Search

Your search keyword '"Zhang, Bikui"' showing total 179 results
Start Over Author "Zhang, Bikui" Search Limiters Full Text
179 results on '"Zhang, Bikui"'

10. Chinese consensus guidelines for therapeutic drug monitoring of polymyxin B, endorsed by the Infection and Chemotherapy Committee of the Shanghai Medical Association and the Therapeutic Drug Monitoring Committee of the Chinese Pharmacological Society

Author

Liu, Xiaofen, Huang, Chenrong, Bergen, Phillip J., Li, Jian, Zhang, Jingjing, Chen, Yijian, Chen, Yongchuan, Guo, Beining, Hu, Fupin, Hu, Jinfang, Hu, Linlin, Li, Xin, Qiu, Hongqiang, Shao, Hua, Sun, Tongwen, Wang, Yu, Xu, Ping, Yang, Jing, Yang, Yong, Yu, Zhenwei, Zhang, Bikui, Zhu, Huaijun, Zuo, Xiaocong, Zhang, Yi, Miao, Liyan, and Zhang, Jing

Published
2023
Full Text
View/download PDF

17. Strategies to improve the therapeutic efficacy of mesenchymal stem cell‐derived extracellular vesicle (MSC-EV): a promising cell-free therapy for liver disease

Author

Zheng, Lijuan, primary, Gong, Hui, additional, Zhang, Jing, additional, Guo, Linna, additional, Zhai, Zhuofan, additional, Xia, Shuang, additional, Hu, Zhiyu, additional, Chang, Jing, additional, Jiang, Yizhu, additional, Huang, Xinran, additional, Ge, Jingyi, additional, Zhang, Bikui, additional, and Yan, Miao, additional

Published
2023
Full Text
View/download PDF

23. High-fat diets enhance and delay ursodeoxycholic acid absorption but elevate circulating hydrophobic bile salts

Author

Huang, Liang, primary, Wei, Wei, additional, Huang, Xiaomei, additional, Li, Xuejing, additional, Liu, Haisha, additional, Gui, Lanlan, additional, Jiang, Jinping, additional, Wan, Linfei, additional, Zhou, Xiangxiang, additional, Ding, Jingsong, additional, Jiang, Xuehua, additional, Zhang, Bikui, additional, and Lan, Ke, additional

Published
2023
Full Text
View/download PDF

24. Multidisciplinary Guidelines for the Rational Use of Topical Non-Steroidal Anti-Inflammatory Drugs for Musculoskeletal Pain (2022)

Author

Shi, Chen, primary, Ye, Zhaoming, additional, Shao, Zengwu, additional, Fan, Bifa, additional, Huang, Cibo, additional, Zhang, Yuan, additional, Kuang, Xinying, additional, Miao, Liyan, additional, Wu, Xin’an, additional, Zhao, Rongsheng, additional, Chen, Xiao, additional, Zhang, Bikui, additional, Tong, Rongsheng, additional, Hu, Xin, additional, Fu, Zhijian, additional, Lin, Jianhao, additional, Li, Xiaomei, additional, Sun, Tiezheng, additional, Liu, Guoqiang, additional, Dai, Haibin, additional, Guo, Cheng, additional, Zhang, Bo, additional, Xu, Ting, additional, Wen, Aidong, additional, Zuo, Xiaocong, additional, Liu, Jinmei, additional, Chen, Xu, additional, Li, Huibo, additional, Wang, Jing, additional, Luo, Min, additional, Fan, Tingting, additional, Qian, Yulan, additional, Li, Xiu’mao, additional, Qiu, Wenjie, additional, Lin, Xiaowen, additional, Pang, Yingchang, additional, Hou, Yunfei, additional, Yao, Difei, additional, Kou, Wen, additional, Sun, Bao, additional, Hu, Can, additional, Xia, Yanzhe, additional, Zhao, Ming, additional, Zhu, Changyu, additional, Li, Qian, additional, and Zhang, Yu, additional

Published
2023
Full Text
View/download PDF

28. Sunitinib induced hepatotoxicity in L02 cells via ROS-MAPKs signaling pathway

Author

Tang, Ting-Li, Yang, Yan, Guo, Lin, Xia, Shuang, Zhang, Bikui, and Yan, Miao

Subjects
Pharmacology, Pharmacology (medical)
Abstract

Sunitinib is a multi-targeted tyrosine kinase inhibitor with remarkable anticancer activity, while hepatotoxicity is a potentially fatal adverse effect of its administration. The aim of this study was to elucidate the mechanism of hepatotoxicity induced by Sunitinib and the protective effect of glycyrrhetinic acid (GA). Sunitinib significantly reduced the survival of human normal hepatocytes (L02 cells), induced the increase of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH). Chloroquine (CQ) and Z-VAD-FMK were applied to clarify the cell death patterns induced by Sunitinib. Sunitinib significantly induced L02 cells death by triggering apoptosis and autophagy acted as a self-defense mechanism to promote survival. Sunitinib exposure caused excessive ROS generation which activated mitogen-activated protein kinases (MAPKs) signaling. Mechanistically, SP600125 (JNK inhibitor) and SB203580 (p38 inhibitor) respectively blocked apoptosis and autophagy induced by Sunitinib. And inhibition of ROS by NAC pretreatment ameliorated the effect of Sunitinib on MAPKs phosphorylation. GA alleviated Sunitinib-induced cell damage by inhibiting apoptosis and autophagy. These results suggested ROS/MAPKs signaling pathway was responsible for Sunitinib-induced hepatotoxicity and GA could be a preventive strategy to alleviate liver injury caused by Sunitinib.

