Gene Reports 26 (2022) 101522
Available online 22 January 2022
2452-0144/© 2022 Elsevier Inc. All rights reserved.
N-Acetyl-L-cysteine effects on oxidative stress-induced high
glucose-cultured human dermal fbroblasts
Mohammad Hossein Rashnavadi , Zahra Tahmasebi , Zeinab Piravar
*
,
Azadeh Mohammad Gholi
Department of Biology, Faculty of Sciences, Central Tehran Branch, Islamic Azad University, Tehran, Iran
A R T I C L E INFO
Edited by Hee-Jeong Im Sampen
Keywords:
High glucose
Oxidative stress
Nrf2
Catalase
Glutathione
N-acetyl cysteine
ABSTRACT
Background: Wound healing in diabetic patients is delayed, but the mechanism of this impairment is unclear. We
sought to investigate molecular changes in human dermal fbroblasts (HDFs) in a high-glucose state and
improving effect of N-acetyl-L-cysteine (NAC).
Methods: HDFs were cultured in 5.5, 25, 50, and 75 mM glucose concentrations for 72 h. Cell proliferation and
migration were examined via in vitro scratch and 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium
bromide (MTT) assays. Cytotoxicity was determined through the measurement of lactate dehydrogenase (LDH).
The level of intracellular reactive oxygen species (ROS) was also measured in the HDFs. Oxidative stress markers
of nuclear factor erythroid 2 (NFE2)- related factor 2 (NRF2), Catalase (CAT) and Glutathione (GSH) were
quantifed with Real time polymerase chain reaction (PCR). The antioxidant effect of NAC, 1 mM was examined
to evaluate the involvement of ROS and LDH and oxidative markers in the glucose effects on the HDFs.
Results: The in vitro scratch assay showed that high glucose concentrations signifcantly reduced fbroblast
migration and proliferation at 12, 24, and 48 h. The MTT assay revealed a decline in cell viability in 50 and 75
mM glucose concentrations. A signifcant increase in LDH and ROS levels was observed in the HDFs incubated in
50 and 75 mM glucose concentrations after 72 h. mRNA level of Nrf2, CAT and GSH were downregulated. The
antioxidant addition of NAC reduced the inhibitory effect of the high-glucose state on the migration and pro-
liferation of the HDFs.
Conclusions: A high-glucose state impairs the in vitro proliferation and migration of HDFs and may, therefore,
induce increased oxidative stress and cellular dysfunction. The antioxidant effect of NAC ameliorates the
damaging impact of a high-glucose state.
1. Introduction
Diabetes is a disease characterized by elevated blood sugar levels.
The impaired metabolism of glucose, lipids, and proteins in diabetes
increases the risk of affiction to other diseases such as retinopathy,
neuropathy, nephropathy, and cardiovascular disease (Pang et al.,
2016). Delayed wound healing is another complication of diabetes,
which may cause chronic ulcers and even amputation (Liu et al., 2011),
with the latter not only diminishing the quality of life of the victims but
also imposing substantial economic burdens on communities. Wound
healing is a complex process that involves various chemical and bio-
logical interactions between cells, growth and infammatory factors, and
extracellular matrix compounds (Kulprachakarn et al., 2017). Hyper-
glycemia delays wound healing by creating an infammatory state and
inhibiting tissue angiogenesis. Laboratory studies have indicated that
hyperglycemia stymies the migration, proliferation, and synthesis of
vital factors such as collagen in cells and amplifes the rate of apoptosis
(Chen et al., 2018). Wound healing requires coordination between
Abbreviations: HDFs, Human Dermal Fibroblasts; NAC, N-Acetyl-L-cysteine; MTT, 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide; LDH,
lactate dehydrogenase; ROS, reactive oxygen species; PCR, polymerase chain reaction; CAT, Catalase; NRF2, nuclear factor erythroid 2 (NFE2)- related factor 2;
DMEM, Dulbecco's Modifed Eagle's Medium; FBS, fetal bovine serum; AUC, area under the percent migration curve; OD, optical density; DMSO, dimethyl sulfoxide;
DCFDA, dichlorodihydrofuorescein diacetate.
* Corresponding author at: Department of Biology, Faculty of Sciences, Central Tehran Branch, Islamic Azad University, Ashraf Isfahani Highway, Imam Hassan
Blvd., Orchid code: 0000-0001-8949-362X, Tehran 1955847881, Iran.
E-mail address: saba.piravar@gmail.com (Z. Piravar).
Contents lists available at ScienceDirect
Gene Reports
journal homepage: www.elsevier.com/locate/genrep
https://doi.org/10.1016/j.genrep.2022.101522
Received 2 October 2021; Received in revised form 23 December 2021; Accepted 14 January 2022
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