Objective To investigate the predictive value of vitamin D,sex hormones and their receptors in the development and regression of male patients with clinical isolated syndrome(CIS).Methods A total of 40 male CIS patients were included in the CIS group and 30 healthy subjects matched in age and long-term res-idence were included in the control group.The levels of vitamin D[1,25(OH)2D2 and 1,25(OH)2D3]inpe-ripheral blood of the included individuals and the first relapsed multiple sclerosis patients(MS group)were detected by ultra-high-performance liquid chromatography-tandem mass spectrometry.The levels of testoster-one(T),progesterone(P),and estradiol(E2)in peripheral blood were detected by electrochemiluminescence.Estrogen receptor(ERα,ERβ),androgen receptor(AR)and vitamin D receptor(VDR)levels in lymphocyte supernatant were detected by enzyme-linked immunosorbent assay(ELISA).Results After a median follow-up of 31.5 months,29 patients(72.5％)with CIS were converted to multiple sclerosis.Compared with pa-tients with non-recurrent CIS patients,patients with multiple sclerosis had a younger age of onset and were prone to positive oligoclonal bands.Compared with HC group,vitamin D levels were reduced in CIS patients,and the difference was statistically significant(P＜0.05).When CIS patients reverted to multiple sclerosis,se-rum levels of E2,ERα,and ERβ were elevated compared with those before relapse,and the levels of testosteroneand AR were decreased,and the difference was statistically significant(P＜0.05).Correlation analysis showed no correlation between peripheral blood levels of vitamin D,sex hormones and their receptors and EDSS in CIS patients.Conclusion Male CIS patients with younger onset age and positive oligoclonal bands are prone to transition to multiple sclerosis.The decrease of vitamin D level may be associated with the onset of male CIS.Vitamin D,sex hormones,and their receptors have no predictive value in the conversion of CIS to multiple sclerosis.

Objective To investigate the effect of scutellarin(STR)on the proliferation and migration of human prostate cancer cell line(PC-3)and its underlying mechanism.Methods PC-3 cells were divided into low-dose STR group,medium-dose STR group,high-dose STR group,colivelin(STAT3 activator)group,high-dose STR+colivelin group and control group.CCK-8 assay and colony formation experiments were applied to detect cell prolif-eration;Scratch experiment was applied to detect cell migration;Transmission electron microscopy was applied to observe the mitochondrial ultrastructure of PC-3 cells.The intracellular free Fe2+,malondialdehyde(MDA)content and reactive oxygen species(ROS)levels were detected by colorimetric method;RT-qPCR was applied to detect the mRNA expression of member 11 of solute vector family(SLC7A11),proliferating cell nuclear antigen(PCNA)and matrix metalloproteinase-9(MMP-9)in cells;Western blot was used to detected p-STAT3 and GPX4 proteins in cells.Results Compared to control group,the mitochondrial structure of PC-3 cells in the low-dose STR group,medium-dose STR group and high-dose STR group was significantly disrupted.The A450 value,colony formation rate,scratch healing rate,PCNA,SLC7A11,MMP-9 mRNA expression,and p-STAT3,GPX4 protein all reduced.While Fe2+,MDA content,and that ROS level increased with dose-dependent way(P＜0.05).Compared with control group,the destruction of mitochondrial structure in cells from colivelin group improved;The A450 value,colony formation rate,scratch healing rate,PCNA,SLC7A11,MMP-9 mRNA expression and p-STAT3,GPX4 protein all increased,while Fe2+MDA content,and ROS level decreased(P＜0.05).Compared with high-dose STR group,the damage of mitochondrial structure in PC-3 cells in the high-dose STR+colivelin group was re-duced.The A450 value,colony formation rate,scratch healing rate,PCNA,SLC7A11,MMP-9 mRNA expression,and p-STAT3,GPX4 protein increased,while Fe2+,MDA content and ROS level decreased(P＜0.05).Conclusions The mechanism by of STR reducing proliferation and migration of prostate cancer cells is potentially related to the inhibition of STAT3/GPX4 pathway.