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PubMed2002

GAP-43 expression and pathological changes of temporal infarction in rats and effects of batroxobin.

UNLABELLED: To study the changes of the expression of growth-associated protein-43 (GAP-43) and pathology in temporal infarction of rats photochemically induced and the effects of batroxobin. METHODS: Immunohistochemical technique and hematoxylin-eosin stain was used to show the changes of the expression of GAP-43 and pathology. RESULTS: In infarction group, GAP-43 expression was markedly increased on the infarction and surrounding tissues at 24 h cerebral infarction. The expression reached peak level at 72 h after cerebral infarction and was decreased at 7 d after cerebral infarction. However, in batroxobin-treated group, GAP-43 expression was increased and the pathological changes were much slight as compared with infarction group. CONCLUSION: The expression of GAP-43 increases in infarction of temporal neocortex and batroxobin promotes the expression of GAP-43 and ameliorates the pathological changes in infarction of temporal neocortex.

Animals↗
PubMed2003

[The effect of batroxobin on atherosclerosis].

To study the effect of batroxobin(DF-521) on atherosclerosis, we divided 50 Japanese big ear rabbits into control group and high-lipid group. After the atherosclerosis model was successfully established, the high-lipid rabbits were divided into 3 groups(placebo group, treatment group 1 and treatment group 2). Batroxobin was injected in the treatment groups, and saline was injected in placebo group and control group. Getting the aorta before, inter and after treatment, dyeing the lipid, endothelium, smooth muscle, collagen fibers of the vascular plaque(the elastic fibers are of autofluorescence), we observed them with the light microscope and laser scanning confocal microscope. From the results, we found that the atherosclerotic plaque in the treatment groups, tended to be static four weeks later, but there was no obvious difference between treatment group 1 and treatment group 2. These implied that batroxobin possessed the action of stabilizing the atherosclerotic plaque, but the dosage-effect was not clear and the principle needed more study.

Animals↗
PubMed1995

Carbohydrate structure analysis of batroxobin, a thrombin-like serine protease from Bothrops moojeni venom.

The carbohydrate side chains of batroxobin were liberated from tryptic glycopeptides by treatment with peptide-N4-(N-acetyl-beta-glucosaminyl)asparagine amidase F, pyridylaminated and separated by two-dimensional HPLC. Neutral oligosaccharide derivatives obtained after desialylation were characterized by methylation analysis, liquid secondary-ion mass spectrometry, digestion with exoglycosidases and endoglycosidases and, in part, by acetolysis, whereas sialic acid constituents were identified by reverse-phase HPLC after conjugation with 1,2-diamino-4,5-methylene-dioxybenzene. The overall glycosylation status of the protein was studied by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). The results revealed that batroxobin is heterogeneously glycosylated carrying predominantly diantennary, partially incomplete complex-type glycans in addition to hybrid-type species. Most glycans were core-fucosylated at C6 of the innermost GlcNAc. As a characteristic feature, galactose was completely replaced by GalNAc beta 4-substituents in complex-type antennae, the GlcNAc-residues of which were, in part, fucosylated at C3. Furthermore, evidence was obtained that suggested the presence of a novel type of glycoprotein-N-glycan comprising two GalNAc beta 4GlcNAc beta 4GlcNAc beta 2Man-antennae. Sialic acid residues represented a mixture of N-acetylneuraminic acid (Neu5Ac) and N-acetyl-4-O-acetylneuraminic acid (Neu4,5Ac2), which were exclusively linked to C3 of subterminal GalNAc. A precise assignment of these sialic acid derivatives to distinct oligosaccharide structures or antennae, however, was not carried out. Finally, MALDI-TOF-MS demonstrated that both potential N-glycosylation sites of batroxobin are substituted by carbohydrate chains. In conclusion, our studies revealed that this snake venom glycoprotein is characterized by a unique oligosaccharide pattern partly comprising novel structural elements.

Animals↗
PubMed1993

The cleavage sequence of fibrinopeptide A from fibrinogen fragment E by thrombin, atroxin or batroxobin.

