Ankaferd hemostat: from molecules to medicine

Ankaferd hemostat (ABS; Ankaferd Blood Stopper®, Istanbul, Turkey) is a hemostatic agent having an impact on red blood cell­ fibrinogen interactions. The hemostatic effect of ABS depends upon the quick promotion of a protein network, particularly fibrinogen gamma, in relation to the erythrocyte aggregation. The entire physiological process involves ABS-induced formation of the protein network by vital erythrocyte aggregation. Vital erythrocyte aggregation occurs with the spectrine, ankyrin, and actin proteins on the membrane of the red blood cells. ABS notably affects cell metabolism and cell cycle mechanisms. Meanwhile, ABS has antiproliferative effects on cancer cells. The aim of this review is to assess molecular basis of ABS as a hemostatic drug. The literature search on ABS was performed in PubMed, Web of Science (SCI expanded), and Scopus with particular focus on the studies of molecular basis of ABS, in vivo research, case series, and controlled randomized clinical studies. Current perspective for the utilization of ABS is to provide hemostasis with accelerating wound healing. Future controlled trials are needed to elucidate the pleiotropic clinical effects of ABS such as antineoplastic, antiinflammatory, antiinfective, antifungal, and antioxidative effects.

Effects of Ankaferd Hemostat on Helicobacter pylori strains and antibiotic resistance

Background/aim: Ankaferd hemostat (ABS; Ankaferd blood stopper, Istanbul, Turkey) is a folkloric medicinal plant extract. The aim of this study was to determine the effect of Ankaferd hemostat (ABS) on the fate of Helicobacter pylori strains. The study also aims to determine alterations in the antimicrobial resistance of three different H. pylori strains in response to ABS exposure. Materials and methods: H. pylori Strain 1 was obtained from the culture collection ATCC 43504 and passaged three times for viability. Strain 2 was isolated from a gastric ulcer patient and Strain 3 was isolated from a gastritis patient. 1% of ABS was added to all of the strains and antimicrobial susceptibility was observed on 30 and 60 min after application. Results: The efficacy of ABS solutions in achieving significant logarithmic reduction in foodborne pathogens of H. pylori was observed in this study. This study showed that ABS has antibacterial (Anti-H. pylori) effects. Conclusion: Our present study indicated, for the first time, that ABS could act against H. pylori. ABS is clinically used for the management of GI bleeding due to benign and malignant GI lesions. Thus, the possible anti-H. pylori effect of ABS shall expand the therapeutic spectrum of the drug in GI lesions in relation to H. pylori infection such as peptic ulser disease (PUD) and lymphoid tissue (MALT) lymphomagenesis.

Effects of Ankaferd Hemostat on red blood cell aggregation: a hemorheological study

Background/aim: Ankaferd hemostat (ABS; Ankaferd blood stopper, Istanbul, Turkey) is a prohemostatic agent affecting erythrocytes. The hemostatic action of ABS depends upon fibrinogen gamma chain, prothrombin, and red blood cells. The aim of this study was to assess the effects of ABS on erythrocyte aggregation via hemorheological analyses. Materials and methods: To measure erythrocyte aggregation, blood samples were obtained from healthy, nonsmoker volunteers who had not taken any medication in the previous 10 days. One mL of blood was placed into the laser-assisted optical rotational cell analyzer (LORCA), into the chamber formed by the gap between two concentric glass cylinders. The solution prepared with ABS and saline was added to blood in incremental amounts of 10 µL, 20 µL, 30 µL, 40 µL, 50 µL, 60 µL, 70 µL, and 100 µL. Erythrocyte aggregation was determined by laser-assisted optical rotational cell analyzer at 37 °C Results: AMPwas found to be 17.7 ± 2.1 au in the blood without ABS, whereas it was lower in the blood with ABS. AMP was 16.0 ± 3.3 in the ABS-added blood group. RBC aggregates did not form faster when cells contacted ABS. The t t½ value was 4.6 ± 2.6 in the ABS-added blood group and 1.9 ± 0.20 in the control group. Aggregation was faster in the control group (P = 0.03). AI, which is a combination of AMP and t½, was lowered in the ABS group (48.7 ± 12.3) compared to the control group (65.8 ± 1.6) (P = 0.02). It was notable that the γIsc max (sec-1) value of the control was higher (200 ± 106) than the ABS-added blood group (141 ± 51.0). Conclusion: ABS has antierythroid aggregation effect. ABS inhibits pathological aggregation of red blood cells. Antithrombotic clinical effects of ABS may be ascribed to the antierythroid aggregan actions of the drug.