Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2023 Nov 28;21(1):145.
doi: 10.1186/s43141-023-00624-4.

Dual action of epigallocatechin-3-gallate in virus-induced cell Injury

Affiliations

Dual action of epigallocatechin-3-gallate in virus-induced cell Injury

Ahmed Mostafa et al. J Genet Eng Biotechnol. .

Abstract

Background: Viral infections cause damage and long-term injury to infected human tissues, demanding therapy with antiviral and wound healing medications. Consequently, safe phytochemical molecules that may control viral infections with an ability to provide wound healing to viral-induced tissue injuries, either topically or systemically, are advantageous. Herein, we hypothesized that epigallocatechin-3-gallate (EGCG), the most abundant polyphenol in green tea, might be effective as a wound healing, antiviral, and antifibrotic therapy.

Results: The antiviral activities of EGCG against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and Herpes simplex virus type 2 (HSV-2) as well as its wound healing activities against different monolayer tissue (continuous and primary) systems were investigated. Consider its possible wound-healing advantages as well. To determine the safe concentrations of EGCG in green monkey kidney (Vero) and Vero-E6 cell lines, MTT assay was performed and showed high CC50 values of 405.1 and 322.9 μM, respectively. The antiviral activities of EGCG against SARS-CoV-2 and HSV-2, measured as half-maximal concentration 50 (IC50) concentrations, were 36.28 and 59.88 μM, respectively. These results confirm that the EGCG has remarkable viral inhibitory activities and could successfully suppress the replication of SARS-CoV-2 and HSV-2 in vitro with acceptable selectivity indices (SI) of 11.16 and 5.39, respectively. In parallel, the EGCG exhibits significant and dose/time-dependent anti-migration effects in human breast cancer cells (MCF-7), its resistant variation (MCF-7adr), and human skin fibroblast (HSF) indicating their potential to heal injuries in different internal and topical mammalian systems.

Conclusions: The EGCG has proven to be an efficient antiviral against SARS-CoV-2 and HSV-2, as well as a wound-healing phytochemical. We assume that EGCG may be a promising option for slowing the course of acute cellular damage induced by systemic (Coronavirus Disease 2019 (COVID-19)) or topical (HSV-2) viral infections.

Keywords: Antiviral activity; COVID-19; Cellular injury; EGCG; Green tea extract; Herpes simplex virus; Wound healing.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the review.

Figures

Fig. 1
Fig. 1
Cytotoxicity and antiviral activity of EGCG against SARS-CoV-2 (a) and HSV-2 (b). The Cytotoxicity and antiviral activity were determined in Vero E6 and Vero cells against NRC-03-nhCoV and HSV-2, respectively. Half maximal cytotoxic (CC50) and inhibitory (IC50) concentrations were calculated using nonlinear regression analysis of GraphPad Prism software (version 5.01) by plotting log inhibitor versus normalized response (variable slope)
Fig. 2
Fig. 2
Stage of antiviral activity of EGCG. The EGCG (50 μM) has been tested against SARS-CoV-2 (a) and HSV-2 (b) at different stages of the viral replication cycle including cell-free status “virucidal effect”, adsorption inhibition, and interference with viral replication
Fig. 3
Fig. 3
The effect of EGCG on MCF-7 and MCF-7adr cell migration. MCF-7 and MCF-7adr cell monolayer sheets were scratched and treated with EGCG (1 and 10 μM). Images for the wound gap distance were taken for treated and control cells after 24 h, 48 h, and 72 h (a & c). Wound gap distances were optically measured and displayed over time (b & d). Data are shown as mean ± SD; n = 3. *P < 0.05, versus the control group
Fig. 4
Fig. 4
The effect of EGCG on HSF cell migration. HSF cell monolayer sheets were scratched and treated with EGCG (1 and 10 μM). Images for the wound gap distance were taken for treated and control cells after 24 h, 48 h, and 72 h (a). Wound gap distances were optically measured and displayed over time (b). Data are shown as mean ± SD; n = 3. *P < 0.05, versus the control group

Similar articles

References

    1. Al-Karmalawy AA, Soltane R, Abo Elmaaty A, Tantawy MA, Antar SA, Yahya G, Chrouda A, Pashameah RA, Mustafa M, Abu Mraheil M, Mostafa A. Coronavirus Disease (COVID-19) Control between Drug Repurposing and Vaccination: A Comprehensive Overview. Vaccines (Basel). 2021;9(11):1317. doi: 10.3390/vaccines9111317. - DOI - PMC - PubMed
    1. Alqarni AA, Alamoudi AA, Allam RM, Ajabnoor GM, Harakeh SM, Al-Abd AM. The influence of antioxidant dietary-derived polyphenolic combination on breast cancer: Molecular study. Biomed Pharmacother. 2022;149:112835. doi: 10.1016/j.biopha.2022.112835. - DOI - PubMed
    1. Balikji J, Kiani P, Hendriksen PA, Hoogbergen MM, Garssen J, Verster JC. Impaired wound healing is associated with poorer mood and reduced perceived immune fitness during the COVID-19 pandemic: A retrospective survey. Health Sci Rep. 2022;5:e764. doi: 10.1002/hsr2.764. - DOI - PMC - PubMed
    1. Cantatore A, Randall SD, Traum D, Adams SD. Effect of black tea extract on herpes simplex virus-1 infection of cultured cells. BMC Complement Altern Med. 2013;13:139. doi: 10.1186/1472-6882-13-139. - DOI - PMC - PubMed
    1. Carneiro BM, Batista MN, Braga ACS, Nogueira ML, Rahal P. The green tea molecule EGCG inhibits Zika virus entry. Virology. 2016;496:215–218. doi: 10.1016/j.virol.2016.06.012. - DOI - PubMed

LinkOut - more resources

-