Calculations of data from fibrin polymerization and cross-linking experiments infer that thrombin-catalysed release of the second of the two fibrinopeptides A (FpA2) from fibrinogen is concerted, although other data suggest that FpA2 release is random. In the concerted pattern of FpA release, divalent monomer (des AA-fibrin) formation predominates throughout the enzymatic conversion of fibrinogen to fibrin, an effect leading to relatively rapid fibril assembly. Alternatively, random FpA2 release would result in a substantial population of monovalent monomer (des A-fibrin) intermediates during early and intermediate phases of the enzymatic conversion to fibrin. Their formation would cause a delay in fibrin fibril assembly. In order to address the question of the pattern of FpA release directly, we purified plasmic fibrinogen fragment E1 isoforms containing both FpA sequences and studied the sequence of FpA release by thrombin or batroxobin. Des A-fragment E1 intermediates formed by loss of one FpA (FpA1), and des AA-fragment E1 products (lacking both FpA1 and FpA2) were identified by analytical isoelectric focusing and quantified by densitometry. The catalytic rate of release of FpA1 (k1) and FpA2 (k2) by thrombin or batroxobin was similar. The ratio of these rates, k2:k1, was 1.10 +/- 0.42 for thrombin and 1.34 +/- 0.26 for batroxobin. These findings indicate that these enzymes cleave FpA2 randomly from fragment E1.

Batroxobin↗
PubMed1992

Novel structure of the N-acetylgalactosamine containing N-glycosidic carbohydrate chain of batroxobin, a thrombin-like snake venom enzyme.

The structure of the Asn-linked carbohydrate chain of batroxobin, a thrombin-like enzyme from Bothrops atrox moojeni snake venom, has been determined. The sugar chain was isolated from batroxobin by hydrazinolysis followed by pyridylamination (PA). The PA-oligosaccharide chain was purified by HPLC on an anion exchange or reverse phase columns, and its structure was examined by sequential exoglycosidase digestion, 600 MHZ 1H NMR spectroscopy and methylation analysis. The results indicate that the oligosaccharide chain has the following structure involving a novel linkage, NeuAc alpha 2----3GalNAc.

Acetylgalactosamine↗
PubMed2003

Activated thrombin-activatable fibrinolysis inhibitor attenuates spontaneous fibrinolysis of batroxobin-induced fibrin deposition in rat lungs.

Studies have shown that inhibition of TAFI by small peptides enhances pharmacological effects of tPA in animal models of thrombosis, suggesting that TAFI modulates the fibrinolytic system. In this study, we investigated the effect of activated human TAFI (TAFIa) on endogenous fibrinolysis in a rat model of intravascular fibrin deposition. (125)I-labeled fibrinogen was injected intravenously followed by a bolus injection of batroxobin, a thrombin-like enzyme. Batroxobin cleaved fibrinogen to form insoluble fibrin that was deposited in tissues, including the lungs. This was shown by a decrease of radioactivity in the blood as a result of consumption of (125)I-labeled fibrinogen and an elevation of radioactivity in the lungs 5 min following batrox-obin administration. Endogenous fibrinolysis was detected by a gradual increase in radioactivity in the blood and a decrease in radioactivity in the lungs at 30 min, an indication of radiolabeled fibrin degradation products (FDPs) being released into the circulation from the tissues. Intravenous administration of human TAFIa dose-dependently attenuated the later phase reduction of radioactivity in the lungs. When the dose of TAFIa was 218 micro g/kg, giving a peak plasma level of TAFIa 0.9 +/- 0.05 micro g/ml, the spontaneous fibrinolysis was completely prevented. These results provide direct evidence that an increase in circulating TAFIa impairs endogenous clot lysis in a rat model of fibrin deposition.

Animals↗
PubMed1986

Metabolic fate of 125I-labeled batroxobin in rats and dogs.

