Pine Cone Extract Research Articles

Interaction of pine cone extract fraction VI with mutagens

Pine cone extract fraction VI (PC-VI) inhibited the mutagenicity of the promutagens tested: the polycyclic aromatic hydrocarbon benzo[ a]pyrene (B[a]P) dose-dependently, and the aromatic amines 2-aminoanthracene (AA) and 2-acetylaminofluorene (AAF) at high concentrations. PC-VI had no effect on the mutagenicity of the direct-acting mutagens 2-(2-furyl)-3-(5-nitrofuryl)acrylamide (AF-2) and N-methyl- N′-nitro- N-nitrosoguanidine (MNNG), but inhibited the mutagenicity of the direct-acting mutagen N-hydroxy 2-acetylaminofluorene (N-OH AAF, proximate mutagen of AAF). The addition of PC-VI to rat hepatic microsomes resulted in a decrease of their enzyme activities, especially NADPH-cytochrome c reductase. By gas-chromatographic analysis of B[a]P or AA contents after incubation of B[a]P or AA and PC-VI and S9 mix, the inhibition of hepatic metabolizing enzymes and the interaction between AA and PC-VI were confirmed. On the other hand, PC-VI had no effect on the DNA repair systems for B[a]P- or AA-induced mutagenesis. We conclude that PC-VI shows indirect antimutagenicity by interfering with cytochrome P-450-dependent bioactivation and by direct interaction with AA and the proximate mutagenic product of AAF.

Antimutagenicity of pine cone extract Fr. VI (PC-VI)

Antimutagenicity of pine cone extract Fr. VI (PC-VI)

Polymeric phenylpropenoids are the active components in the pine cone extract that inhibit the replication of type-1 human immunodeficiency virus in vitro.

We have previously shown that an alkaline extract from cones of pine trees could significantly inhibit HIV-1 replication in vitro. Ultraviolet, infrared, thin-layered chromatography and nuclear magnetic resonance analyses showed that polymeric phenylpropenoids might be the active ingredient in the alkaline extract that inhibited HIV-1 replication. We synthesized polymeric phenylpropenoids by dehydrogenation of caffeic acid, p-coumaric acid, ferulic acid and coniferyl alcohol. All 4 synthetic isopolymers had anti-HIV activity comparable to that found in the alkaline pine cone extract. Additionally, 3 of the 4 polymers blocked infection of cell by herpes simplex type-1 virus. Among the monomers, only caffeic acid had anti-HIV activity, but was also toxic to cells. None of the monomers had impact on herpes simplex virus infection.

Possible involvement of lignin structure in anti-influenza virus activity

Commercial lignins suppressed the growth of influenza A virus infecting MDCK cells, and the RNA-dependent RNA synthesis, as efficiently as the high-molecular weight fractions extracted from pine cone of Pinus parviflora Sieb. et Zucc. The anti-influenza A virus activity of both pine cone extract and commercial alkali-lignin was considerably reduced by treatment with sodium chlorite, but was not affected by sulfuric acid or trifluoroacetic acid. The degraded components of lignin, various synthesized polyphenols unrelated to lignin, and natural and chemically modified glucans, were not appreciably inhibitory. The data suggest that the polymerized phenolic structure of lignified materials is responsible for the anti-influenza A virus activity.

Inhibition of influenza virus infection by pine cone antitumor substances

The anti-influenza virus activity of polysaccharides and other high molecular weight fractions from pine cone extract (PCE) of Pinus parviflora Sieb. et Zucc. was investigated. None of the fractions affected the growth of MDCK cells. The acidic PCE substances markedly suppressed the growth of the influenza virus in MDCK cells. Significant inhibition of both the viral protein synthesis in infected cells and virion-associated RNA-dependent RNA polymerase activity was observed with these acidic fractions. Although amantadine inhibited virus plaque formation as effectively as PCE fractions, it was less effective in inhibiting the RNA polymerase activity. These results suggest that PCE, which has been shown to contain antitumor substance(s), also contains anti-influenza virus substance(s).