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- 저자 : ( Suying Wang ) (검색결과 4 건)
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Effective of high salt diet (HSD) on letrozole-induced polycystic ovarian syndrome (PCOS) mice
Suying Liang,Xiaoying Tang,Minmin Chen,Huiwen Liu,Wanying Li,Zixian Wang,Qi Qi Pang,Jia-Le Song 한국식품영양과학회 2021 한국식품영양과학회 학술대회발표집 Vol.2021 No.10
To investigate the effect of high salt diet (HSD, 8% NaCl) on the letrozole induced PCOS mice. At the total of experimental periods (35 days), all female C57BL/6J mice were randomly divided into normal groups, PCOS group (ingested letrozole daily for 21 days) and HSD+PCOS group. The body weight (BW) and histologic changes were evaluated. The serum levels of testosterone (T), LH, E2, FSH, INS, TG, TC, LDL, HDL were determined by ELISA kits. Compared with normal groups, the BW, T, LH, INS, TG, TC LDL-C in PCOS rats were significantly increased, and the levels of E2, FSH and HDL-C were significantly decreased. In addition, compared with the PCOS group, the BW, T, LH, INS, TG, TC LDL-C in HSD+PCOS rats were significantly increased, and the levels of E2, FSH and HDL-C were significantly decreased. Our results showed that HSD exacerbates metabolic disorders and hormonal imbalances in PCOS mice.
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( Yuan Wang ),( Hanmei Zhang ),( Suying Feng ) 대한피부과학회 2021 Annals of Dermatology Vol.33 No.4
Papillon-Lefevre syndrome (PLS) (OMIM: 245000) is a rare autosomal recessive disorder characterized by palmoplantar hyperkeratosis and early onset periodontitis, resulting in the premature loss of the deciduous and permanent teeth. PLS is caused by mutations in the cathepsin C (CTSC) gene (OMIM: 602365), which has been mapped to chromosome 11q14- q21. Genetic analysis can help early and rapid diagnosis of PLS. Here we report on a Chinese PLS pedigree with two affected siblings. We have identified two novel compound heterozygous mutations c.763T>C (p.C255R) and c.1015C> A (p.R339S) in the CTSC gene. The two mutations expand the spectrum of CTSC mutations in PLS. (Ann Dermatol 33(4) 369∼ 372, 2021)
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Activation of PXR inhibits LPS-induced NF-κB activation by increasing IκBα expression in HepG2 cells
Nanhui Ye,Hang Wang,Qiaoling Li,Chaotong Lin,Huahua Feng,Suying Lin,Jing Hong,Chunn Meng 대한독성 유전단백체 학회 2018 Molecular & cellular toxicology Vol.14 No.1
A limited number of xenobiotic-induced inflammatory episodes occur in the human liver and small intestine under normal physiological conditions, although many xenobiotic agents are metabolized in these organs every day. In this study, we found that rifampicin-activated pregnane X receptor (PXR) plays an important role in the suppression of lipopolysaccharide-activated nuclear factor kappa B (NF-κB) activity by increasing the expression of the inhibitor of κBα (IκBα) in HepG2 cells. Rifampicin did not increase the expression of IκBα in PXR knockdown HepG2 cells. Furthermore, we found that the activation of PXR could inhibit the lipopolysaccharide-stimulated nuclear translocation of NF-κB p50/p65 using electrophoretic mobility shift assay, immunoprecipitation assays, and microscopy. High levels of IκBα directly interacted with NF-κB and prevented its nuclear translocation, thus inhibiting its binding to consensus DNA sequences in nuclei. Xenobiotic-activated tissue-specific PXR might exert anti-inflammatory actions by antagonizing the xenobiotic-induced transcriptional activity of NFκB in the liver and small intestine. The results also showed that activation of PXR arrested the HepG2 cell cycle in the G0/G1 phase and exhibited cancer prevention potential by inhibiting inflammatory reactions in cells.
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( Yongjie Xu ),( Rui Li ),( Kaili Zhang ),( Wei Wu ),( Suying Wang ),( Pengpeng Zhang ),( Haixia Xu ) 생화학분자생물학회(구 한국생화학분자생물학회) 2018 BMB Reports Vol.51 No.7
HnRNPK is a multifunctional protein that participates in chromatin remodeling, transcription, RNA splicing, mRNA stability and translation. Here, we uncovered the function of hnRNPK in regulating the proliferation and differentiation of myoblasts. hnRNPK was mutated in the C2C12 myoblast cell line using the CRISPR/Cas9 system. A decreased proliferation rate was observed in hnRNPK-mutated cells, suggesting an impaired proliferation phenotype. Furthermore, increased G2/M phase, decreased S phase and increased sub-G1 phase cells were detected in the hnRNPK-mutated cell lines. The expression analysis of key cell cycle regulators indicated mRNA of Cyclin A2 was significantly increased in the mutant myoblasts compared to the control cells, while Cyclin B1, Cdc25b and Cdc25c were decreased sharply. In addition to the myoblast proliferation defect, the mutant cells exhibited defect in myotube formation. The myotube formation marker, myosin heavy chain (MHC), was decreased sharply in hnRNPK-mutated cells compared to control myoblasts during differentiation. The deficiency in hnRNPK also resulted in the repression of Myog expression, a key myogenic regulator during differentiation. Together, our data demonstrate that hnRNPK is required for myoblast proliferation and differentiation and may be an essential regulator of myoblast function. [BMB Reports 2018; 51(7): 350-355]
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