125I-Labeled batroxobin was prepared and following its intravenous and subcutaneous administrations to rats and dogs, the blood radioactivity was determined. In the both species following the intravenous injections, the decrease in radioactivity was biexponential. Following subcutaneous administration, radioactivity became maximal at 6h and decreased in a manner similar to that of the beta-phase of the intravenous injection. The blood concentration of fibrinogen in dogs was also determined. After the intravenous injection, fibrinogen became undetectable 1h later, and appeared again in the blood at 24h. After the subcutaneous injection, the decrease was not so rapid. Fibrinogen resumed its original levels at 7 day after the administration in both the routes. Radioactivity after the both injections was excreted generally in the urine in about the same amounts. The total urinary and fecal excretions in rats and dogs were 80 and 95%, respectively. The distribution of radioactivity in the tissues was examined by counting technique and whole-body autoradiography. Radioactivity predominantly accumulated in the thyroid and stomach and could also be found in the kidneys and liver in fair amounts. The distribution patterns of radioactivity for both the routes of administrations and also for male and pregnant rats were basically the same. In fetus rats, a slight distribution was noted. From the results of gel filtration chromatography and trichloroacetic acid fractionation, [125I] batroxobin was metabolized soon after the administration to afford low molecular substances such as 125I-ion in the plasma and urine.

Animals↗
PubMed2006

[Batroxobin in patients with ischemic stroke in the carotid system (the multicenter study)].

A randomized placebo-controlled study has been carried out in 3 Moscow hospitals. A sample included 90 patients who survived hemispheric ischemic stroke caused by pathology in the internal carotid artery 72 h before the treatment. Forty-five patients were given standard (basic) therapy and 45 patients received adjuvant batroxobin intravenously by 1,0 ml (10BU) drops on day 1, 3 and 5 and by 0,5 ml (5BU) drops on day 7 and 9 after admitting in a hospital. Assessment of the patients' state was conducted before the treatment, on day 3, 6 and 15. The European Stroke Scale was used to measure severity of clinical symptoms. The results suggest efficacy of batroxobin the use of which provides rapid good results, especially improvement in movement disorders. The use of this drug is accompanied by defibrinating effect. The drug is well tolerated.

Batroxobin↗
PubMed1997

Application of thrombin based fibrin glue and non-thrombin based batroxobin glue on intact human blood vessels: evidence for transmural thrombin activity.

An alternative method of uniting small diameter vessels to obtain tissue union while limiting the thrombogenic effect of suture placement at a vessel anastomosis involves the use of a thrombin based fibrin glue as a surgical sealant. This investigation addresses whether the in vitro application of a thrombin based glue (TG), or batroxobin glue (BG), a non-thrombin based glue made with the snake venom enzyme batroxobin, alters intravascular platelet deposition (PD) or cleaves blood fibrinogen, as measured by fibrinopeptide A (FPA) production, when the respective glue is applied to the external surface of an intact human placental artery or an artery with an anastomosis. When TG was applied to the adventitial surface of an intact vessel or an anastomosis (n = 7) of control and experimental vessels, there was a significant increase in intraluminal platelet deposition, an effect not realized with BG (n = 12, intact vessel TG p = 0.01, BG p = 0.66, anastomosis TG p <0.01, BG p <0.01). Both TG and BG significantly increased FPA levels when human whole blood was perfused through both intact vessels or vessels containing an anastomosis when compared to control vessels (intact vessel TG and BG p <0.01, anastomosis TG and BG p <0.01). Labelled thrombin studies document the rapid passage of thrombin through an intact vessel wall or vessels with an anastomosis when TG was applied to the adventitial surface of the vessel. The data suggest that TG and BG are drug delivery systems for their respective enzymes that either pass through or transfer a message across not only a surgically created anastomosis, but also an intact vessel wall.

Batroxobin↗
PubMed1989

[The use of Soviet substitutes for batroxobin in the determination of fibrinogen].

Plasma fibrinogen was measured by kinetic photometry with two Soviet analogs of the foreign agent batroxobin: ancistron-N and agichal, obtained from Central Asian Aspidelaps lubricus venom by different techniques. Both the preparations of thrombin-like enzyme from the venom have proved to be adequate substituents of batroxobin; the optimal concentration of ancistron-N for this test was found to be 20 micrograms/ml or 0.04 U/ml, that of agichal 0.5 micrograms/ml.

