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1.
Chinese Journal of Contemporary Pediatrics ; (12): 172-178, 2023.
Article in Chinese | WPRIM | ID: wpr-971056

ABSTRACT

OBJECTIVES@#To investigate the change in the distribution of memory B cell subsets in children with frequently relapsing nephrotic syndrome (FRNS) during the course of the disease.@*METHODS@#A total of 35 children with primary nephrotic syndrome (PNS) who attended the Department of Pediatrics of the Affiliated Hospital of Xuzhou Medical University from October 2020 to October 2021 were enrolled as subjects in this prospective study. According to the response to glucocorticoid (GC) therapy and frequency of recurrence, the children were divided into two groups: FRNS (n=20) and non-FRNS (NFRNS; n=15). Fifteen children who underwent physical examination were enrolled as the control group. The change in memory B cells after GC therapy was compared between groups, and its correlation with clinical indicators was analyzed.@*RESULTS@#Before treatment, the FRNS and NFRNS groups had significantly increased percentages of total B cells, total memory B cells, IgD+ memory B cells, and IgE+ memory B cells compared with the control group, and the FRNS group had significantly greater increases than the NFRNS group (P<0.05); the FRNS group had a significantly lower percentage of class-switched memory B cells than the NFRNS and control groups (P<0.05). After treatment, the FRNS and NFRNS groups had significant reductions in the percentages of total B cells, total memory B cells, IgM+IgD+ memory B cells, IgM+ memory B cells, IgE+ memory B cells, IgD+ memory B cells, and IgG+ memory B cells (P<0.05) and a significant increase in the percentage of class-switched memory B cells (P<0.05). The FRNS group had a significantly higher urinary protein quantification than the NFRNS and control groups (P<0.05) and a significantly lower level of albumin than the control group (P<0.05). In the FRNS group, urinary protein quantification was negatively correlated with the percentage of class-switched memory B cells and was positively correlated with the percentage of IgE+ memory B cells (P<0.05).@*CONCLUSIONS@#Abnormal distribution of memory B cell subsets may be observed in children with FRNS, and the percentages of IgE+ memory B cells and class-switched memory B cells can be used as positive and negative correlation factors for predicting recurrence after GC therapy in these children.


Subject(s)
Child , Humans , B-Lymphocyte Subsets/metabolism , Immunoglobulin E , Immunoglobulin M , Nephrotic Syndrome/immunology , Prospective Studies , Glucocorticoids/therapeutic use
2.
Chinese Journal of Applied Physiology ; (6): 106-109, 2011.
Article in Chinese | WPRIM | ID: wpr-301489

ABSTRACT

<p><b>OBJECTIVE</b>To investigate molecular mechanisms underlying in the treatment of inflammatory bowel disease by Pulsatilla decoction.</p><p><b>METHODS</b>Wistar male rats were randomly divided into control group, model group, model + positive control group (mesalazine), traditional Chinese medicine treatment group, in addition, the Chinese medical treatment group was divided into middle and high dose group ( n = 8). Intragastric administration was used in the positive control group and traditional Chinese medicine treatment group. The expression of Smad7 and p-Smad3 in the colons were detected by immunohistochemistry and Western blot.</p><p><b>RESULTS</b>Compared with the model group, positive medicine and traditional Chinese medicine group, especially high-dose group, could effectively inhibit the expression of Smad7, while enhancing the p-Smad3 expression.</p><p><b>CONCLUSION</b>The activation of TGF-beta1/Smad3 signaling pathway may be the molecular mechanism underlying in the anti-inflammatory effect of inflammatory bowel disease by Pulsatilla decoction.</p>


Subject(s)
Animals , Male , Rats , Drugs, Chinese Herbal , Therapeutic Uses , Inflammatory Bowel Diseases , Drug Therapy , Phytotherapy , Pulsatilla , Chemistry , Rats, Wistar , Signal Transduction , Smad3 Protein , Metabolism , Smad7 Protein , Metabolism , Transforming Growth Factor beta1 , Metabolism
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