scholarly journals In VitroAntiophidian Mechanisms ofHypericum brasilienseChoisy Standardized Extract: Quercetin-Dependent Neuroprotection

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Cháriston André Dal Belo ◽  
Ana Paula de Bairros Lucho ◽  
Lúcia Vinadé ◽  
Leandro Rocha ◽  
Hildegardo Seibert França ◽  
...  

The neuroprotection induced byHypericum brasilienseChoisy extract (HBE) and its main active polyphenol compound quercetin, againstCrotalus durissus terrificus(Cdt) venom and crotoxin and crotamine, was enquired at both central and peripheral mammal nervous system. Cdt venom (10 μg/mL) or crotoxin (1 μg/mL) incubated at mouse phrenic nerve-diaphragm preparation (PND) induced an irreversible and complete neuromuscular blockade, respectively. Crotamine (1 μg/mL) only induced an increase of muscle strength at PND preparations. At mouse brain slices, Cdt venom (1, 5, and 10 μg/mL) decreased cell viability. HBE (100 μg/mL) inhibited significantly the facilitatory action of crotamine (1 μg/mL) and was partially active against the neuromuscular blockade of crotoxin (1 μg/mL) (data not shown). Quercetin (10 μg/mL) mimicked the neuromuscular protection of HBE (100 μg/mL), by inhibiting almost completely the neurotoxic effect induced by crotoxin (1 μg/mL) and crotamine (1 μg/mL). HBE (100 μg/mL) and quercetin (10 μg/mL) also increased cell viability in mice brain slices. Quercetin (10 μg/mL) was more effective than HBE (100 μg/mL) in counteracting the cell lysis induced by Cdt venom (1 and 10 μg/mL, resp.). These results and a further phytochemical and toxicological investigations could open new perspectives towards therapeutic use ofHypericum brasiliensestandardized extract and quercetin, especially to counteract the neurotoxic effect induced by snake neurotoxic venoms.

Toxins ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 801
Author(s):  
Isadora Oliveira ◽  
Edson Yoshida ◽  
Murilo Dini ◽  
Ana Paschoal ◽  
José Cogo ◽  
...  

Systemic envenomation by Crotalus durissus terrificus (South American rattlesnake) can cause coagulopathy, rabdomyolysis, acute kidney injury, and peripheral neuromuscular blockade, the latter resulting in flaccid paralysis. Previous studies have shown that plant products such as tannic acid and theaflavin can protect against the neuromuscular blockade caused by C. d. terrificus venom in vitro. In this work, we used mouse-isolated phrenic nerve-diaphragm preparations to examine the ability of caffeic acid, chlorogenic acid, and quercetin to protect against C. d. terrificus venom-induced neuromuscular blockade in vitro. In addition, the ability of tannic acid to protect against the systemic effects of severe envenomation was assessed in rats. Preincubation of venom with caffeic acid (0.5 mg/mL), chlorogenic acid (1 mg/mL), or quercetin (0.5 mg/mL) failed to protect against venom (10 μg/mL)-induced neuromuscular blockade. In rats, venom (6 mg kg−1, i.p.) caused death in ~8 h, which was prevented by preincubation of venom with tannic acid or the administration of antivenom 2 h post-venom, whereas tannic acid given 2 h post-venom prolonged survival (~18.5 h) but did not prevent death. Tannic acid (in preincubation protocols or given 2 h post-venom) had a variable effect on blood creatinine and urea and blood/urine protein levels and prevented venom-induced leukocytosis. Tannic acid attenuated the histological lesions associated with renal damage in a manner similar to antivenom. The protective effect of tannic acid appeared to be mediated by interaction with venom proteins, as assessed by SDS-PAGE. These findings suggest that tannic acid could be a potentially useful ancillary treatment for envenomation by C. d. terrificus.


BMJ Open ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. e043935
Author(s):  
Xuan Wang ◽  
Yingyuan Li ◽  
Chanyan Huang ◽  
Wei Xiong ◽  
Qin Zhou ◽  
...  

IntroductionDespite the use of quantitative neuromuscular monitoring together with the administration of reversal drugs (neostigmine or sugammadex), the incidence of residual neuromuscular blockade defined as a train-of-four ratio (TOFr) <0.9 remains high. Even TOFr >0.9 cannot ensure adequate recovery of neuromuscular function when T1 height is not recovered completely. Thus, a mathematical correction of TOFr needs to be applied because the return of a normal TOFr can precede the return of a normal T1 twitch height. On the other hand, different muscles have different sensitivities to neuromuscular blockade agents; thus, complete recovery of one specific muscle group does not represent complete recovery of all other muscles. Therefore, our study aims to assess the muscle strength recovery of respiratory-related muscle groups by ultrasound and evaluate global strength using handgrip dynamometry in the early postoperative period when TOFr=0.9 and corrected TOFr (cTOFr)=0.9 with comparison of neostigmine versus sugammadex as reversal drugs.Methods and analysisThis study will be a prospective, single-blinded, randomised controlled trial involving 60 patients with American Society of Anesthesiologists physical status I–II and aged between 18 and 65 years, who will undergo microlaryngeal surgery. We will assess geniohyoid muscle, parasternal intercostal muscle, diaphragm, abdominal wall muscle and handgrip strength at four time points: before anaesthesia, TOFr=0.9, cTOFr=0.9 and 30 min after admission to the post anaesthesia care unit. Our primary objective will be to compare the effects of neostigmine and sugammadex on the recovery of muscle strength of different muscle groups in the early postoperative period when TOFr=0.9 and cTOFr=0.9. The secondary objective will be to observe the difference of muscle strength between the time points of TOFr=0.9 and cTOFr=0.9 to find out the clinical significance of cTOFr >0.9.Ethics and disseminationThe protocol was reviewed and approved by the Ethics Committee of The First Affiliated Hospital, Sun Yat-sen University. The findings will be disseminated to the public through peer-reviewed scientific journals.Trial registration numberChiCTR2000033832.


