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11 results on '"Shao, Xiaoni"'

1. A Novel Approach Based on Gut Microbiota Analysis and Network Pharmacology to Explain the Mechanisms of Action of Cichorium intybus L. Formula in the Improvement of Hyperuricemic Nephropathy in Rats

Author

Amatjan,Mukaram, Li,Na, He,Pengke, Zhang,Boheng, Mai,Xianyan, Jiang,Qianle, Xie,Haochen, and Shao,Xiaoni

Subjects
Pharmacology, Drug Design, Development and Therapy, Drug Discovery, Pharmaceutical Science
Abstract

Mukaram Amatjan,1 Na Li,1 Pengke He,1 Boheng Zhang,1 Xianyan Mai,1 Qianle Jiang,1 Haochen Xie,2 Xiaoni Shao1 1Immunotherapy Laboratory, College of Pharmacology, Southwest Minzu University, Chengdu, 610225, People’s Republic of China; 2Qinghai Tibet Plateau Research Institute, Southwest Minzu University, Chengdu, 610225, People’s Republic of ChinaCorrespondence: Xiaoni Shao, Immunotherapy Laboratory, College of Pharmacology, Southwest Minzu University, #168 Dajian Street, Shuangliu District, Chengdu, 610225, People’s Republic of China, Tel +86-28-85738423, Email xnshao@swun.edu.cnBackground: Cichorium intybus L. formula (CILF) is a traditional Chinese medicine (TCM) widely used in the treatment of gout and hyperuricemic nephropathy (HN). The aim of this research was to investigate the potential protective effect of CILF against HN and elucidated the underlying mechanism.Methods: CILF water extract was administered to an HN rat model established by adenine combined with ethambutol. The levels of uric acid (UA), serum urea nitrogen (UREA), and creatinine (CREA) were detected. Changes in the pathology and histology of the kidney were observed by hematoxylin-eosin staining. The 16S rRNA of the gut microbiota was sequenced. The binding ability of the main ingredients of CILF to key targets was analyzed by network pharmacology and molecular docking. The expression levels of the related mRNAs and proteins in the kidney were evaluated by RT-qPCR and immunohistochemistry analysis.Results: CILF administration significantly alleviated increases in UA, UREA, and CREA, structural damage, and kidney dysfunction. Gut microbiota analysis was applied to explore the pharmacological mechanism of the effects of CILF on bacterial diversity and microbiota structure in HN. CILF decreased the abundance of Bacteroides. In addition, it increased the abundance of Lactobacillaceae, Erysipelotrichaceae, Lachnospiraceae, Ruminococcaceae, and Bifidobacterium. Based on network pharmacology and molecular docking analysis, CILF profoundly influenced the IL17, TNF and AGE-RAGE signaling pathway. Additionally, CILF inhibited the expression of STAT3, VEGFA and SIRT1 to improve the symptoms of nephropathy. Our research suggested that CILF protects against kidney dysfunction in rats with HN induced by adenine combined with ethambutol.Conclusion: Our findings on the anti-HN effects of CILF and its mechanism of action, from the viewpoint of systems biology, and elaborated that CILF can alter the diversity and community structure of the gut microbiota in HN, providing new approaches for the prevention and treatment of HN.Keywords: Cichorium intybus L. formula, hyperuricemic nephropathy, gut microbiota, network pharmacology, molecular docking

Published
2023

9. ¹H NMR-based metabolic profiling of human rectal cancer tissue

Author

Wang, Huijuan, primary, Wang, Liang, additional, Zhang, Hailong, additional, Deng, Pengchi, additional, Chen, Jie, additional, Zhou, Bin, additional, Hu, Jing, additional, Zou, Jun, additional, Lu, Wenjie, additional, Xiang, Pu, additional, Wu, Tianming, additional, Shao, Xiaoni, additional, Li, Yuan, additional, Zhou, Zongguang, additional, and Zhao, Ying-Lan, additional

Published
2013
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10. 1H-NMR based metabonomic profiling of human esophageal cancer tissue

Author

Wang, Liang, primary, Chen, Jie, additional, Chen, Longqi, additional, Deng, Pengchi, additional, bu, Qian, additional, Xiang, Pu, additional, Li, Manli, additional, Lu, Wenjie, additional, Xu, Youzhi, additional, Lin, Hongjun, additional, Wu, Tianming, additional, Wang, Huijuan, additional, Hu, Jing, additional, Shao, Xiaoni, additional, Cen, Xiaobo, additional, and Zhao, Ying-Lan, additional

Published
2013
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11. Uric Acid Induces Cognitive Dysfunction through Hippocampal Inflammation in Rodents and Humans.

Author

Shao X, Lu W, Gao F, Li D, Hu J, Li Y, Zuo Z, Jie H, Zhao Y, and Cen X

Subjects
Administration, Oral, Animals, Cognition drug effects, Cytokines immunology, Hippocampus drug effects, Humans, Inflammation Mediators immunology, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Rats, Rats, Wistar, Species Specificity, Uric Acid administration & dosage, Cognition Disorders chemically induced, Cognition Disorders immunology, Encephalitis chemically induced, Encephalitis immunology, Hippocampus immunology, Uric Acid toxicity
Abstract

Uric acid (UA) is a purine metabolite that in most mammals is degraded by the hepatic enzyme uricase to allantoin. Epidemiological studies have shown that an elevated UA level predicts the development of cognition and memory deficits; however, there is no direct evidence of this relationship, and the underlying mechanism is largely undefined. Here, we show that a high-UA diet triggers the expression of proinflammatory cytokines, activates the Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB pathway, and increases gliosis in the hippocampus of Wistar rats. We, subsequently, identify a specific inhibitor of NF-κB, BAY11-7085, and show that stereotactic injections of the inhibitor markedly ameliorate UA-induced hippocampal inflammation and memory deficits in C57BL/6 mice. We also found that NF-κB is activated in the primary cultured hippocampal cells after UA administration. Additionally, C57BL/6 mice that lack TLR4 are substantially protected against UA-induced cognitive dysfunction, possibly due to a decrease in inflammatory gene expression in the hippocampus. Importantly, magnetic resonance imaging confirms that hyperuricemia in rats and humans is associated with gliosis in the hippocampus. Together, these results suggest that UA can cause hippocampal inflammation via the TLR4/NF-κB pathway, resulting in cognitive dysfunction. Our findings provide a potential therapeutic strategy for counteracting UA-induced neurodegeneration., Significance Statement: This work demonstrates that a high-uric acid (UA) diet triggers the expression of proinflammatory cytokines, activates the Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB pathway, and increases gliosis in the hippocampus of Wistar rats. Inhibition of the NF-κB signaling pathway markedly ameliorates UA-induced hippocampal inflammation and cognitive dysfunction in C57BL/6 mice. TLR4-knock-out mice are substantially protected against UA-induced cognitive dysfunction, possibly due to a decrease in inflammatory gene expression in the hippocampus. Moreover, magnetic resonance imaging confirms that hyperuricemia in rats and humans are associated with gliosis in the hippocampus. Together, this study suggests that there is an important link between UA-induced cognitive dysfunction and hippocampal inflammation in rodents and humans, which may have remarkable implications in the treatment of UA-induced neurodegeneration., (Copyright © 2016 the authors 0270-6474/16/3610990-16$15.00/0.)

Published
2016
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