Fibrinogen↗
PubMed1977

The activation of plasma factor XIII with the snake venom enzymes ancrod and batroxobin marajoensis.

The snake venom enzymes Ancrod and Batroxobin marajoensis are able to activate human plasma factor XIII as shown by the formation of the gamma-dimers. The concentration of gamma-dimers increases with the concentration of the activating enzymes. Factor XIII activated by Ancrod or Batroxobin marajoensis is, however, unable to catalyse the incorporation of the amine dansyl-cadaverine into casein. The partially activated factor XIII is therefore not demonstrable by means of the artificial test system. This factor XIII loses little activity and remains activable by thrombin.

Ancrod↗
PubMed1987

Release of plasminogen activator by batroxobin.

In the isolated perfused pig ear, batroxobin caused a dose-dependent increase in the release of plasminogen activator. The activator-releasing effect required the presence of the active enzyme. The activator released was of the tissue-type.

Animals↗
PubMed1992

The effect of batroxobin on cochlear blood flow.

Cochlear blood flow is considered to be closely related to cochlear function. Among several etiologic factors implicated in inner ear diseases, disturbance of local blood flow is held to be one of the most important. With this in view, various pharmaceuticals are currently being used to increase local blood flow in patients with inner ear diseases. In the control of blood flow there are three major factors; systemic blood pressure (perfusion pressure), vascular tone, and blood viscosity. Batroxobin (BX) was developed to increase local blood flow by lowering blood viscosity through defibrinogenation; it is used in the treatment of thrombosis and occasionally for the treatment of sudden deafness. In the present study, we observed the effect of BX on cochlear blood flow in guinea pigs, using a laser Doppler flowmeter, and measured the blood fibrinogen concentration after BX infusion. There was an obvious increase in cochlear blood flow during the observation period of 3 h after 10 BU/kg were infused, and a slight increase when 2 BU/kg were infused. Blood fibrinogen levels decreased dramatically by 30 min after BX infusion (10 BU/kg), and the extremely low level attained was maintained throughout the 3-h observation period. Hemorrhage from the surgically opened ear was noted in 2 animals during the experiment and rectal bleeding in one.

Animals↗
PubMed2000

Effect of batroxobin against dog heart ischemia/reperfusion injury.

AIM: To study the effect of batroxobin(Bat) on dog heart ischemia/reperfusion (I/R) injury. METHODS: Dog heart I/R injury was induced by occluding the left anterior descending coronary artery for 30 min and restoring blood perfusion for 90 min. Bat was intravenously injected before heart ischemia and 15 min before reperfusion. Plasma creatine kinase (CK), lactate dehydrogenase (LDH), and myocardial malondiaedehyde (MDA) concentrations were measured. The pathologic changes of I/R myocardium were observed. RESULTS: Bat reduced the mortality rate of I/R dog (I/R group 65.0% vs Bat-I group 30.0% and Bat-II group 28.6%, P < 0.05). Myocytes of I/R heart showed intracellular edema, damaged mitochondria, and concentrated nucleus. Bat decreased these changes. In Bat-I and Bat-II group, plasma CK and LDH level were reduced, the +dp/dtmax and -dp/dtmax at 30 min after ischemia and 90 min after reperfusion were elevated, and left ventricular end dilation pressure (LVEDP) was lowered. The myocardial MDA contents were decreased by 42.3% and 38.1% (P < 0.01) in Bat-I and Bat-II group, respectively. CONCLUSION: Bat may exert an apparent role against dog heart ischemia/reperfusion injury and improve myocardial function.

Animals↗
PubMed2000

Influence of batroxobin on cerebral ischemia-reperfusion injury in gerbils.

