied and has shown great potential for elucidating the intricacies of female reproductive health. This review provides an extensive discussion of the influence of EVs on oocytes, emphasizing their involvement in normal physiology and altered cargo under pathological conditions. In addition, the positive impact of therapeutic EVs on oocyte quality and their role in alleviating ovarian pathological conditions are summarized.
Humans
;
Extracellular Vesicles/physiology*
;
Oocytes/cytology*
;
Female
;
Animals
;
Cell Communication/physiology*
2.Research progress on programmed death receptor 1/ ligand 1 inhibitor in immunotherapy of head and neck squamous cell carcinoma
ZENG Fei ; LU Jie ; SUN Renhao ; FANG Yikang ; YU Wenyi ; YANG Fang ; ZHAO Lu
Journal of Prevention and Treatment for Stomatological Diseases 2021;29(10):706-710
Head and neck squamous cell carcinoma (HNSCC) is a common malignant tumor that seriously threatens human health and life. With increasing studies on the mechanism of tumor immune escape, programmed death receptor 1 (PD-1) and programmed death ligand receptor 1 (PD-L1) have been proven to be involved in tumor immune escape. The primary mechanism is that PD-1 recruits protein tyrosine phosphatase (SHP-2) to dephosphorylate downstream tyrosine kinase (SyK) and phosphatidylinositol 3-kinase (PI3K), thereby inhibiting downstream protein kinase B (AKT), extracellular regulated protein kinases (ERK) and other important signaling pathways, ultimately inhibiting T cell activation. In recent years, PD-1/PD-L1 inhibitors have become popular immunotherapies. Pembrolizumab and nivolumab have been approved for HNSCC patients by the U.S. Food and Drug Administration. Both durvalumab and atezolizumab are still in clinical trials, and published data show that both have certain safety and efficacy but still need much clinical data to support them. Meanwhile, the combination of PD-1/PD-L1 inhibitors with radiotherapy, chemotherapy and immunotherapy is still controversial in terms of clinical efficacy and adverse events, and further research is needed. However, serious immune-related adverse reactions limit the clinical application of PD-1/PD-L1 inhibitors, despite promising curative effects. Therefore, developing novel inhibitors and investigating stable and effective biomarkers and upstream and downstream signaling mechanisms are urgent issues.
3.Protective effects of ethyl docosahexaenoate on brain oxidative injury and edema induced by cerebral ischemic reperfusion
Renhao XUE ; Dehua CAO ; Weifa ZHENG ; Liang SUN ; Zhili LIU
Chinese Journal of Marine Drugs 2001;0(05):-
Objective To investigate the protective effects of ethyl docosahexaenoate on brain oxidative injury and edema induced by cerebral ischemic/reperfusion in gerbils. Methods The gerbils were subjected to both common carotid arteries occlusion. The contents of MDA and GSH, the activities of GSH-PX, CAT, SOD and ATPase, the water content and the concentrations of Na + and Ca 2+ were measured. Histopathological examination was also done. Results The pretreatment with E-DHA significantly prevented the raise of MDA level, the decline of GSH content, the activities of GSH-Px, CAT, ATPase and the increases of Ca 2+, Na + and water content. Conclusion E-DHA has protective effect on brain ischemic injury and edema, which may be due to an inhibitory action on hydroxyl radical formation and brain edema.


Result Analysis
Print
Save
E-mail