Published
2022
Full Text
View/download PDF

35. Medication therapy of high‐dose methotrexate: An evidence‐based practice guideline of the Division of Therapeutic Drug Monitoring, Chinese Pharmacological Society

Author

Song, Zaiwei, primary, Hu, Yang, additional, Liu, Shuang, additional, Wang, Guanru, additional, Zhai, Suodi, additional, Zhang, Xianglin, additional, Li, Youping, additional, Du, Guanhua, additional, Shi, Yuankai, additional, Chen, Yaolong, additional, Dong, Mei, additional, Guo, Ruichen, additional, Guo, Wei, additional, Huang, Hongbing, additional, Huang, Xiaojun, additional, Jing, Hongmei, additional, Ke, Xiaoyan, additional, Li, Guohui, additional, Miao, Liyan, additional, Niu, Xiaohui, additional, Qiu, Feng, additional, Shen, Jingnan, additional, Tang, Jingyan, additional, Wang, Tianyou, additional, Wang, Xiaoling, additional, Wang, Zhuo, additional, Wu, Jiuhong, additional, Zhan, Siyan, additional, Zhang, Bikui, additional, Zhang, Lingli, additional, Zhang, Yanhua, additional, Zhang, Wei, additional, Zhao, Limei, additional, Zhao, Libo, additional, Zhen, Jiancun, additional, Zheng, Huyong, additional, Zhu, Zhu, additional, Jiang, Dan, additional, Huang, Zhencheng, additional, Tan, Zhiyuan, additional, Lin, Qiaonan, additional, and Zhao, Rongsheng, additional

Published
2022
Full Text
View/download PDF

38. Association of Pulmonary Sepsis and Immune Checkpoint Inhibitors: A Pharmacovigilance Study.

Author

Xia, Shuang, Gong, Hui, Zhao, Yichang, Guo, Lin, Wang, Yikun, Zhang, Bikui, Sarangdhar, Mayur, Noguchi, Yoshihiro, and Yan, Miao

Subjects
GLUCOCORTICOIDS, CARDIOTOXICITY, IMMUNE checkpoint inhibitors, LUNG diseases, CANCER chemotherapy, MONOCLONAL antibodies, RETROSPECTIVE studies, SEPSIS, CANCER patients, DRUG interactions, RESEARCH funding, ODDS ratio, PHARMACODYNAMICS, DISEASE risk factors
Abstract

Simple Summary: This study investigates the association of pulmonary sepsis with immune checkpoint inhibitors by conducting an analysis using data from the Food and Drug Administration pharmacovigilance database. Compared to chemotherapy or targeted therapy, a robust signal emerged for nivolumab and atezolizumab. Co-administration of immune checkpoint inhibitors and glucocorticoids or proton pump inhibitors synergistically increased the risk of pulmonary sepsis. These signals should promote both prospective research and multidisciplinary proactive monitoring by healthcare professionals. Background: Although some sepsis cases were reported with immune checkpoint inhibitors (ICIs) in clinical trials, the link between pulmonary sepsis and ICIs remains mostly unknown. We aim to investigate the association between pulmonary sepsis and ICIs, and to describe the clinical features. Methods: A disproportionality analysis was performed using FAERS data and compared rates of pulmonary sepsis in cancer patients receiving ICIs vs. other drug regimens (such as chemotherapy and targeted therapy). Associations between ICIs and sepsis were assessed using reporting odds ratios (ROR) and information component (IC). We also detected drug interaction signals based on the Ω shrinkage measure. Age and gender distribution were compared between pulmonary sepsis and all adverse events associated with ICIs. Results: We identified 120 reports of pulmonary sepsis associated with ICIs between Q1, 2011 to Q3, 2021. A total of 82 of 120 (68.3%) patients on ICIs suffered from pulmonary sepsis and progressed to death. In addition, there is no significant difference in age and gender in the occurrence of pulmonary sepsis in cancer patients on ICIs. Overall ICIs, nivolumab, and atezolizumab still have a significant signal of pulmonary sepsis (ROR025 > 1, IC025 > 0, p < 0.001) compared with targeted therapy (such as tyrosine kinase inhibitors) or chemotherapy. Co-administration of ICIs and glucocorticoids or proton pump inhibitors synergistically increased the risk of pulmonary sepsis (Ω025 > 0). Conclusions: Our study suggested ICIs, especially nivolumab and atezolizumab, tended to increase the risk of pulmonary sepsis more than other anticancer regimens. Clinicians should be vigilant in the prevention and management of pulmonary sepsis during ICIs therapy. [ABSTRACT FROM AUTHOR]

