TL;DR: This study demonstrates that Phe193 plays a more significant role than His192 in determining substrate specificity and inhibition resistance in TSV-PA, and possesses a 8–9-fold increased activity for plasminogen and becomes sensitive to bovine pancreatic trypsin inhibitor.
TL;DR: In this article, a process for preparing an autologous platelet gel and membranes thereof comprising mixing a platelet concentrate with a calcium salt and batroxobin is described, which allows to overcome the prior art processes drawbacks connected with the use of human of bovine thrombin.
Abstract: A process is disclosed for preparing an autologous platelet gel and membranes thereof comprising mixing a platelet concentrate with a calcium salt and batroxobin. This process encompassing the use of batroxobin as the gel activator allows to overcome the prior art processes drawbacks connected with the use for the same purpose of human of bovine thrombin. A kit is also described for carrying out this process.
TL;DR: Since all these three enzymes enhance fibrinolysis similarly during defibrination therapy, the neutralization or inactivation of the inhibitors of fibrinelysis appeared not to represent the main mechanism for the enhancement.
Abstract: Reptilase, defibrase and ancrod are thrombin-like venom enzymes that cleave fibrinogen to release fibrinopeptide-A and generate fibrin monomers. Although these enzymes decrease fibrinogen levels in vivo, presumably by enhancing fibrinolytic activity, the mechanism has not been identified. In the present study, we analyzed their effects on the inhibitors of fibrinolysis. Plasminogen activator inhibitor-1 (PAI-1) was cleaved at its C-terminus by reptilase and lost its specific activity. Alpha2-antiplasmin (alpha2-AP) was cleaved both at the Pro19-Leu20 peptide bond and at its C-terminus by reptilase, and also lost its specific activity. The apparent second-order rate constants (mol/l per min per Batroxobin unit) were 0.22 for the cleavage of PAI-1 (3.2 micromol/l) and 0.19 for that of alpha2AP (6.4 micromol/l), which were approximately 200-fold lower than that (47.0) for the cleavage of fibrinogen (1.1 micromol/l). Neither defibrase nor ancrod cleaved and inactivated these inhibitors. Only reptilase enhanced euglobulin clot lysis in vitro at high concentration, due probably to PAI-1 inactivation. Since all these three enzymes enhance fibrinolysis similarly during defibrination therapy, the neutralization or inactivation of the inhibitors of fibrinolysis appeared not to represent the main mechanism for the enhancement.
TL;DR: In this paper, a process for preparing an autologous platelet gel and membranes thereof comprising mixing a platelet concentrate with a calcium salt and batroxobin is described, which allows to overcome the prior art processes drawbacks connected with the use of human of bovine thrombin.
Abstract: A process is disclosed for preparing an autologous platelet gel and membranes thereof comprising mixing a platelet concentrate with a calcium salt and batroxobin. This process encompassing the use of batroxobin as the gel activator allows to overcome the prior art processes drawbacks connected with the use for the same purpose of human of bovine thrombin. A kit is also described for carrying out this process.
TL;DR: Batroxobin can improve spatial memory disorder in temporal ischemic rats, and the down-regulation of the expression of c-Jun is probably related to the neuroprotective mechanism.
TL;DR: Batroxobin can improve spatial memory disorder of temporal ischemic rats; and the down-regulation of the expression of HSP32 and HSP70 is probably related to the attenuation of isChemic injury.
TL;DR: The neurological function was recovered significantly better than the control group even at 10 days after batroxobin treatment had been stopped, and the serum fibrinogen level was decreased significantly in the test group,and the side effects were well tolerated.
