Demonstration of the histopathological and immunohistochemical effects of a novel hemostatic agent, ankaferd blood stopper, on vascular tissue in a rat aortic bleeding model

Abstract

BackgroundAnkaferd Blood Stopper® (ABS) is a folkloric medicinal plant extract used as a hemostatic agent in traditional Turkish medicine. This experimental study investigated the histopathological and immunohistochemical effects of ABS on vascular tissue in a rat model of aortic bleeding.MethodsFour groups of 11 Wistar albino rats were used. The abdominal aortas of the rats were wounded; an ABS-soaked tampon was applied to rats in Groups 1 and 3, and a plain gauze tampon was applied to rats in Groups 2 and 4 until the bleeding stopped. The bleeding time was recorded. Immediately following sacrificing, the arteriotomy sites from Groups 1 and 2 were removed. The abdominal incisions in Groups 3 and 4 were closed following hemostasis. On Day 7 of the study, Group 3 and 4 rats were sacrificed and the abdominal aorta arteriotomy sites were removed for histopathological and immunohistochemical evaluation.ResultsThe mean bleeding time in 15 animals in Groups 2 and 4 was 4.9 ± 0.6 s, and in 22 animals in Groups 1 and 3 was 3.1 ± 0.6 s. Distal aortic occlusion was not observed on either Day 1 or 7 in any group. Significantly more widespread and dense endothelial nitric oxide synthase (eNOS) staining was observed in Group 1 animals than Group 2. On Days 1 and 7 after application of ABS, histopathological changes, consisting of necrosis, inflammation, and endothelial cell loss, in the rat abdominal aortas did not differ between Groups 1 and 2. The basophilic discoloration in the ABS group on the operation day was a result of a foreign body reaction and hemosiderin-loaded histiocyte accumulation, which occurred on Day 7.ConclusionsIn this study, hemostasis was successfully achieved with ABS in rat abdominal aortas. No histopathological change was found in the rat abdominal aortas between the ABS and control groups on Days 1 and 7. Further studies on the long-term effects of foreign body reactions and hemosiderin-loaded histiocyte accumulation are required.

New hemostatic agent: the effect of Ankaferd Blood Stopper on healing wounds in experimental skin incision model

“…The activation of plasma fibrinogen decreases, and the fibrinogen antigen levels decrease with an extension of the thrombin time. In addition, the total protein, albumin, and globulin levels decrease (1)(2)(3)(4)(5)(6).…”

“…As observed by electron microscopy, ABS aggregates blood cells, especially erythrocytes and active leukocytes. The basic mechanism of ABS involves the formation of encapsulated proteins, which serve as foci of erythrocyte aggregation (1)(2)(3)(4)(5)(6).…”

Histopathological Alterations in the Kidney Tissue Following Topical Ankaferd Hemostat Application in a Rat Renal Injury Model

“…Therefore, there are molecular links underlying ABSpleiotropic cellular actions acting on anti-infective, wound healing, and apoptotic processes. 1,6,7,10,13,17,[24][25][26][27][28][29][30][31][32] Since renal system is located at the crossroads of cellular neoplastic development and protein secretions, the unique effects of ABS on distinct renal cell types shall be investigated in future in vivo animal models mimicking cancer models. Our present study represent true basis for the design of such experimental animal trials.…”

Striking Promotion of the in vitro Myeloma Monoclonal Immunoglobulin Aggregation by Ankaferd Hemostat

“…The concept of ABS-induced hemostatic network has been developed via MALDI-TOF proteomic molecular analyses, cytometric arrays, transciption analysis, and SEM ultrastructural examinations as well as numerous investigations interacting with in vitro and in vivo research settings. [1][2][3][15][16][17][18][19][20] Essential erythroid proteins (Ankrin recurrent and FYVE bundle containing protein 1, Spectrin alpha, Actin-depolimerisation factor, Actin-depolimerizing factor, LIM bundle and actine binding subunit 1 isoform a, LIM bundle and actine binding subunit 1 isoform b, NADP-dependent malic enzyme, NADH dehydrogenase (Ubiquinone) 1 alpha subcomplex, Mitochondrial NADP (+) dependent malic enzyme 3, Ribulose bisphosphatecarbocsilase large chain, Maturase K) and the required ATP bioenergy (ATP synthase, ATP synthase beta subunit, ATP synthase alpha subunit, ATP-binding protein C12, TP synthase H+ transporter protein, ADF, Alpha-1,2-glycosyltransferase ALG10-A) are included in the protein library of ABS. ABS also upregulates GATA/FOG transcription system affecting erythroid functions and urotensin II.…”

“…15,16 Those concepts have been developed via MALDI-TOF proteomic molecular analyses, cytometric arrays, transciption analysis, and SEM ultrastructural examinations as well as numerous investigations interacting with in vitro and in vivo research settings. [1][2][3][15][16][17][18][19][20] ABS has many cellular effects. 1,[21][22][23] ABS has been shown to affect renal tubular apoptosis based on the level of hemorrhage.…”