Exploring the efficacy of naturally occurring biflavone based antioxidants towards the inhibition of the SARS-CoV-2 spike glycoprotein mediated membrane fusion

Mondal, Samiran; Karmakar, Abhijit; Mallick, Tamanna; Begum, Naznin Ara

doi:10.1016/j.virol.2021.01.015

Cited by 16 publications

(12 citation statements)

References 60 publications

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“… 120 Meanwhile, biflavone-based anti-HIV drugs, such as hinokiflavone and robustaflavone, could prevent SARS-CoV-2 S-mediated virus entry by blocking the HR1-HR2 interaction. 121 …”

Section: Small-molecule Compounds That Block the Hr1-hr2 Interactionmentioning

confidence: 99%

Targetable elements in SARS-CoV-2 S2 subunit for the design of pan-coronavirus fusion inhibitors and vaccines

Guo

Lin

Chen

et al. 2023

Sig Transduct Target Ther

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The ongoing global pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), has caused devastating impacts on the public health and the global economy. Rapid viral antigenic evolution has led to the continual generation of new variants. Of special note is the recently expanding Omicron subvariants that are capable of immune evasion from most of the existing neutralizing antibodies (nAbs). This has posed new challenges for the prevention and treatment of COVID-19. Therefore, exploring broad-spectrum antiviral agents to combat the emerging variants is imperative. In sharp contrast to the massive accumulation of mutations within the SARS-CoV-2 receptor-binding domain (RBD), the S2 fusion subunit has remained highly conserved among variants. Hence, S2-based therapeutics may provide effective cross-protection against new SARS-CoV-2 variants. Here, we summarize the most recently developed broad-spectrum fusion inhibitors (e.g., nAbs, peptides, proteins, and small-molecule compounds) and candidate vaccines targeting the conserved elements in SARS-CoV-2 S2 subunit. The main focus includes all the targetable S2 elements, namely, the fusion peptide, stem helix, and heptad repeats 1 and 2 (HR1-HR2) bundle. Moreover, we provide a detailed summary of the characteristics and action-mechanisms for each class of cross-reactive fusion inhibitors, which should guide and promote future design of S2-based inhibitors and vaccines against new coronaviruses.

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“… 120 Meanwhile, biflavone-based anti-HIV drugs, such as hinokiflavone and robustaflavone, could prevent SARS-CoV-2 S-mediated virus entry by blocking the HR1-HR2 interaction. 121 …”

Section: Small-molecule Compounds That Block the Hr1-hr2 Interactionmentioning

confidence: 99%

Targetable elements in SARS-CoV-2 S2 subunit for the design of pan-coronavirus fusion inhibitors and vaccines

Guo

Lin

Chen

et al. 2023

Sig Transduct Target Ther

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“…The binding interactions of antioxidant compounds with S protein RBD and other SARS-CoV-2 proteins involved in COVID-19 infection have been studied. According to recent studies compounds like quercetin, withanolides, anaferine, ashwagandhanolide, nefamostat, hinokiflavone and robustaflavone showed high affinity for the S2 domain of the spike protein of SARS-CoV-2 [ 205 , 206 ]. These compounds interact with SARS-CoV-2 through its aromatic amino acid residues through non-covalent bonds (H-bonds) with the SARS-CoV-2 S2 protein.…”

Section: Mechanisms Of Antioxidants Compounds Against Sars-cov-2 In Covid-19mentioning

confidence: 99%

“…These compounds interact with SARS-CoV-2 through its aromatic amino acid residues through non-covalent bonds (H-bonds) with the SARS-CoV-2 S2 protein. Moreover, hinokiflavone and robustaflavone interacted strongly with the residues of heptad repeat 1 and 2 regions of S2 proteins of SARS-CoV-2, inhibiting the fusion between the virus and target cell membranes [ 205 ]. Kamferol, curcumin, pterostilbene, and hydroxychloroquine have also been reported to interact with the C-terminal of the S1 domain and fisetin, quercetin, isorhamnetin, genistein, luteolin, resveratrol, and apigenin interact with the S2 domain of the SARS-CoV-2 spike protein [ 207 ].…”

