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7 results on '"Xin-Yi Fang"'

1. Interactions Between Therapeutics for Metabolic Disease, Cardiovascular Risk Factors, and Gut Microbiota

Author

Qi-You Ding, Jia-Xing Tian, Min Li, Feng-Mei Lian, Lin-Hua Zhao, Xiu-Xiu Wei, Lin Han, Yu-Jiao Zheng, Ze-Zheng Gao, Hao-Yu Yang, Xin-Yi Fang, and Xiao-lin Tong

Subjects
metabolic therapy, gut microbiota, cardiovascular diseases, metformin, microbiota-targeted therapies, Microbiology, QR1-502
Abstract

With improved standards of living, the incidence of multiple metabolic disorders has increased year by year, especially major risk factors for cardiovascular disease such as hyperglycemia and hyperlipidemia, continues to increase. Emerging epidemiological data and clinical trials have shown the additional protective effects of some metabolic therapy drugs against cardiovascular diseases. A series of studies have found that these drugs may work by modulating the composition of gut microbiota. In this review, we provide a brief overview of the contribution of the gut microbiota to both metabolic disorders and cardiovascular diseases, as well as the response of gut microbiota to metabolic therapy drugs with cardiovascular benefits. In this manner, we link the recent advances in microbiome studies on metabolic treatment drugs with their cardiovascular protective effects, suggesting that intestinal microorganisms may play a potential role in reducing cardiovascular risk factors. We also discuss the potential of microorganism-targeted therapeutics as treatment strategies for preventing and/or treating cardiovascular disease and highlight the need to establish causal links between therapeutics for metabolic diseases, gut microbiota modulation, and cardiovascular protection.

Published
2020
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3. Research Progress on the Pathological Mechanisms of Podocytes in Diabetic Nephropathy

Author

Xinmiao Wang, Lin Han, Xiaolin Tong, Xin-Yi Fang, Yu Wei, Linhua Zhao, Lili Zhang, Yu-Jiao Zheng, Zhige Wen, and Qing Wang

Subjects
0301 basic medicine, Endocrinology, Diabetes and Metabolism, Apoptosis, Review Article, Diseases of the endocrine glands. Clinical endocrinology, Muscle hypertrophy, Podocyte, Diabetic nephropathy, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Diabetes mellitus, medicine, Autophagy, Animals, Humans, Diabetic Nephropathies, skin and connective tissue diseases, Pathological, business.industry, Podocytes, Research, Transdifferentiation, RC648-665, medicine.disease, 030104 developmental biology, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Cell Transdifferentiation, Cancer research, Disease Progression, sense organs, Signal transduction, business, Signal Transduction
Abstract

Diabetic nephropathy (DN) is not only an important microvascular complication of diabetes but also the main cause of end-stage renal disease. Studies have shown that the occurrence and development of DN are closely related to morphological and functional changes in podocytes. A series of morphological changes after podocyte injury in DN mainly include podocyte hypertrophy, podocyte epithelial-mesenchymal transdifferentiation, podocyte detachment, and podocyte apoptosis; functional changes mainly involve podocyte autophagy. More and more studies have shown that multiple signaling pathways play important roles in the progression of podocyte injury in DN. Here, we review research progress on the pathological mechanism of morphological and functional changes in podocytes associated with DN, to provide a new target for delaying the occurrence and development of this disorder.

Published
2020

4. Corrigendum to 'A new xanthatin analogue 1β-hydroxyl-5α-chloro-8-epi-xanthatin induces apoptosis through ROS-mediated ERK/p38 MAPK activation and JAK2/STAT3 inhibition in human hepatocellular carcinoma' [Biochimie 152C (2018) 43-52]

Author

Lin Zhao, Xin-Yi Fang, Shuai Tan, Qing-Cuo Ren, Hai Zhang, Lun Wang, and Xiaofei Shen

Subjects
MAPK/ERK pathway, Chemistry, Apoptosis, p38 mitogen-activated protein kinases, Hepatocellular carcinoma, Jak2 stat3, medicine, Cancer research, General Medicine, medicine.disease, Biochemistry
Published
2020

5. The P2Y

Author

Jiu, Lin, Yan-Yan, Zhang, Fei, Liu, Xin-Yi, Fang, Meng-Ke, Liu, Chao-Lan, Huang, Hang, Wang, Da-Qing, Liao, Cheng, Zhou, and Jie-Fei, Shen

