Caffeine:
Following the previously published preclinical studies, caffeine showed
anti-inflammatory effects in the lungs of rat pups following its
administration at a low neonatal dose
(Köroğlu et al. 2014). Further
preclinical studies showed that caffeine reduced the production of
proinflammatory cytokines in a rat model of endotoxic shock
(Tofovic et al. 2001) and also
suppressed the TNF-α-induced apoptosis and hepatitis in mice model
(Sugiyama et al. 2001). Besides, it was
also reported in another preclinical study that acute caffeine treatment
at a high dose or chronic caffeine treatment at a low dose reduced lung
damage and inflammatory cytokines like TNF-α and IL-1 levels in a lung
injury mice model. However, a chronic caffeine treatment at a low dose
enhanced inflammation and lung damage (Li
et al. 2011). On a similar note, in vitro studies showed the presence
of coffee extracts on lipopolysaccharide (LPS)-treated murine
macrophage-like cells showed a decrease in mRNA levels of TNF-α and IL-6
(Jung et al. 2017). Such an
anti-inflammatory effect of caffeine correlates with reduced expression
of IL-6, IL-3, and IL-12 by LPS-treated murine macrophage cells
(Samieirad et al. 2017). In another
study, 50µM caffeine treatment on LPS-activated cord blood (neonatal)
monocytes showed a 20% decrease of TNF-α production
(Chavez-Valdez et al. 2009) and at a
concentration of 100µM caffeine suppressed the TNF-α production by
LPS-stimulated human whole blood by approximately 40%
(Horrigan et al. 2004). In addition to
preclinical and in vitro data, there is epidemiological evidence showing
that caffeine intake as a protective factor for diseases like
Alzheimer’s disease (Maia and De Mendonça
2002). The neuroprotective effects could be due to its
anti-inflammatory properties. The extensive studies showing
anti-inflammatory and anti-oxidative properties of caffeine(Figure 2) suggests that it may play a potential therapeutic
role and a possible treatment of inflammation and oxidations in COVID-19
patients.