Section: Mechanisms Of Antioxidants Compounds Against Sars-cov-2 In Covid-19mentioning

confidence: 99%

Use of Antioxidants for the Neuro-Therapeutic Management of COVID-19

et al. 2021

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Coronavirus Disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), is an emergent infectious disease that has caused millions of deaths throughout the world. COVID-19 infection’s main symptoms are fever, cough, fatigue, and neurological manifestations such as headache, myalgias, anosmia, ageusia, impaired consciousness, seizures, and even neuromuscular junctions’ disorders. In addition, it is known that this disease causes a series of systemic complications such as adverse respiratory distress syndrome, cardiac injury, acute kidney injury, and liver dysfunction. Due to the neurological symptoms associated with COVID-19, damage in the central nervous system has been suggested as well as the neuroinvasive potential of SARS-CoV-2. It is known that CoV infections are associated with an inflammation process related to the imbalance of the antioxidant system; cellular changes caused by oxidative stress contribute to brain tissue damage. Although anti-COVID-19 vaccines are under development, there is no specific treatment for COVID-19 and its clinical manifestations and complications; only supportive treatments with immunomodulators, anti-vascular endothelial growth factors, modulating drugs, statins, or nutritional supplements have been used. In the present work, we analyzed the potential of antioxidants as adjuvants for the treatment of COVID-19 and specifically their possible role in preventing or decreasing the neurological manifestations and neurological complications present in the disease.

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“…spring and other plants [ 7 – 9 ]. It has diverse pharmacological activities, including anti-inflammation [ 10 ], antivirus [ 11 ] and antioxidant [ 12 ]. In addition, HF modulates pre-mRNA splicing and inhibits sentrin-specific protease 1 (SENP1) [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Hinokiflavone induces apoptosis, cell cycle arrest and autophagy in chronic myeloid leukemia cells through MAPK/NF-κB signaling pathway

Qin

Chen

Liu

et al. 2022

BMC Complement Med Ther

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Background Chronic myeloid leukemia (CML) is a myeloproliferative tumor originating from hematopoietic stem cells, and resistance to tyrosine kinase inhibitors (TKI) has become a major cause of treatment failure. Alternative drug therapy is one of the important ways to overcome TKI resistance. Hinokiflavone (HF) is a C-O-C type biflavonoid with low toxicity and antitumor activity. This study investigated the antitumor effect and possible mechanisms of HF in CML cells. Methods Cell viability was measured by CCK-8 assay. Cell apoptosis and cell cycle distribution were analyzed by flow cytometry. Western blotting was used to assess protein expression levels. Results Our results showed that HF significantly inhibited the viability of K562 cells in a concentration- and time-dependent manner and induced G2/M phase arrest by up-regulating p21 and down-regulating Cdc2 protein. Furthermore, HF induced caspase-dependent apoptosis by activating JNK/p38 MAPK signaling pathway and inhibiting NF-κB activity. In addition, HF induced autophagy by increasing LC3-II expression and p62 degradation. Pretreatment with CQ, a late autophagy inhibitor, significantly increased the levels of LC3-II and p62 proteins and promoted cell survival. Conclusion HF shows a good anti-leukemia effect and is expected to become a potential therapeutic drug for CML.

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Exploring the efficacy of naturally occurring biflavone based antioxidants towards the inhibition of the SARS-CoV-2 spike glycoprotein mediated membrane fusion

Cited by 16 publications

References 60 publications

Targetable elements in SARS-CoV-2 S2 subunit for the design of pan-coronavirus fusion inhibitors and vaccines

Targetable elements in SARS-CoV-2 S2 subunit for the design of pan-coronavirus fusion inhibitors and vaccines

Use of Antioxidants for the Neuro-Therapeutic Management of COVID-19

Hinokiflavone induces apoptosis, cell cycle arrest and autophagy in chronic myeloid leukemia cells through MAPK/NF-κB signaling pathway

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