Abstract: Objective This paper is to evaluate the efficacy and safety of batroxobin in treatment of acute cerebral infarctions.Methods A multicenter,randomized,doubleblind,placebo controlled clinical trial was conducted,including a test group and a control group.The patients in each group were treated with wei nao lu tong injection(a kind of traditional treatment in acute cerebral infarctions)as a basic treatment.Batroxobin was added to the test group,while the placebo (normal saline) was added to the control group every other day for 3 days altogether.Results The clinical effects in the test group were observed significantly earlier than the control group,and the neurological function was recovered significantly better than the control group even at 10 days after batroxobin treatment had been stopped.The serum fibrinogen level was decreased significantly in the test group,and the side effects were well tolerated.Conclusion Batroxobin is effective and safe in treatment for patients with acute cerebral infarctions.
TL;DR: A method of inhibiting apoptosis, comprising administering an effective ingredient batroxobin, was proposed by as discussed by the authors, which is a method of reducing the number of apoptosis cells.
Abstract: A method of inhibiting apoptosis, comprising administering an effective ingredient batroxobin.
TL;DR: In this paper, a process for preparing an autologous platelet gel and membranes thereof comprising mixing a platelet concentrate with a calcium salt and batroxobin is described, which allows to overcome the prior art processes drawbacks connected with the use of human of bovine thrombin.
Abstract: A process is disclosed for preparing an autologous platelet gel and membranes thereof comprising mixing a platelet concentrate with a calcium salt and batroxobin. This process encompassing the use of batroxobin as the gel activator allows to overcome the prior art processes drawbacks connected with the use for the same purpose of human of bovine thrombin. A kit is also described for carrying out this process.
TL;DR: Batroxobin might restore the blood circulation of stasis band of burn wound, so as to accelerate wound healing and to improve the quality of healed skin.
Abstract: Objective To investigate the effects of batroxobin on the healing of and microcirculatory blood flow in deep partial thickness burn wound in rats. Methods Wistar rat inflicted by 4 cmx 4 cm deep partial thickness scalding on the back was taken as the model. Twenty male rats were randomly divided into scalding burn group and batroxobin treatment group. Cutaneous blood flow volume was measured before and at 0.5, 2, 4, 6, 12, 24 and 72 postburn hours (PBH). Scalding and residual burn wound areas were measured immediately and on the 14th and 18th postburn day (PBD). The rats were sacrificed on 30th PBD and the cutaneous samples were harvested for hair follicle counting and histological examination with LM. Results The cutaneous blood flow volume of rats in single burn group decreased progressively during 2-72 PBHs. But in batroxobin treating group, cutaneous blood flow volume improved evidently and the wound healing accelerated obviously with increased cutaneous appendages formation. Conclusion Batroxobin might restore the blood circulation of stasis band of burn wound, so as to accelerate wound healing and to improve the quality of healed skin.
TL;DR: Bat may exert an apparent role against dog heart ischemia/reperfusion injury and improve myocardial function.
Abstract: 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.
TL;DR: The presence of two new forms of a thrombin-like enzyme, both with apparent molecular masses of 38 kDa, in Bothrops atrox venom are described, sharing 80% homology with batroxobin and flavoxobin.
Abstract: This article describes the presence of two new forms of a thrombin-like enzyme, both with apparent molecular masses of 38 kDa, in Bothrops atrox venom. Both share the ability to cleave fibrinogen into fibrin and to digest casein. Both present identical K(m) on the substrate BApNA. Their N-terminal amino acid sequences are identical for 26 residues, sharing 80% homology with batroxobin and flavoxobin. Two groups of monoclonal antibodies (mAbs) raised against the purified enzyme forms recognized different epitopes of the putative corresponding enzymes present in B. atrox crude venom. On Western blotting analysis of B. atrox crude venom, mAbs 5DB2C8, 5AA10 and 5CF11, but not mAbs 6CC5 and 6AD2-G5, revealed two or more protein bands ranging from 25 to 38 kDa. By immunoprecipitation assays, the 6AD2-G5 mAb was able to precipitate protein bands of 36-38 kDa from B. atrox, B. leucurus, B. pradoi, B. moojeni, B. jararaca and B. neuwiedii crude venoms. Fibrinogen-clotting activity was inhibited when the same venom specimens were pre-incubated with mAb 6AD2-G5, except for B. jararaca and B. neuwiedii.