Year-end Sale % OFF 
Abstract
Although epigallocatechin-3-gallate (EG) is well-known as a potent antioxidant and free radical scavenger for neurodegenerative diseases, it still has disadvantages that reduce its treatment effectiveness due to low bioavailability, slow absorption, and water solubility. Therefore, the aim of this study is to improve the bioavailability of EG and increase the effectiveness of anti-inflammatory properties to microglial cells by using Poly(Lactide-co-Glycolide) (PLGA) microspheres as carriers. In this study, we used UV–Vis spectroscopy to show the formation of the complex of β-cyclodextrin (β-CD) and EG (CD-EG). The loading efficiency of EG in PLGA microspheres was optimized by the addition of β-CD. The highest loading efficiency of 16.34% was found among other formulations. The results of Fourier transform infrared spectroscopy indicated the loading of CD-EG in PLGA microspheres. The scanning electron microscopic images demonstrated the spherical PLGA particles with controlled particles size ranging from 1–14 µm. Moreover, the in vitro release of EG was conducted to explore the sustained release property of the PLGA formulations. In the in vitro model of mouse microglial cells (BV-2 cells) stimulated by lipopolysaccharide, the cytotoxicity test showed that for up to 1 mg/mL of PLGA microspheres no toxicity to BV-2 cells was found. PLGA microspheres can significantly suppress the nitric oxide production from BV-2 cells, indicating EG loaded in PLGA microspheres can suppress the inflammation of activated microglial cells. Furthermore, the intracellular iNOS in BV-2 cells was also found to be down regulated. In summary, we have successfully shown that the use of β-CD can increase the loading efficiency of EG in PLGA microspheres and provide neuroprotective effect on the activated microglial cells.
Highlights
Microglia are the primary immune cells of the brain that play a crucial role in neurodegenerative diseases [1,2]
In regards to brain injury caused by toxic reagents, trauma, ischemia, and cell debris, the microglial cells are stimulated to generate excessive factors of pro-inflammation consisting of tumor necrosis factor (TNF-α) [3,4], interleukin (IL-1β) [5,6], nitric oxide (NO) [7,8], and reactive oxygen species (ROS) [9] to induce death of neurons
These results revealed that various ratios of β-cyclodextrin interacted with EG lead to the shifting of maximum adsorption wavelength of complexes compared to original EG (274 nm) [42]
Summary
Microglia are the primary immune cells of the brain that play a crucial role in neurodegenerative diseases [1,2]. Activated microglia is described to present in two functionally various states, including innate and adaptive activation, which is determined by their stimulatory environment. The inequality of these activation in microglial cells may lead to either neural benefit or damage. The activation of microglial cells in terms of chronicity is believed to be related to neurodegenerative disorders (Alzheimer’s disease [10,11,12] and Parkinson’s disease [13,14,15]). The inhibition of microglial activation has been suggested for potential treatment of neurodegenerative diseases [16,17]
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