AIM: To study the effects of batroxobin (Bat) on neurons survival, neurobehavioral test, ATP levels and hydroxyl radical outputs in hippocampus during forebrain ischemia-reperfusion in gerbils. METHODS: The forebrain ischemia was induced by occluding the bilateral common carotid arteries for 10 min in gerbils, and ATP levels and 2, 3-dihydroxybenzoic acid (DHBA) outputs were assayed by HPLC. The neurons survival were assessed by histology, and behavioral tests of gerbils were assessed by open field test. RESULTS: The number of neurons survival in Ir at d 7 postischemic insult were (7 +/- 4)% of sham-operated gerbils, much less than that in Bat (45 +/- 16)%. The levels of explore activities of ischemic gerbils was 175% and 159% of sham-operated gerbils at d 3 and d 6 postischemic insult, much more than that in Bat (120% d 3 and 140% d 6). Hippocampal ATP levels in Ir were 64% of sham-operated gerbils at reperfusion 60 min, much less than that in Bat I and II (82% and 89% respectively). The hippocampal 2,3-DHBA outputs in Ir increased by 4.5 folds of sham-operated gerbils at reperfusion 60 min, but the 2,3-DHBA outputs in Bat I and Bat II were only 2.6 and 2.4 folds respectively. CONCLUSION: Bat possesses the inhibitory effects on DND and OH. production following cerebral ischemia-reperfusion in gerbils.

Adenosine Triphosphate↗
PubMed2004

Batroxobin reduces intracellular calcium concentration and inhibits proliferation of vascular smooth muscle cells.

BACKGROUND: Batroxobin (BX), a serine protease used in defibrinogenation and thrombolysis, also has an effect on c-fos gene and growth factor. This study attempted to determine the effects of BX on the proliferation of vascular smooth muscle cells (VSMCs) and calcium metabolism. METHODS: VSMCs were treated with BX at concentrations of 0.1, 0.3, or 1.0 mmol/L and cell numbers were determined at 0, 24, 48, and 72 hours. Intracellular calcium concentration ([Ca2+]i) was measured using direct fluorescence methods. RESULTS: BX was found to suppress proliferation of VSMCs in a dose-dependent fashion with inhibition rates of 18% and 31% by 48 and 72 hours, respectively. In addition, BX decreases basal [Ca2+]i significantly. The basal level in untreated cells was 162.7 +/- 33.8 nmol/L, and decreased to 131.5 +/- 27.7 nmol/L, 128.3 +/- 28.5 nmol/L, and 125.6 +/- 34.3 nmol/L with the three concentrations of BX, respectively. Noradrenaline (NE)-induced [Ca2+]i stimulation was also attenuated by BX (0.1 mmol/L BX, 20% +/- 8% inhibition; 0.3 mmol/L BX, 54% +/- 11% inhibition; 1.0 mmol/L BX, 62% +/- 15% inhibition). The ability of NE to stimulate [Ca2+]i was attenuated in cultures in Ca(2+)-free medium, as was the ability of BX to blunt NE-induced stimulation. CONCLUSION: These findings demonstrate that BX can effectively inhibit proliferation of VSMCs, probably by blocking the release and uptake of Ca2+, thus influencing [Ca2+]i.

Animals↗
PubMed1991

[Kinetic fibrinogen determination with batroxobin (reptilase)].

A kinetic turbidity-producing method for fibrinogen determination on the basis of reptilase reagent (batroxobin) is described. The method, which is in good agreement with method by Clauss shows comparable precision, is marked out by the possibility of objective photometric measurement. Reagent stability, use of undiluted test plasma and single-point calibration are further advantages. The method is insensitive to heparin. With regards to FDP it is less disturbed than the method by Clauss. In case of adaptation to a modern photometer a clear rationalization effect can be achieved.

Batroxobin↗
PubMed1976

Comparison of the actions of thrombin and the thrombin-like venom enzymes ancrod and batroxobin.

Thrombin acts on several coagulant proteins to produce products with physiologic, pharmacologic and pathologic potential. The most sensitive thrombin substrate seems to be factor VIII. Some thrombin dependent reactions studied in vitro and proposed as control reactions seem too insensitive to the action of thrombin to be of in vivo significance. The only enzymic reaction the thrombin-like venom enzymes, Ancrod and Batroxobin, have in common with thrombin is the removal of fibrinopeptide A.

Ancrod↗