布鲁顿酪氨酸激酶
血管生成
类风湿性关节炎
趋化因子
癌症研究
化学
药理学
关节炎
酪氨酸激酶
免疫学
医学
炎症
生物化学
信号转导
作者
Nageen Hussain,Mohsin Mumtaz,Mohammad Adil,Abad Ali Nadeem,Abid Sarwar,Tariq Aziz,Metab Alharbi,Abdulrahman Alshammari,Abdullah F. Alasmari,Mousa Essa Alharbi
标识
DOI:10.18388/abp.2020_6654
摘要
Mutation in the VEGF gene disturbs the production of chondrocytes and angiogenesis which are essential for cartilage health. Cytokines and chemokines produced by auto-activation of B-cells degrade cartilage. Bruton's Tyrosine Kinase (BTK) plays a crucial role in the activation of these B-cells. VEGF has a central part in angiogenesis, in the recruitment of endothelial cells, and is involved in mechanisms that result in tumour formation. The objective of this research is to investigate the potential role of VEGF polymorphism in the development of Rheumatoid Arthritis (RA) and the screening of potential natural, synthetic BTK inhibitor compounds as possible in-silico chemotherapeutic agents to control auto-activation of B-cells and cartilage degrading cytokines. In this study, it had been shown that allele A frequency was significantly higher than that of allele C in RA-positive patients as compared to controls. Hence it depicts that allele A of VEGF (rs699947) can increase the risk of RA while allele C has a protective role. The phytochemicals which showed maximum binding affinity at the inhibitory site of BTK include beta boswellic acid, tanshinone, and baicalin. These phytochemicals as BTK inhibitor give insights to use them as anti-arthritic compounds by nanoparticle drug delivery mechanism.
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