Thiyagarajan, P., R. Senthil Murugan, et al. (2012). „Dietary chlorophyllin inhibits the canonical NF-kappaB signaling pathway and induces intrinsic apoptosis in a hamster model of oral oncogenesis.“ Food Chem Toxicol50(3-4): 867-876.
Chlorophyllin, a water-soluble, semi-synthetic derivative of the ubiquitous green pigment chlorophyll is shown to exert potent anticarcinogenic effects. In the present study, we investigated the chemopreventive effects of chlorophyllin on 7,12-dimethylbenz(a)anthracene (DMBA)-induced hamster buccal pouch (HBP) carcinogenesis by analyzing the expression of NF-kappaB family members and markers of intrinsic apoptosis. Dietary administration of chlorophyllin (4 mg/kg bw) suppressed the development of HBP carcinomas by inhibiting the canonical NF-kappaB signaling pathway by downregulating IKKbeta, preventing the phosphorylation of IkappaB-alpha, and reducing the expression of nuclear NF-kappaB. Inactivation of NF-kappaB signaling by chlorophyllin was associated with the induction of intrinsic apoptosis as evidenced by modulation of Bcl-2 family proteins, enforced nuclear localization of survivin, upregulation of apoptogenic molecules, activation of caspases, and cleavage of PARP. The results of the present study demonstrate that chlorophyllin inhibits the development of DMBA-induced HBP carcinogenesis by targeting NF-kappaB and the intrinsic apoptotic pathway. Thus, dietary agents such as chlorophyllin that simultaneously target divergent pathways of cell survival and cell death are novel candidates for cancer chemoprevention.
Deutsche Zusammenfassung der aktuellen wissenschaftlichen Arbeit von 2012:
Bei Hamstern mit Wangenkrebs konnte nachgewiesen werden, dass Chlorophyllin einen starken krebshemmenden Effekt hat. Über den sogenannten NF-kappa-B-Signalweg wird die Entwicklung von Krebszellen gehemmt.
Auch die folgende Arbeit beweist die gute Wirksamkeit bei einem experimentell erzeugten Krebs (im Tierversuch):
Carcinogenesis. 2009 Feb;30(2):315-20. doi: 10.1093/carcin/bgn280. Epub 2008 Dec 10.
Identifying efficacious approaches to chemoprevention with chlorophyllin, purified chlorophylls and freeze-dried spinach in a mouse model of transplacental carcinogenesis.
Castro DJ, Löhr CV, Fischer KA, Waters KM, Webb-Robertson BJ, Dashwood RH, Bailey GS, Williams DE.
Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331-7301, USA.
The carcinogenic potential of dibenzo[a,l]pyrene (DBP) has been well characterized in numerous animal models. We have previously documented that a single dose of 15 mg/Kg DBP to pregnant mice late in gestation (GD 17) produces an aggressive T-cell lymphoma as well as lung and liver cancer in offspring. The current study examines the chemopreventative properties of chlorophyllin (CHL) and chlorophyll (Chl) in this transplacental carcinogenesis model. Pregnant B6129SF1 females, bred to 129S1/SvIm males, received purified diets incorporated with either 2000 p.p.m. CHL, 2000 p.p.m. Chl or 10% freeze-dried spinach beginning at gestation day 9. Lymphoma-dependent mortality was not significantly altered by maternal consumption of any of the diet and little effect on lung tumor burden in mice surviving to 10 months of age was observed. However, coadministration of CHL at 380 mg/Kg with DBP by gavage (molar ratio of 10:1, CHL:DBP) provided significant protection against DBP-initiated carcinogenesis. Offspring born to dams receiving CHL co-gavaged with DBP exhibited markedly less lymphoma-dependent mortality (P < 0.001). The degree of protection by CHL, compared with controls dosed with DBP in tricaprylin (TCP) as the vehicle, was less marked, but still significant. Coadministration of CHL (TCP as vehicle) also reduced lung tumor multiplicity in mice by approximately 50% and this was observed throughout the study (P < 0.005). This is the first demonstration that CHL can provide potent chemoprotection in a transplacental carcinogenesis model and support a mechanism involving complex-mediated reduction of carcinogen uptake.
Fazit: Chlorophyllin gibt einen signifikant wirksamen Schutz gegen die Entwicklung von experimentell ausgelöstem Krebs.