Hamamelitannin

Biological & Pharmaceutical Bulletin, 1995, 18(1):59-63.

Protective activity of hamamelitannin on cell damage induced by superoxide anion radicals in murine dermal fibroblasts.[Pubmed: 7735252]

METHODS AND RESULTS:
Previously we demonstrated that Hamamelitannin (2',5-di-O-galloyl hamamelose) in Hamamelis virginiana L. exhibits potent superoxide-anion scavenging activity. We then examined the physiological and pharmacological activities of Hamamelitannin as well as its functional homologues, gallic acid and syringic acid. The following results were obtained: (1) Hamamelitannin has a higher protective activity against cell damages induced by superoxide anions than gallic acid which is the functional moiety of Hamamelitannin. The protective activity of Hamamelitannin on murine fibroblast-damage induced by superoxide anions was found at a minimum concentration of 50 microM, while the corresponding figure for gallic acid was 100 microM. (2) Pre-treatment of fibroblasts with Hamamelitannin enhances cell survival. (3) The superoxide-anion scavenging activity of the compound in terms of its IC50 value (50% inhibition concentration of superoxide anion radicals generated) was evaluated by ESR spin-trapping.
CONCLUSIONS:
Both Hamamelitannin (IC50 = 1.31 +/- 0.06 microM) and gallic acid (IC50 = 1.01 +/- 0.03 microM) exhibited high superoxide-anion scavenging activity followed by syringic acid (IC50 = 13.90 +/- 2.38 microM). (4) When Hamamelitannin was treated with superoxide anions generated by a KO2-crown ether system, HPLC analysis showed the disappearance of Hamamelitannin and the concomitant formation of Hamamelitannin-derived radicals (g = 2.005, delta H1 = 2.16 G, delta H2 = 4.69 G) was detected by ESR spectrometry.

Sci Rep. 2016 Feb 1;6:20321.

The Quorum Sensing Inhibitor Hamamelitannin Increases Antibiotic Susceptibility of Staphylococcus aureus Biofilms by Affecting Peptidoglycan Biosynthesis and eDNA Release.[Pubmed: 26828772 ]

Treatment of Staphylococcus aureus infections has become increasingly challenging due to the rapid emergence and dissemination of methicillin-resistant strains. In addition, S. aureus reside within biofilms at the site of infection. Few novel antibacterial agents have been developed in recent years and their bacteriostatic or bactericidal activity results in selective pressure, inevitably inducing antimicrobial resistance. Consequently, innovative antimicrobials with other modes of action are urgently needed. One alternative approach is targeting the bacterial quorum sensing (QS) system. Hamamelitannin (2',5-di-O-galloyl-d-hamamelose; HAM) was previously suggested to block QS through the TraP QS system and was shown to increase S. aureus biofilm susceptibility towards vancomycin (VAN) although mechanistic insights are still lacking.
METHODS AND RESULTS:
In the present study we provide evidence that HAM specifically affects S. aureus biofilm susceptibility through the TraP receptor by affecting cell wall synthesis and extracellular DNA release of S. aureus. We further provide evidence that HAM can increase the susceptibility of S. aureus biofilms towards different classes of antibiotics in vitro.
CONCLUSIONS:
Finally, we show that HAM increases the susceptibility of S. aureus to antibiotic treatment in in vivo Caenorhabditis elegans and mouse mammary gland infection models.

Journal of Antimicrobial Chemotherapy, 2013, 68(1):126-130.

In vivo antibiofilm effect of cerium, chitosan and hamamelitannin against usual agents of catheter-related bloodstream infections.[Pubmed: 22991425]

Catheter-related bloodstream infections (CRBSIs) are common healthcare-associated infections associated with increased morbidity and medical costs. Antiseptic- and antibiotic-coated central venous catheters (CVCs) have been proposed to reduce the incidence of CRBSIs, with variable success. The aim of this study was to determine the in vivo antibiofilm activity of biocompatible and inexpensive compounds, such as cerium nitrate, chitosan and Hamamelitannin, against usual agents of CRBSIs.
METHODS AND RESULTS:
The antibiofilm effect of cerium nitrate, chitosan and Hamamelitannin was tested against Staphylococcus epidermidis, Staphylococcus aureus, Acinetobacter baumannii and Candida albicans in a mouse foreign body infection model, using polyurethane catheter segments. Biofilm formation was assessed with a crystal violet assay to quantify the total biomass, with a tetrazolium reduction assay to quantify the metabolic activity and with scanning electron microscopy. At subinhibitory concentrations, cerium nitrate significantly reduced biofilm formation by C. albicans, chitosan significantly decreased biofilm formation by S. epidermidis and C. albicans, and Hamamelitannin significantly inhibited all bacterial biofilms.
CONCLUSIONS:
The in vivo antibiofilm effect of cerium nitrate against C. albicans and of chitosan against C. albicans and S. epidermidis, at subinhibitory concentrations, makes them promising alternatives to coat CVCs. Moreover, the microbicidal effect on a wider range of CVC colonizers was previously reported in vitro for both compounds, at higher concentrations. For all bacterial strains, the highest in vivo antibiofilm efficacy was achieved with Hamamelitannin. For A. baumannii, this is the first report of in vivo inhibition.

Journal of Natural Products, 2012, 75(1):26-33.

Hamamelitannin from witch hazel (Hamamelis virginiana) displays specific cytotoxic activity against colon cancer cells.[Pubmed: 22216935]

Hamamelis virginiana (witch hazel) bark is a rich source of condensed and hydrolyzable tannins reported to exert a protective action against colon cancer. The present study characterizes different witch hazel tannins as selective cytotoxic agents against colon cancer.
METHODS AND RESULTS:
To cover the structural diversity of the tannins that occur in H. virginiana bark, the hydrolyzable tannins, Hamamelitannin and pentagalloylglucose, together with a proanthocyanidin-rich fraction (F800H4) were selected for the study. Treatment with these compounds reduced tumor viability and induced apoptosis, necrosis, and S-phase arrest in the cell cycle of HT29 cells, with Hamamelitannin being the most efficient. Owing to polyphenol-mediated H(2)O(2) formation in the incubation media, the antiproliferative effect was determined in the presence and absence of catalase to rule out any such interference. The presence of catalase significantly changed the IC(50) only for F800H4. Furthermore, at concentrations that inhibit the growth of HT29 cells by 50%, Hamamelitannin had no harmful effects on NCM460 normal colonocytes, whereas pentagalloylglucose inhibited both cancerous and normal cell growth.
CONCLUSIONS:
Using the TNPTM assay, we identified a highly reactive phenolic position in Hamamelitannin, which may explain its efficacy at inhibiting colon cancer growth.