Potential Protective Effects of Vitamin K3 on SARS-CoV-2-Induced Inflammation and Cell Damage: A Promising Therapeutic Strategy for COVID-19


The ongoing COVID-19 pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has led to significant global health and economic challenges.

The disease is characterized by a dysregulated inflammatory response that can lead to severe organ damage and even death.

In this context, the search for effective therapeutics that can mitigate inflammation and protect against SARS-CoV-2-induced cell damage is of paramount importance.

In this study, the researchers investigated the potential protective effects of vitamin K3, also known as Menadione, on the inflammatory response and cell damage induced by SARS-CoV-2 N protein and E protein. The findings shed light on the potential use of vitamin K3 as a preventive or therapeutic strategy for COVID-19.

The Role of Vitamin K3 in Inflammation and Physiology

Vitamin K is an essential micronutrient that plays a vital role in various physiological processes, including blood coagulation, bone mineralization, soft tissue physiology, and neurological development. The vitamin K family includes natural forms derived from plants (vitamin K1 and K2) and synthetic congeners (vitamin K3 and K4).

Among them, vitamin K3, or Menadione, is a hydrophilic compound that is not obtained through the diet and is often used as a clotting drug and vitamin supplement.

In recent years, research has highlighted the anti-inflammatory effects of vitamin K3. Previous studies have demonstrated that vitamin K3 can inhibit the activation of NF-κB, a major pro-inflammatory signaling pathway, and reduce the production of pro-inflammatory cytokines.

Additionally, vitamin K3 and its analogs have been shown to target the NLRP3 inflammasome, a multiprotein complex involved in the inflammatory response, further reinforcing their anti-inflammatory properties.

The Relationship Between Vitamin K and COVID-19

Emerging evidence has suggested that vitamin K may be linked to COVID-19 outcomes. COVID-19 patients have been shown to have increased vitamin K utilization, and low levels of vitamin K have been associated with higher mortality in COVID-19 patients.

Moreover, vitamin K3 and its analogs have been investigated for their potential to inhibit the activity of SARS-CoV-2 3CLPro, an enzyme crucial for viral replication, suggesting that vitamin K3 may have a direct antiviral effect.

The Study’s Objectives and Methodology

The present study aimed to investigate the protective effects of vitamin K3 on SARS-CoV-2-induced inflammation and cell damage, particularly focusing on the effects of the SARS-CoV-2 N protein and E protein. Endothelial activation, a key feature of the inflammatory response in COVID-19, was selected as a primary target in this study, as it is associated with increased vascular permeability, microvascular thrombosis, and organ failure.

The researchers utilized cellular models to assess the impact of vitamin K3 on SARS-CoV-2 protein-induced inflammation and damage. Endothelial cells and THP-1 cells (a human monocytic cell line) were exposed to SARS-CoV-2 N protein and E protein, and the protective effects of vitamin K3 were evaluated based on changes in cell activation, pyroptosis, and cytokine expression.

Results and Discussion

The study demonstrated that vitamin K3 effectively suppressed SARS-CoV-2 N protein-induced endothelial cell activation by inhibiting monocyte adherence and reducing the expression of key adhesion molecules. Additionally, vitamin K3 exerted potent anti-inflammatory activity by preventing the expression of multiple pro-inflammatory cytokines, possibly through the inhibition of the NF-κB signaling pathway.

These findings suggested that vitamin K3 may have beneficial effects on SARS-CoV-2-induced endothelial activation and dysfunction, which are critical in the pathogenesis of COVID-19.

Furthermore, the researchers observed that vitamin K3 significantly reduced SARS-CoV-2 E protein-induced pyroptosis in THP-1 cells. Pyroptosis is a form of programmed cell death triggered by pro-inflammatory signals, and its occurrence has been reported in COVID-19 patients.

The protective effect of vitamin K3 against E protein-induced pyroptosis may be associated with the inhibition of the NLRP3/GSDMD pathway, which is regulated by the NF-κB transcription factor.

This suggests that vitamin K3 may interfere with pyroptosis through its anti-inflammatory properties, further supporting its potential as a therapeutic strategy for COVID-19.


In conclusion, the present study provides valuable insights into the potential protective effects of vitamin K3 on the inflammatory response and cell damage induced by SARS-CoV-2 N and E proteins.

The observed suppression of endothelial activation and pyroptosis, as well as the inhibition of pro-inflammatory cytokine expression, highlights vitamin K3 as a promising candidate for the prevention and treatment of COVID-19-associated inflammation and organ injury.

As with any scientific study, further investigation is warranted to fully understand the mechanisms underlying vitamin K3’s protective effects and its potential applications in clinical settings. Nevertheless, these findings contribute to the growing body of knowledge on the interplay between inflammation and SARS-CoV-2 proteins and suggest vitamin K3 as a potential adjunctive therapy in the fight against COVID-19.



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