Subjects
Inflammation, Male, Behavior, Animal, MAP Kinase Signaling System, Freund's Adjuvant, Trigeminal Neuralgia, p38 Mitogen-Activated Protein Kinases, Rats, Up-Regulation, Rats, Sprague-Dawley, Trigeminal Ganglion, Facial Pain, Hyperalgesia, Receptors, Purinergic P2Y, Animals, Cytokines, Phosphorylation
Abstract

P2Y purinergic receptors expressed in neurons and satellite glial cells (SGCs) of the trigeminal ganglion (TG) contribute to inflammatory and neuropathic pain. P2Y

Published
2019

6. P2Y

Author

Jiu, Lin, Fei, Liu, Yan-Yan, Zhang, Ning, Song, Meng-Ke, Liu, Xin-Yi, Fang, Da-Qing, Liao, Cheng, Zhou, Hang, Wang, and Jie-Fei, Shen

Subjects
Male, Rats, Sprague-Dawley, Receptors, Purinergic P2Y, Interleukin-1beta, Animals, Satellite Cells, Perineuronal, Chemokine CCL2, Rats
Abstract

Satellite glial cells (SGCs) activation in the trigeminal ganglia (TG) is critical in various abnormal orofacial sensation in nerve injury and inflammatory conditions. SGCs express several subtypes of P2 purinergic receptors contributing to the initiation and maintenance of neuropathic pain. The P2Y

Published
2018

7. A new xanthatin analogue 1β-hydroxyl-5α-chloro-8-epi-xanthatin induces apoptosis through ROS-mediated ERK/p38 MAPK activation and JAK2/STAT3 inhibition in human hepatocellular carcinoma

Author

Qing-Cuo Ren, Hai Zhang, Xiaofei Shen, Xin-Yi Fang, Lun Wang, Lin Zhao, and Shuai Tan

Subjects
0301 basic medicine, MAPK/ERK pathway, STAT3 Transcription Factor, Carcinoma, Hepatocellular, p38 mitogen-activated protein kinases, Apoptosis, Biochemistry, p38 Mitogen-Activated Protein Kinases, 03 medical and health sciences, Cell Line, Tumor, Malondialdehyde, Survivin, Humans, STAT3, Protein kinase A, Extracellular Signal-Regulated MAP Kinases, Furans, Protein Kinase Inhibitors, Cell Proliferation, biology, Cell growth, Chemistry, Liver Neoplasms, General Medicine, Janus Kinase 2, Glutathione, Acetylcysteine, Enzyme Activation, Oxidative Stress, 030104 developmental biology, Cancer cell, biology.protein, Cancer research, Reactive Oxygen Species
Abstract

1β-hydroxyl-5α-chloro-8-epi-xanthatin (XTT), a sesquiterpene lactone isolated from Xanthium sibiricum, possessed potent cytotoxicity on cancer cells in vitro. The objective of this study was to investigate the anti-tumor effect and underlying mechanisms of XTT on human hepatocellular carcinoma (HCC). Firstly, XTT inhibited the cell growth and induced apoptosis in human HCC cells, which was associated with the induction of Bax and cleaved-caspase-3, inhibition of Bcl-2 and survivin expression. Importantly, XTT induced the generation of reactive oxygen species (ROS) and malondialdehyde (MDA), and depletion of glutathione (GSH) in HCC cells through covalently modification of GSH. Furthermore, XTT caused obvious activation of extracellular regulated protein kinase (ERK) and p38 mitogen-activated protein kinase (p38 MAPK) and inactivation of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) in HCC cells. ROS scavenger N-acetyl cysteine abrogated the effects of XTT on ERK/p38 MAPK activation and JAK2/STAT3 inhibition, and rescued HCC cells from XTT-induced apoptosis. Additionally, inhibitors of ERK/p38 MAPKs or activator of JAK2/STAT3 partially abolished XTT-mediated effect. In summary, XTT inhibited cell growth and induced apoptosis in HCC cells through ROS-mediated ERK/p38 MAPK activation and JAK2/STAT3 inhibition by GSH depletion. These findings also show the therapeutic potential of XTT in HCC.

Published
2018

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