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BACKGROUND:Mangiferin is a biphenylpyridone compound extracted from mango leaves,bark and roots.Previous studies have shown that mangiferin can exert anti-systemic inflammatory effects through the activation of transcription factors such as NF-κB and JAK/STAT. OBJECTIVE:To investigate the effects and mechanisms of mangiferin on proliferation,migration and inflammatory factor release of rheumatoid arthritis fibroblast-like synovial cells(RA-FLS). METHODS:RA-FLS were divided into blank group,R848(TLR7/8 agonists)stimulated group,mangiferin low-,medium-,high-dose groups(2,4 and 8 μg/mL)and positive control group(Cu-CPT8,TLR8 pathway inhibitor).The cytotoxic effect of different mass concentrations of mangiferin was detected using cell counting kit-8 method and the final cellular dosing mass concentration was screened.The proliferation ability of RA-FLS was detected by cell clone formation assay,the migration ability of RA-FLS was detected by scratch assay and Transwell migration assay,and the expression of interleukin 1β,interleukin 6 and tumor necrosis factor α mRNA in RA-FLS was detected by qRT-PCR. RESULTS AND CONCLUSION:Compared with the blank group,the viability of RA-FLS was inhibited after treatment with mangiferin at 2-10 μg/mL,but there was no significant difference among groups(P>0.05),indicating that the toxic effect on RA-FLS was minimal.Compared with the R848-stimulated group,mangiferin decreased the number of cell clones,the scratch healing rate and the number of migrating cells in all dosing groups(P<0.01);and the expression of interleukin 1β,interleukin 6 and tumor necrosis factor α mRNA was also reduced in the mangostin medium-and high-dose groups(P<0.01).Compared with the R848-stimulated group,the number of cell clones,the scratch healing rate and the number of migrating cells as well as the expression levels of interleukin 6 and tumor necrosis factor α mRNA were significantly reduced in the positive control group(P<0.05,P<0.01).But there was no significant difference in the expression level of interleukin 1β.To conclude,mangiferin may exert its anti-rheumatoid arthritis effects through the TLR7/8 signaling pathway by inhibiting RA-FLS proliferation,migration,and inflammatory factor release.
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ObjectiveTo investigate the changes in peripheral blood mononuclear cells ［CD8+ T lymphocytes and natural killer (NK) cells］ and levels of perforin and granzyme B in these cells in children with infectious mononucleosis (IM), as well as their clinical significance in liver injury. MethodsA total of 60 children who met the diagnostic criteria for IM were enrolled, and 30 healthy children were enrolled as control group. With the help of cell surface markers and cytokine staining, flow cytometry was performed to analyze CD8+ T lymphocytes, NK cells, and the expression of perforin and granzyme B. The t-test was used for comparison of continuous data between groups; a one-way analysis of variance was used for comparison between three groups, and the Dunnett-t test was used for further comparison between two groups. ResultsAmong the 60 children with IM, the incidence rate of liver injury was 50% (30/60); 18 (60%) children had an alanine aminotransferase (ALT) level of ＜200 IU/L, 10 (33.3%) had an ALT level of ≥200 IU/L and ＜400 IU/L, and 2 (6.67%) had an ALT level of ≥400 IU/L. All children had normal liver functions after one month of treatment. Compared with the control group, the non-liver injury IM group and the liver injury IM group had significant increases in the expression of perforin and granzyme B in CD8+ T lymphocytes (all P＜0.05). Compared with the non-liver injury subgroup of IM patients, the liver injury subgroup had a significantly higher percentage of CD8+ T lymphocytes and significantly higher expression of perforin and granzyme B in NK cells (all P＜0.05). ConclusionThere is a high incidence rate of liver injury in children with IM, mainly mild or moderate elevation of aminotransferases, which are self-limiting and can be returned to normal. High levels of perforin and granzyme B in NK cells and a high percentage of CD8+ T lymphocytes are the cause of liver injury.
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We report 3 cases of polycystic ovary syndrome (PCOS) in which the patients had successful pregnancy after repeated implantation failure in at least 8 in vitro fertilization and embryo transfer (IVF-ET) cycles. The patients were treated with gonadotropin-releasing hormone antagonist (GnRH-ant) protocol and gonadotropin-releasing hormone angonist (GnRHa) for triggering ovulation, and successful pregnancy and normal deliveries were achieved after 9 IVT-ET cycles. For young patients with PCOS but a good ovarian reserve and a high ovarian response, treatment with GnRH antagonist protocol and GnRHa alone with appropriate management of the factors that may affect implantation can prevent severe ovarian hyperstimulation syndrome to achieve favorable clinical outcomes.