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| 1 | Cell–cell contact with proinflammatory macrophages enhances the immunotherapeutic effect of mesenchymal stem cells in two abortion models显示文摘Mesenchymal stem cells(MSCs),which are pluripotent cells with immunomodulatory properties,have been considered good candidates for the therapy of several immune disorders,such as inflammatory bowel diseases,concanavalin A-induced liver injury,and graft-versus-host disease.The embryo is a natural allograft to the maternal immune system.A successful pregnancy depends on the timely extinction of the inflammatory response induced by embryo implantation,followed by the switch to a tolerant immune microenvironment in both the uterus and the system.Excessive infiltration of immune cells and serious inflammatory responses are triggers for embryo rejection,which results in miscarriage.Here,we demonstrated that adoptive transfer of MSCs could prevent fetal loss in a lipopolysaccharide(LPS)-induced abortion model and immune response-mediated spontaneous abortion model.The immunosuppressive MSCs alleviated excessive inflammation by inhibiting CD4+T cell proliferation and promoting the decidual macrophage switch to M2 in a tumor necrosis factor-stimulated gene-6(TSG-6)-dependent manner.Cell-tocell contact with proinflammatory macrophages increased the TSG-6 production by the MSCs,thereby enhancing the suppressive regulation of T cells and macrophages.Moreover,proinflammatory macrophages in contact with the MSCs upregulated the expression of CD200 on the stem cells and facilitated the reprogramming of macrophages towards an anti-inflammatory skew through the interaction of CD200 with CD200R on proinflammatory macrophages.Therefore,the results demonstrate that a TSG-6-mediated paracrine effect,reinforced by cell-to-cell contact between MSCs and proinflammatory macrophages,is involved in the mechanism of MSC-mediated abortion relief through the induction of immune tolerance.Our study also indicates the potential application of MSCs in clinical recurrent miscarriages. | Yanhong Li Di Zhang Ling Xu Lin Dong Ji Zheng Yikong Lin Jiefang Huang Yanyun Zhang Yu Tao Xingxing Zang Dajin Li Meirong Du | 2019 | Cellular & Molecular Immunology2019，16，12： | 23 |
| 2 | SCM-198 protects endometrial stromal cells from oxidative damage through Bax/Bcl-2 and ERK signaling pathways显示文摘In creasi ng amounts of evidence dem on strated that accumulative reactive oxyge n species (ROS) and apoptosis of human endometrial stromal cells (ESCs) are closely associated with endometrial dysfunction induced by oxidative stress, which plays an important role in the pathological process of multiple gyn ecological and reproduction-related diseases. SCM-198, an alkaloid active component of Leonurus japonicas Houtt, has been reported to have anti-oxidative activity. However, the specific mechanisms of SCM-198 in the prevention of endometrial damage remain unknown. In the present study, we assessed the effect of SCM-198 on hydrogen peroxide (H2O2Hnduced oxidative injury in ESCs. ESCs were pretreated with SCM-198 for 4 h and then challenged with H2O2.Morphology ch a nges, apoptosis rate, and intracellular ROS producti on were measured to assess the level of oxidative injury. Flow cytometry and western blot analysis were performed to detect the expression levels of Bax, Bcl-2, active-caspase-3, and mitogen-activated protein kinases pathways. Classic inflammation cytokines were measured by real-time polymerase chain reactions. Our results showed that SCM-198 attenuated apoptosis and ROS generation of ESCs induced by H2O2. H2O2 induced the apparent apoptotic characteristics, including fragmentation of DNA, upregulation of Bax/Bcl2, activation of caspase-3, and secretion of inflammation cytokines, which were all ameliorated by SCM-198. Furthermore, H2O2-induced apoptosis-related ERK1/2 pathway activation was restrained by SCM-198 pretreatme nt. These fin dings suggested that SCM-198 could protect ESCs from oxidative injury, mainly by inhibiting oxidative stress and reducing apoptosis. | Yunyun Li Yikong Lin Xixi Huang Chunfang Xu Xinhua Liu Li Wang Min Yu Dajin Li Yizhun Zhu Meirong Du | 2019 | Acta Biochimica et Biophysica Sinica2019，51，6： | 10 |
| 3 | SCM-198 ameliorates endometrial inflammation via suppressing the LPS-JNK-cJUN/cFOS-TLR4-NF-κB pathway显示文摘Endometritis is an inflammatory disease of the endometrium,which is responsible for endometrial dysfunction,decidualization failure,and increased incidence of early pregnancy loss.SCM-198,a synthetic form of leonurine,is well known to possess anti-inflammatory effects.SCM-198 has been reported to display beneficial effects on endometritis.However,the specific mechanisms of SCM-198 in preventing endometritis remain unknown.In this study,we focused on the molecular mechanism of SCM-198 in inhibiting endometritis.The anti-inflammatory effects and the related signaling pathways of SCM-198 were studied in vitro using human endometrial stromal cells(hESCs).Reverse transcriptase-polymerase chain reaction and western blot analysis results demonstrated that SCM-198 markedly inhibited lipopolysaccharide(LPS)-induced endometrial inflammatory response by suppressing the LPS-JNK-cJUN/cFOS-TLR4-NF-κB pathway.The preventive and therapeutic effects of SCM-198 on endometrial inflammation were explored by using a mouse model of LPS-induced endometritis.SCM-198 produced essentially the same effects when administered either post-treatment(after LPS)or pre-treatment(before LPS)via vaginal or intraperitoneal administration.In vivo results indicated that SCM-198 is a potential effective drug for the treatment of endometritis. | Yikong Lin Yunyun Li Xinyi Li Xinhua Liu Xiaolin Wang Min Yu Yizhun Zhu Meirong Du | 2021 | Acta Biochimica et Biophysica Sinica2021，53，9： | 1 |
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