Hyaluronic acid-graphene oxide quantum dots nanoconjugate as dual purpose drug delivery and therapeutic agent in meta-inflammation

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Abstract

Type 2 diabetes mellitus (T2DM) predominantly considered a metabolic disease is now being considered an inflammatory disease as well due to the involvement of meta-inflammation. Obesity-induced adipose tissue inflammation (ATI) is one of the earliest phenomena in the case of meta-inflammation, leading to the advent of insulin resistance (IR) and T2DM. The key events of ATI are orchestrated by macrophages, which aggravate the inflammatory state in the tissue upon activation, ultimately leading to systemic chronic low-grade inflammation and Non-Alcoholic Steatohepatitis (NASH) through the involvement of proinflammatory cytokines. The CD44 receptor on macrophages is overexpressed in ATI, NASH, and IR. Therefore, we developed a CD44 targeted Hyaluronic Acid functionalized Graphene Oxide Quantum Dots (GOQD-HA) nanocomposite for tissue-specific delivery of metformin. Metformin-loaded GOQD-HA (GOQD-HA-Met) successfully downregulated the expression of proinflammatory cytokines and restored antioxidant status at lower doses than free metformin in both palmitic acid-induced RAW264.7 cells and diet induced obese mice. Our study revealed that the GOQD-HA nanocarrier enhanced the efficacy of Metformin primarily by acting as a therapeutic agent apart from being a drug delivery platform. The therapeutic properties of GOQD-HA stem from both HA and GOQD having anti-inflammatory and antioxidant properties respectively. This study unravels the function of GOQD-HA as a targeted drug delivery option for metformin in meta-inflammation where the nanocarrier itself acts as a therapeutic agent.

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Supplementary Information

The online version contains supplementary material available at 10.1186/s12951-023-02015-w.

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Chronic inflammation in the etiology of disease across the life span

David Furman, Judith Campisi, Eric Verdin … (2019)

Although intermittent increases in inflammation are critical for survival during physical injury and infection, recent research has revealed that certain social, environmental and lifestyle factors can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that collectively represent the leading causes of disability and mortality worldwide, such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders. In the present Perspective we describe the multi-level mechanisms underlying SCI and several risk factors that promote this health-damaging phenotype, including infections, physical inactivity, poor diet, environmental and industrial toxicants and psychological stress. Furthermore, we suggest potential strategies for advancing the early diagnosis, prevention and treatment of SCI.

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The mechanisms of action of metformin

Graham Rena, D Hardie, Ewan Pearson (2017)

Metformin is a widely-used drug that results in clear benefits in relation to glucose metabolism and diabetes-related complications. The mechanisms underlying these benefits are complex and still not fully understood. Physiologically, metformin has been shown to reduce hepatic glucose production, yet not all of its effects can be explained by this mechanism and there is increasing evidence of a key role for the gut. At the molecular level the findings vary depending on the doses of metformin used and duration of treatment, with clear differences between acute and chronic administration. Metformin has been shown to act via both AMP-activated protein kinase (AMPK)-dependent and AMPK-independent mechanisms; by inhibition of mitochondrial respiration but also perhaps by inhibition of mitochondrial glycerophosphate dehydrogenase, and a mechanism involving the lysosome. In the last 10 years, we have moved from a simple picture, that metformin improves glycaemia by acting on the liver via AMPK activation, to a much more complex picture reflecting its multiple modes of action. More work is required to truly understand how this drug works in its target population: individuals with type 2 diabetes. Electronic supplementary material The online version of this article (doi:10.1007/s00125-017-4342-z) contains a slideset of the figures for download, which is available to authorised users.

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Author and article information

Contributors

Madhusudan Das: madhuzoo@yahoo.com

Journal

Journal ID (nlm-ta): J Nanobiotechnology

Journal ID (iso-abbrev): J Nanobiotechnology

Title: Journal of Nanobiotechnology

Publisher: BioMed Central (London )

ISSN (Electronic): 1477-3155

Publication date (Electronic): 1 August 2023

Publication date PMC-release: 1 August 2023

Publication date Collection: 2023

Volume: 21

Electronic Location Identifier: 246

Affiliations

[1 ]GRID grid.59056.3f, ISNI 0000 0001 0664 9773, Department of Zoology, , University of Calcutta, ; 35 Ballygunge Circular Road, Kolkata, 700019 India

[2 ]GRID grid.59056.3f, ISNI 0000 0001 0664 9773, Department of Polymer Science and Technology, , University of Calcutta, ; 92 A.P.C. Road, Kolkata, 700009 India

[3 ]Department of Allied Health Sciences, Brainware University, Kolkata, 700129 India

[4 ]GRID grid.59056.3f, ISNI 0000 0001 0664 9773, Department of Zoology, , Vidyasagar College for Women, ; Kolkata, 700006 India

[5 ]GRID grid.59056.3f, ISNI 0000 0001 0664 9773, Molecular and Applied Mycology and Plant Pathology Laboratory, Department of Botany, , University of Calcutta, ; Kolkata, 700019 India

Article

Publisher ID: 2015

DOI: 10.1186/s12951-023-02015-w

PMC ID: 10394801

PubMed ID: 37528408

SO-VID: 07b9a26c-bac1-4302-bfd9-3dcd845c2ff9

License:

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 21 March 2023

Date accepted : 21 July 2023

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100001407, Department of Biotechnology, Ministry of Science and Technology, India;

Award ID: BT/PR25080/NER/95/999/2017

Award Recipient : Madhusudan Das

Custom metadata

ScienceOpen disciplines: Biotechnology

Keywords: graphene oxide quantum dots,hyaluronic acid,metformin,nanocomposite,meta-inflammation,adipose tissue inflammation,hepatic steatosis

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ScienceOpen disciplines: Biotechnology

Keywords: graphene oxide quantum dots, hyaluronic acid, metformin, nanocomposite, meta-inflammation, adipose tissue inflammation, hepatic steatosis

Hyaluronic acid-graphene oxide quantum dots nanoconjugate as dual purpose drug delivery and therapeutic agent in meta-inflammation

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Supplementary Information

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Most cited references 86

A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding

Chronic inflammation in the etiology of disease across the life span

The mechanisms of action of metformin

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