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407 results on '"Tang, Yiping"'

4. Cognitive enhancing effect of rTMS combined with tDCS in patients with major depressive disorder: a double-blind, randomized, sham-controlled study

Author

Li, Xingxing, Liu, Junyao, Wei, Shuochi, Yu, Chang, Wang, Dongmei, Li, Yuchen, Li, Jiaxin, Zhuang, Wenhao, Luo, Rui-Chen-Xi, Li, Yanli, Liu, Zhiwang, Su, Yuqiu, Liu, Jimeng, Xu, Yongming, Fan, Jialin, Zhu, Guidong, Xu, Weiqian, Tang, Yiping, Yan, Hui, Cho, Raymond Y., Kosten, Thomas R., Zhou, Dongsheng, and Zhang, Xiangyang

Published
2024
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28. Didymin Ameliorates Dextran Sulfate Sodium (DSS)-Induced Ulcerative Colitis by Regulating Gut Microbiota and Amino Acid Metabolism in Mice.

Author

Chu, Zhongxing, Hu, Zuomin, Yang, Feiyan, Zhou, Yaping, Tang, Yiping, and Luo, Feijun

Subjects
ULCERATIVE colitis, AMINO acid metabolism, TRANSCRIPTION factors, GUT microbiome, CITRUS fruits
Abstract

Background: Didymin is a dietary flavonoid derived from citrus fruits and has been shown to have extensive biological functions, especially anti-inflammatory effects, but its mechanism is unclear. The purpose of this study was to investigate the potential mechanism of didymin that alleviates ulcerative colitis. Methods and Results: Our results indicated that didymin could alleviate the symptoms of ulcerative colitis, as it inhibited the expressions of interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Didymin also promoted the expressions of claudin-1 and zona occludens-1(ZO-1), which are closely related with restoring colon barrier function. Didymin also increased the abundance of Firmicutes and Verrucomicobiota, while decreasing the abundance of Bacteroidota and Proteobacteria. Meanwhile, didymin significantly altered the levels of metabolites related to arginine synthesis and metabolism, and lysine degradation in the colitis mice. Utilizing network pharmacology and molecular docking, our results showed that the metabolites L-ornithine and saccharin could interact with signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa-B (NF-κB). In this in vitro study, L-ornithine could reduce the expressions of transcription factors STAT3 and NF-κB, and it also inhibited the expressions of IL-6 and IL-1β in the lipopolysaccharides (LPS) induced in RAW264.7 cells, while saccharin had the opposite effect. Conclusions: Taken together, didymin can regulate gut microbiota and alter metabolite products, which can modulate STAT3 and NF-κB pathways and inhibit the expressions of inflammatory factors and inflammatory response in the DSS-induced colitis mice. [ABSTRACT FROM AUTHOR]

Published
2024
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29. Role and Mechanism of Sialic Acid in Alleviating Acute Lung Injury through In Vivo and In Vitro Models.

Author

Li, Dan, Li, Fangyan, Zhou, Yaping, Tang, Yiping, Hu, Zuomin, Wu, Qi, Xie, Tiantian, Lin, Qinlu, Wang, Hanqing, and Luo, Feijun

Subjects
SIALIC acids, LUNG injuries, PULMONARY edema, PNEUMONIA, ANTIOXIDANTS
Abstract

Excessive inflammatory reactions are the most important pathological injury factor in acute lung injury (ALI). Our recent study found that sialic acid had an anti-colitis effect. In this study, the effect of sialic acid (SA) on acute lung inflammation was investigated. A lipopolysaccharide (LPS)-induced ALI animal model and LPS-stimulated HUVEC cell model were used to evaluate the anti-inflammatory effect of SA and study its molecular mechanisms. Compared with the LPS group, the lung index of the SA group decreased from 0.79 ± 0.05% to 0.58 ± 0.06% (LPS + 50 SA) and 0.62 ± 0.02% (LPS + 100 SA), with p < 0.01, suggesting that SA could improve the pulmonary edema of mice and alleviate LPS-induced lung injury. Transcriptome research identified 26 upregulated genes and 25 downregulated genes involved in the protection of SA against ALI. These genes are mainly related to the MAPK and NF-κB signaling pathways. Our study also proved that SA markedly downregulated the expression of inflammatory factors and blocked the JNK/p38/PPAR-γ/NF-κB pathway. Meanwhile, SA treatment also upregulated the expression of HO-1 and NQO1 in ALI mice. In vitro, SA obviously repressed the expressions of inflammatory cytokines and the JNK/p38-NF-κB/AP-1 pathway. SA also regulated the expression of oxidative stress-related genes through the Nrf2 pathway. Taken together, SA exhibits a protective role by modulating the anti-inflammatory and anti-oxidation pathways in ALI, and it may be a promising candidate for functional foods to prevent ALI. [ABSTRACT FROM AUTHOR]

Published
2024
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