Toxicon ◽  
2019 ◽  
Vol 168 ◽  
pp. S13
Author(s):  
Leonardo Melo ◽  
Lidiane Nunes Barbosa ◽  
Rui Seabra Ferreira Junior ◽  
Benedito Barraviera ◽  
Luciana Curtolo De Barros ◽  
...  

PLoS ONE ◽  
2017 ◽  
Vol 12 (11) ◽  
pp. e0187857 ◽  
Author(s):  
Jacqueline Farinha Shimizu ◽  
Carina Machado Pereira ◽  
Cintia Bittar ◽  
Mariana Nogueira Batista ◽  
Guilherme Rodrigues Fernandes Campos ◽  
...  

2004 ◽  
Vol 100 (6) ◽  
pp. 1519-1525 ◽  
Author(s):  
Jean-Pierre Estebe ◽  
Robert R. Myers

Background Amitriptyline is a tricyclic antidepressant drug used systemically for the management of neuropathic pain. Antidepressants, as a class of drugs with direct neurologic actions, are becoming widely used for the management of chronic pain, although their mechanisms are not entirely understood. Amitriptyline exerts potent effects on reuptake of norepinephrine and serotonin and blocks alpha 2A adrenoreceptors and N-methyl-D-aspartate receptors. Because amitriptyline is also a particularly potent blocker of sodium channels and voltage-gated potassium and calcium channels, it has been recommended as a long-acting local anesthetic agent. Unfortunately, amitriptyline has significant toxic side effects in the central nervous system and cardiovascular system that are dose-related to its systemic administration. Therefore, before amitriptyline can be used clinically as a local anesthetic agent, it should be thoroughly explored with respect to its direct neurotoxic effect in the peripheral nervous system. Methods The left sciatic nerve of Sprague-Dawley rats (12/ group) received a single topical amitriptyline dose of 0.625, 1.25, 2.5, or 5 mg; a saline group (n = 2) was used as control. Neuropathologic evaluations were conducted in separate animals (n = 4) 1, 3, and 7 days later. Results Amitriptyline topically applied in vivo to rat sciatic nerve causes a dose-related neurotoxic effect. Drug doses of 0.625-5 mg all caused Wallerian degeneration of peripheral nerve fibers, with the number of affected fibers and the severity of the injury directly related to the dose. Conclusion Because the effective local anesthetic dose is within this dose range, the authors strongly recommend that amitriptyline not be used as a local anesthetic agent.


Zoo Biology ◽  
2007 ◽  
Vol 26 (2) ◽  
pp. 155-160 ◽  
Author(s):  
Rogério Loesch Zacariotti ◽  
Kathleen Fernandes Grego ◽  
Wilson Fernandes ◽  
Sávio Stefanini Sant'Anna ◽  
Marcelo Alcindo de Barros Vaz Guimarães

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Rafael M. Ximenes ◽  
Marcelo M. Rabello ◽  
Renata M. Araújo ◽  
Edilberto R. Silveira ◽  
Fábio H. R. Fagundes ◽  
...  

Secretory phospholipases A2(sPLA2) exert proinflammatory actions through lipid mediators. These enzymes have been found to be elevated in many inflammatory disorders such as rheumatoid arthritis, sepsis, and atherosclerosis. The aim of this study was to evaluate the effect of harpalycin 2 (Har2), an isoflavone isolated fromHarpalyce brasilianaBenth., in the enzymatic, edematogenic, and myotoxic activities of sPLA2fromBothrops pirajai, Crotalus durissus terrificus, Apis mellifera,andNaja najavenoms. Har2 inhibits all sPLA2tested. PrTX-III (B. pirajaivenom) was inhibited at about 58.7%, Cdt F15 (C. d. terrificusvenom) at 78.8%, Apis (from bee venom) at 87.7%, and Naja (N. najavenom) at 88.1%. Edema induced by exogenous sPLA2administration performed in mice paws showed significant inhibition by Har2 at the initial step. In addition, Har2 also inhibited the myotoxic activity of these sPLA2s. In order to understand how Har2 interacts with these enzymes, docking calculations were made, indicating that the residues His48 and Asp49 in the active site of these enzymes interacted powerfully with Har2 through hydrogen bonds. These data pointed to a possible anti-inflammatory activity of Har2 through sPLA2inhibition.


1973 ◽  
Vol 135 (1) ◽  
pp. 73-79 ◽  
Author(s):  
J. F. Giorgini ◽  
F. L. De Lucca

Instability of 28S rRNA of Crotalus durissus terrificus liver was observed during hotphenol extraction: purified 28S rRNA is converted into an 18S RNA component by heat treatment. It was also found that ‘6S’ and ‘8S’ low-molecular-weight RNA species were released during the thermal conversion. This conversion and the release of the low-molecular-weight species were also induced by 8m-urea and 80% (v/v) dimethyl sulphoxide at 0°C. Evidence is presented that this phenomenon is an irreversible process and results from the rupture of hydrogen bonds. The 18S RNA product was shown to be homogeneous by polyacrylamide-gel electrophoresis and by sucrose-density-gradient centrifugation. The base composition of the 18S RNA products obtained by heat, urea or dimethyl sulphoxide treatments was similar. The C+G content of the 18S RNA product was different from that of the native 18S rRNA, but similar to that of 28S rRNA.


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