China 
Africa 
Explore chapters and articles related to this topic
Shear Stress, Mechanosensors, and Atherosclerosis
Published in Juhyun Lee, Sharon Gerecht, Hanjoong Jo, Tzung Hsiai, Modern Mechanobiology, 2021
Generally, there are two major types of shear stress: one is the laminar flow and the other is disturbed flow. The different flow patterns were generated by different hemodynamic forces using different shear stress systems, such as plate viscometer, flow chamber, ibidi system, and other microfluidic systems. Mounting evidence in the past has shown that laminar flow protects against endothelial dysfunction and atherosclerosis, by promoting an endothelial protective and atheroprotective transcriptional program, mediated by transcriptional factors, such as Krüppel-like factor-2 (KLF2) [10–12], KLF4 [13–15], and Nrf21 [16]. In contrast, disturbed flow promotes endothelial dysfunction and atherosclerosis via atherogenic transcriptional factors, such as nuclear factor kappa light chain enhancer of activated B cells (NF-icB) [17], yes-associated protein (YAP) [18–20], and HIF12 [21, 22] (Fig. 1.2). Many drugs, such as statins [23, 24], resveratrol [24–26], tannic acids [27], and histone deacetylase inhibitor SAHA3 [28], mimic laminar flow response by upregulating KLF2 expression and activity. On the other hand, many proatherogenic factors, such as lipopolysaccharide (LPS) [29] and tumor necrosis factor-alpha (TNF-α) [30], mimic the disturbed flow– induced response by activating NF-x:B and downregulating KLF2 expression, suggesting the possibility of target mechanosensitive transcriptional factors modulating atherosclerosis.
Genome Editing and Gene Therapies: Complex and Expensive Drugs
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Familial PD is characterized among others by an accumulation of α-synuclein (wt. and mutant) and compounds reducing α-synuclein levels should be able to mitigate or even prevent the development of Parkinsonism phenotypes. Dansithong et al. (2015) developed cell lines expressing SNCA fused to the reporter genes luciferase (luc) or green fluorescent protein (GFP). For inserting the reporter genes in-frame downstream of the SNCA gene they used ZFN genome technique to edit SH-SY5Y neuroblastoma cell lines; for transfection, Invitrogen lipofectamine was employed (Subsection 10.4.3.3.1). In addition, these cells were treated with the histone deacetylase inhibitor valproic acid which led to an increased SNCA-luc and SNCα-GFP expression (via epigenetic mechanisms) and improved the utility of such cells’ efficient high-throughput drug screening.
Drug Targeting to Tumors: Principles, Pitfalls and (Pre-) Clinical Progress
Published in Lajos P. Balogh, Nano-Enabled Medical Applications, 2020
Twan Lammers, Fabian Kiessling, Wim E. Hennink, Gert Storm
In the past few decades, significant progress has been made in understanding the molecular principles of many different diseases. In the case of cancer, these improved insights into the genetic and (patho-) physiological processes contributing to malignant transformation and tumorigenesis have resulted in the development of several novel (classes of) chemotherapeutic drugs. Such “molecularly targeted therapeutics,” like the growth factor receptor inhibitor Herceptin, the proteasome inhibitor Velcade, the histone deacetylase inhibitor Vorinostat and the antiangiogenic agent Avastin, more selectively interfere with certain “hallmarks of cancer” [1, 2], like with the overexpression of growth factors and growth factor receptors, with the altered balance between apoptosis and anti-apo-ptosis, with the numerous genetic and epigenetic changes that are present in cancer cells, and with the development of a dense vascular network, needed to provide tumors with oxygen and nutrients. By means of their pharmacologically and/or physiologically more optimal mechanism(s) of action, “molecularly targeted therapeutics” have been shown to be able to more preferentially kill cancer cells, both in vitro and in vivo, and to improve the balance between the efficacy and the toxicity of systemic anticancer therapy [3–5].
In vitro fermentation assay on the bifidogenic effect of steviol glycosides of Stevia rebaudiana plant for the development of dietetic novel products
Published in Preparative Biochemistry & Biotechnology, 2023
It has been proven that the intestinal microbiota and the type of nutrients taken are beneficial to the host in terms of metabolism. Butyric acid from SCFAs is effective as a primary food source for colon bacteria and also as a histone deacetylase inhibitor.[58] This fatty acid contributes to the maintenance of barrier integrity and reduces intestinal inflammation.[59,60] Acetic acid, propionic acid and butyric acid regulate key metabolic hormones including peptide YY (PYY) and GLP-1 (12, 23), activating G-protein-coupled receptors (GPRs) .[61,62] It has been found in studies that the formation of propionic acid, butyric acid or other SCFAs can improve insulin sensitivity and reduce obesity.[63]
In vitro chemo-protective effect of Eisenia foetida coelomic fluid against histone deacetylase inhibitor-induced oxidative toxicity in breast cancer cells
Published in International Journal of Environmental Health Research, 2022
Asuman Deveci Özkan, Janiah Alimudin, Yasemin Kilciler, Burcu Yuksel, Ozlem Aksoy, Zeynep Betts
Sodium butyrate (NaBu), which is used as a chemotherapeutic agent in the treatment of breast cancer, which is the most common cancer in women in the world, is a short-chain fatty acid found in humans, produced from dietary fibre (Yuksel et al. 2022). It inhibits proliferation in breast cancer cell lines and induces morphological changes, causing growth arrest, differentiation and apoptosis in cells. (Huang et al. 2017). In cancer treatment, necrotic cell death may disrupt membrane integrity and cause the release of mediators associated with inflammation and immunosuppression into the extracellular environment. This situation may pose a threat to the patient by promoting carcinogenesis. Therefore, it is very important to eliminate or reduce the high cytotoxicity of NaBu for both neoplastic and normal cells. Our study investigated the chemoprotective effect of coelomic fluid obtained from Eisenia foetida on the toxicity of NaBu, a histone deacetylase inhibitor, in breast cancer. For this purpose, the cytotoxic and chemoprotective effects of ECF on breast cancer cell viability were determined. To evaluate the effect of ECF on the oxidative toxicity induced by NaBu in MCF-7 cells, changes in ROS production levels and expression of cell death and ROS-related genes (Bax, Bcl-2, SOD and CAT) were detected.