Published
2023
Full Text
View/download PDF

46. Network Pharmacology Prediction and Molecular Docking-Based Strategy to Discover the Potential Pharmacological Mechanism of Huai Hua San Against Ulcerative Colitis

Author

Liu,Jiaqin, Liu,Jian, Tong,Xiaoliang, Peng,Weijun, Wei,Shanshan, Sun,Taoli, Wang,Yikun, Zhang,Bikui, Li,Wenqun, Liu,Jiaqin, Liu,Jian, Tong,Xiaoliang, Peng,Weijun, Wei,Shanshan, Sun,Taoli, Wang,Yikun, Zhang,Bikui, and Li,Wenqun

Abstract

Jiaqin Liu,1,2 Jian Liu,1,2 Xiaoliang Tong,3 Weijun Peng,4 Shanshan Wei,1,2 Taoli Sun,5 Yikun Wang,1,2 Bikui Zhang,1,2 Wenqun Li1,2 1Department of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, People’s Republic of China; 2Institute of Clinical Pharmacy, Central South University, Changsha, Hunan, 410011, People’s Republic of China; 3Department of Dermatology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, 410013, People’s Republic of China; 4Department of Integrated Traditional Chinese & Western Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, People’s Republic of China; 5School of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan, 410208, People’s Republic of ChinaCorrespondence: Wenqun LiDepartment of Pharmacy, The Second Xiangya Hospital, Central South University, No. 139 Renmin Road, Changsha, 410011, People’s Republic of ChinaTel +86-731-85292093Email liwq1204@csu.edu.cnBackground: Huai Hua San (HHS), a famous Traditional Chinese Medicine (TCM) formula, has been widely applied in treating ulcerative colitis (UC). However, the interaction of bioactives from HHS with the targets involved in UC has not been elucidated yet.Aim: A network pharmacology-based approach combined with molecular docking and in vitro validation was performed to determine the bioactives, key targets, and potential pharmacological mechanism of HHS against UC.Materials and Methods: Bioactives and potential targets of HHS, as well as UC-related targets, were retrieved from public databases. Crucial bioactive ingredients, potential targets, and signaling pathways were acquired through bioinformatics analysis, including protein–protein interaction (PPI), as well as the Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Subsequently, molecular docking was carried out to predict the combination of active compounds with core tar

Published
2021

47. Xanthohumol Inhibits TGF-β1-Induced Cardiac Fibroblasts Activation via Mediating PTEN/Akt/mTOR Signaling Pathway

Author

Jiang,Chuanhao, Xie,Ning, Sun,Taoli, Ma,Wanjun, Zhang,Bikui, and Li,Wenqun

Subjects
Drug Design, Development and Therapy
Abstract

Chuanhao Jiang,1,2,* Ning Xie,3,* Taoli Sun,4 Wanjun Ma,2 Bikui Zhang,2 Wenqun Li2 1Department of Laboratory Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, People’s Republic of China; 2Department of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha 410011, People’s Republic of China; 3Department of Breast Cancer Medical Oncology, Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya Medical School, Central South University, Changsha, Hunan 410013, People’s Republic of China; 4Key Laboratory Breeding Base of Hu’nan Oriented Fundamental and Applied Research of Innovative Pharmaceutics, College of Pharmacy, Changsha Medical University, Changsha, Hunan 410219, People’s Republic of China*These authors contributed equally to this workCorrespondence: Wenqun Li Email liwq1204@csu.edu.cnBackground: Xanthohumol (Xn) is the most abundant prenylated flavonoid in Hops (Humulus lupulus L.), and exhibits a range of pharmacological activities. This study aimed to investigate the effect of Xn on TGF-β 1-induced cardiac fibroblasts activation and elucidate the underlying mechanism.Materials and Methods: The cellTiter 96® AQueous one solution cell proliferation assay kit was adopted to determine the cell viability of cardiac fibroblasts, and the proliferation was detected through 5-ethynyl-2ʹ-deoxyuridine (EdU) incorporation assay. The α-SMA protein expression was measured by using immunofluorescence and Western blotting. Western blotting was conducted to test the protein expressions of collagen I and III, PTEN, p-Akt, Akt, p-mTOR, mTOR, p-Smad3, Smad3 and GAPDH. The mRNA levels of α-SMA, collagen I and III were determined by quantitative real-time polymerase chain reaction (PCR).Results: Xn inhibited the TGF-β 1-induced proliferation, differentiation and collagen overproduction of cardiac fibroblasts. TGF-β 1 induced the down-regulated PTEN expression, Akt and mTOR phosphorylation. These effects of TGF-β 1 were suppressed by Xn, while blocking of PTEN reduced Xn-mediated inhibitory effect on cardiac fibroblasts activation induced by TGF-β 1.Conclusion: Xn inhibits TGF-β 1-induced cardiac fibroblasts activation via mediating PTEN/Akt/mTOR signaling pathway.Keywords: xanthohumol; Xn, cardiac fibrosis, cardiac fibroblasts, TGF-β 1, PTEN/AKT/mTOR pathway

Published
2020

Catalog

Books, media, physical & digital resources
See catalog results