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. 2021 Jul 5;26(13):4099. doi: 10.3390/molecules26134099

Figure 1.

Figure 1

Various active principles and their mechanism of action. The infection cycle of SARS-CoV-2 in human cells. The SARS-CoV-2 spike (S) protein binds to ACE2 in host cells followed by priming of protein S by transmembrane protease serine 2 protease (TMPRSS2). Then, the virus produces the polyproteins pp1a and pp1ab, which are processed by viral proteases (3CLpro/Mpro, PLpro) to non-structural proteins (nsps), including RNA-dependent RNA polymerase (RdRp). Viral RdRp synthesizes a full-length complementary negative-strand RNA as a template for the production of the positive strand genome of the virus. Subgenomic mRNAs are then translated into structural proteins in the rough endoplasmic reticulum or in the cytosol. The viral genomic RNA is encapsulated by the nucleocapsid protein N and, finally, the virus is released by exocytosis. The blunt arrows indicate the possible targets of the active principles of medicinal plants. Irreversibly interference with viral docking receptors: Caphtharic acid (o), cichoric acid and echinacoside from Echinacea purpurea (p), vitamins D, C and Zn (q). Entry locks: Emodin (a), lectins (b), quercetin (c), catechin (d), naringenin (e), hesperetin (f), baicalin (g), epigallocatechin (h), gallocatechin gallate (i), prodelphinidin (af), gallocatechin (ag), saikosaponins derivatives of oleanane from Heteromorpha arborescens and Bupleurum spp. (aj), glycyrrhizine (al), Licorice (am), desmethoxyreserpine (ao), dihydrotanshinone I (ay). ACE2 receptor blocking: Emodin (a), hesperetin (f), kaempferol (j), anthocyanins (t), phenolic compounds: tannic acid (aa), 3-isotheaflavin-3-gallate (ab) and theaflavin-3,3′-digallate (ac) from Camellia sinensis. TMPRSS2 receptor blocking: [6]-gingerol (ak). Block the entry of cells through endocytosis: Butanol extract (v) and procyanidins (ai) from Cinnamomum verum. Inhibit 3CLpro: Quercetin (c), kaempferol (j), curcumin (y), sinigrin (z), eugenol (an), betulinic acid (ap), coumaroyltyramine (aq), cryptotanshinone (ar), desmethoxyreserpine (ao), Dihomo-γ-linolenic acid (au), lignan (as), sugiol (at), N-cis-feruloyltyramine (av), Tanshinone IIa (aw). Inhibit PLpro: Quercetin (c), baicalin (g), kaempferol (j), myricetin (n), scutellarein (l), eugenol (an), coumaroyltyramine (aq), cryptotanshinone (ar), N-cis-feruloyltyramine (av), Tanshinone IIa (aw), moupinamide (ax). Affinity with S protein: Eugenol (an), dihydrotanshinone I (ay). Viral replication: Aescin (k), kaempferol (j), resveratrol (s), prodelphinidin (af), gallocatechin (ag), epigallocatechin isomer (ah) from Pelargonium sidoides, essential oils: β-ocimene, 1,8-cineole, α-pinene and β-pinene (ad), phenolic compounds: tannic acid (aa), 3-isotheaflavin-3-gallate (ab) and theaflavin-3,3′-digallate (ac), betulinic acid (ap), desmethoxyreserpine (ao), lignan (as), sugiol (at). Affects the release or assembly of the virus: Phenolic compounds: tannic acid (aa), 3-isotheaflavin-3-galalate (ab) and theaflavin-3,3′-digallate (ac), lectin agglutinin (w) from Hippeastrum striatum. TNF-β, IL-1β expressions: Quercetin (c), luteoloside (m), chlorogenic acid (x) geranylated flavonoids (tomebrin A, B, D and E) (r), resveratrol (s), anthocyanins (t), gallic acid (u), prodelphinidin (af), gallocatechin (ag), epigallocatechin isomer (ah).