Biosynthetic gold nanoparticles of Hibiscus syriacus L. callus potentiates anti-inflammation efficacy via an autophagy-dependent mechanism
- Authors
- Xu, Xing Yue; Thi Hoa My Tran; Perumalsamy, Haribalan; Sanjeevram, Dhandapani; Kim, Yeon-Ju
- Issue Date
- May-2021
- Publisher
- ELSEVIER
- Keywords
- Callus of Hibiscus syriacus L.; Biosynthetic gold nanoparticles; LPS-stimulated inflammation; Mitochondrial dysfunction; Autophagy
- Citation
- MATERIALS SCIENCE & ENGINEERING C-MATERIALS FOR BIOLOGICAL APPLICATIONS, v.124
- Indexed
- SCIE
SCOPUS
- Journal Title
- MATERIALS SCIENCE & ENGINEERING C-MATERIALS FOR BIOLOGICAL APPLICATIONS
- Volume
- 124
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/189722
- DOI
- 10.1016/j.msec.2021.112035
- ISSN
- 0928-4931
- Abstract
- Biological applications of gold nanoparticles (AuNps) have potentially explored an efficient agent attributed to their biocompatibility and high efficiency in drug delivery. Our study applied an extract of Hibiscus syriacus L. callus (HCE) with a pioneer implementation on the induction of mass production. Bioactive compounds present in HCE were identified by Gas chromatography-mass spectrometry (GC-MS) and Liquid chromatography MS (LC-MS), wherein, the Denatonium was exclusively identifiable in HCE. Next, AuNps were synthesized and optimized using HCE (HCE-AuNps), and the comparison was conducted to evaluate the anti-inflammatory effect in lipo-polysaccharide (LPS)-stimulated macrophages. As per result, HCE-AuNps was reported to show a prominent reduction of pro-inflammatory cytokines and renovate the mitochondrial function through restoring the mitochondrial membrane potential changes, decreasing reactive oxygen species (ROS) accumulation, and recovering ATP contents, respectively. Furthermore, the immunoblotting of LC3b/a accumulation, and p62 rapid degradation revealed that HCE-AuNps could induce the autophagy as an intracellular response to reinforce alleviation of pro-inflammatory cytokines and mitochondria dysfunction. Besides, 740 Y-P (PI3K agonist) was used to verify that inhibiting autophagy could partially reverse HCE-AuNps suppressed mitochondrial dysfunction, and thus exacerbated inflammation, supporting a causal role for autophagy in the anti-inflammatory effect of HCE-AuNps. Taken together, we strongly anticipate that HCE-AuNps would act as a potential autophagy inducer for LPS-triggered macrophage's inflammation, providing a novel insight for biosynthetic nanoparticles in the treatment of mitochondria dysfunction and inflammation related diseases.
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